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1
DiSanto, J. P., D. Guy-Grand, A. Fisher, and A. Tarakhovsky. "Critical role for the common cytokine receptor gamma chain in intrathymic and peripheral T cell selection." Journal of Experimental Medicine 183, no. 3 (March 1, 1996): 1111–18. http://dx.doi.org/10.1084/jem.183.3.1111.
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The common cytokine receptor gamma chain (gammac), which is a functional subunit of the receptors for interleukins (IL)-2, -4, -7, -9, and -15, plays an important role in lymphoid development. Inactivation of this molecule in mice leads to abnormal T cell lymphopoiesis characterized by thymic hypoplasia and reduced numbers of peripheral T cells. To determine whether T cell development in the absence of gammac is associated with alterations of intrathymic and peripheral T cell selection, we have analyzed gammac-deficient mice made transgenic for the male-specific T cell receptor (TCR) HY (HY/gammac- mice). In HY/gammac- male mice, negative selection of autoreactive thymocytes was not diminished; however, peripheral T cells expressing transgenic TCR-alpha and -beta chains (TCR-alphaT/betaT) were absent, and extrathymic T cell development was completely abrogated. In HY/gammac- female mice, the expression of the transgenic TCR partially reversed the profound thymic hypoplasia observed in nontransgenic gammac- mice, generating increased numbers of thymocytes in all subsets, particularly the TCR-alphaT/betaT CD8+ single-positive thymocytes. Despite efficient positive selection, however, naive CD8+ TCR-alphaT/betaT T cells were severely reduced in the peripheral lymphoid organs of HY/gammac- female mice. These results not only underscore the indispensible role of gammac in thymocyte development, but also demonstrate the critical role of gammac in the maintenance and/or expansion of peripheral T cell pools.
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Skoglund, G., A. Basmaciogullari, B. Rouot, JC Marie, and G. Rosselin. "Cell-specific localization of G protein alpha-subunits in the islets of Langerhans." Journal of Endocrinology 162, no. 1 (July 1, 1999): 31–37. http://dx.doi.org/10.1677/joe.0.1620031.
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G protein alpha-subunits are involved in the transduction of receptor-mediated regulation of insulin and glucagon secretions. To get further insight into the status of G proteins in alpha- and beta-cells of the Langerhans islets, we have used immunohistochemistry to study the distribution of alpha-subunits in pancreas sections from the rat. Our results show that only insulin-immunoreactive beta-cells display immunoreactivity for selective antibodies directed against the different members of the Galphas and Galpha12-families (alphas, alphaolf, and alpha12, alpha13 respectively). Immunoreactivities for antibodies directed against members of the Galphaq- and Galphai-families showed a more diverse localization: alpha11 and alphao2 were only detected in glucagon-immunoreactive alpha-cells, whereas alphai1 was detected in all beta-cells but only in a few alpha-cells. Even though beta-cells showed immunoreactivities for alphao-non-isoform-selective antibodies, we could not identify the isoform(s) present using selective alphao1 and alphao2 antibodies. Other members of the Galphai- and Galphaq-families (alphai3, alphat2, alphaz and alphaq) were detected in both alpha- and beta-cells. In conclusion, our findings demonstrate a clear difference in the localization of G protein alpha-subunits between alpha- and beta-cells, suggesting the involvement of specific receptor transduction pathways for the neuronal/hormonal regulation of alpha- and beta-cell functions.
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Pasenkiewicz-Gierula, M., and T. Róg. "Conformations, orientations and time scales characterising dimyristoylphosphatidylcholine bilayer membrane. Molecular dynamics simulation studies." Acta Biochimica Polonica 44, no. 3 (September 30, 1997): 607–24. http://dx.doi.org/10.18388/abp.1997_4409.
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The results of molecular dynamics simulation of fully hydrated dimyristoylphosphatidylcholine (DMPC) bilayer membrane in the liquid-crystalline phase are presented. They show that the probability of a gauche conformation varies periodically along the chain with only a slight increase towards the end of the chain. However, the frequency of transition between conformations increases, due to a decrease in the lifetime of the trans conformation, along the chain. The average lifetimes for trans conformations are in the range of 1-2 x 10(-10) s and for gauche conformations in the range of 4-7 x 10(-11) s. The alpha-chain of the DMPC head group has mainly an extended conformation, due to predominantly trans conformation of alpha5 torsion. The rotational correlation time for the P-N vector is 3.7 ns. The C2-C1-O11-P fragment of the DMPC head group (theta1, alpha1, alpha2 torsions) is rigid while the P-O12-C11-C12 fragment (alpha3, alpha4, alpha5 torsions) is flexible. The lateral diffusion coefficient for DMPC self-diffusion in the membrane is 2 x 10(-7) cm2/s; the rate of transverse diffusion is the same. Large differences in the calculated rotational correlation times for the alpha-, beta-, gamma-chains and for the O21-C1 vector indicate that in the liquid-crystalline bilayer each segment of the DMPC molecule exhibits its own rotational freedom, in addition to its internal flexibility resulting from rotational isomerism. The results obtained in these calculations, although in general agreement with some experimental data, shed new light on the dynamical behaviour of phosphatidylcholine molecules in the bilayer membrane in the liquid-crystalline phase.
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Jacques, T. S., J. B. Relvas, S. Nishimura, R. Pytela, G. M. Edwards, C. H. Streuli, and C. ffrench-Constant. "Neural precursor cell chain migration and division are regulated through different beta1 integrins." Development 125, no. 16 (August 15, 1998): 3167–77. http://dx.doi.org/10.1242/dev.125.16.3167.
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Proliferation and tangential migration of neural precursor cells are essential determinants of CNS development. We have established cell culture models of both these processes using neural precursor cells grown as neurospheres. The pattern of migration that we observe in these cells is homotypic and occurs in the absence of a glial or neuronal scaffold, and is therefore equivalent to that previously described as chain migration. To determine the role of integrins in proliferation and migration, we have analysed the expression pattern of integrins on neurosphere cells and then performed blocking peptide and antibody experiments. Neurosphere cells express five major integrins, alpha5 beta1, alpha 6Abeta1, alphav beta1, alphav beta5 and alpha vbeta8 and, in addition, express low levels of alpha 6Bbeta1. Chain migration is inhibited by blocking the alpha 6beta1 integrin. Proliferation, by contrast, is inhibited by blocking the other beta1 integrins, alphav beta1 and alpha5 beta1. These results show that integrins are important regulators of neural precursor cell behaviour, with distinct beta1 integrins regulating proliferation and migration. They also demonstrate a novel role for the alpha6 beta1 integrin in the cell-cell interactions underlying homotypic chain migration.
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Cerenak, Andreja, Zlatko Satovic, and Branka Javornik. "Genetic mapping of hop (Humulus lupulus L.) applied to the detection of QTLs for alpha-acid content." Genome 49, no. 5 (May 1, 2006): 485–94. http://dx.doi.org/10.1139/g06-007.
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The map locations and effects of quantitative trait loci (QTLs) were estimated for alpha-acid content in hop (Humulus lupulus L.) using amplified fragment length polymorphism (AFLP) and microsatellite marker (simple sequence repeat (SSR)) genetic linkage maps constructed from a double pseudotestcross. The mapping population consisted of 111 progeny from a cross between the German hop cultivar 'Magnum', which exhibits high levels of alpha-acids, and a wild Slovene male hop, 2/1. The progeny segregated quantitatively for alpha-acid content determined in 2002, 2003, and 2004. The maternal map consisted of 96 markers mapped on 14 linkage groups defining 661.90 cM of total map distance. The paternal map included 70 markers assigned to 12 linkage groups covering 445.90 cM of hop genome. QTL analysis indicated 4 putative QTLs (alpha1, alpha2, alpha3, and alpha4) on linkage groups (LGs) 03, 01, 09, and 03 of the female map, respectively. QTLs explained 11.9%–24.8% of the phenotypic variance. The most promising QTL to be used in marker-assisted selection is alpha2, the peak of which colocated exactly with the AFLP marker. Three chalcone synthase-like genes (chs2, chs3, and chs4) involved in hop bitter acid synthesis mapped together on LG04 of the female map. Saturation of the maps, particularly the putative QTL regions, will be carried out using SSR markers, and the stability of the QTLs will be tested in the coming years.Key words: Humulus lupulus L., genetic maps, alpha-acid content, QTLs.
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Aramini, J. "NMR solution structures of [d(GCGAAT-3'-3'-alphaT-5'-5'-CGC)2] and its unmodified control." Nucleic Acids Research 26, no. 24 (December 15, 1998): 5644–54. http://dx.doi.org/10.1093/nar/26.24.5644.
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Newberg, M. H., D. H. Smith, S. B. Haertel, D. R. Vining, E. Lacy, and V. H. Engelhard. "Importance of MHC class 1 alpha2 and alpha3 domains in the recognition of self and non-self MHC molecules." Journal of Immunology 156, no. 7 (April 1, 1996): 2473–80. http://dx.doi.org/10.4049/jimmunol.156.7.2473.
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Abstract The importance of the species of different domains of class I MHC molecules in peripheral T cell recognition and positive and negative selection was evaluated in a single system. In transgenic mice expressing AAD (containing the alpha1+alpha2 domains of HLA-A2.1 and the alpha3 domain of H-2Dd), the CTL response to influenza peptide M1(58-66) in the context of the alpha1+alpha2 domains of HLA-A2.1 was as strong as the influenza-specific H-2Db-restricted response. However, this strong response was only discernible if the target cell MHC molecule also contained a murine alpha3 domain. In contrast, the response in HLA-A2.1 transgenic mice was about 30-fold weaker, and these CTL were indifferent to the origin of the target molecule alpha3 domain. Further analysis suggested that the major impact of the murine alpha3 domain of the transgene product was to enhance positive selection of a low affinity population of AAD-restricted T cells, presumably through species-specific interaction with CD8. Surprisingly, the response to non-self human class I MHC determinants was not augmented in AAD mice, indicating that the T cells selected are narrowly focused on AAD-related structures. Further analysis indicated that the alphal+alpha2 domains as well as the alpha3 domain influenced the magnitude of the response to non-self human class I MHC determinants, and this effect was mapped to alpha2. We suggest that the alpha2 domains of murine class I molecules contain conserved structural elements that augment the avidity of T cell-class I interactions, and this is particularly important in the recognition of non-self MHC molecules.
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Caniggia, I., J. Liu, R. Han, J. Wang, A. K. Tanswell, G. Laurie, and M. Post. "Identification of receptors binding fibronectin and laminin on fetal rat lung cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 3 (March 1, 1996): L459—L468. http://dx.doi.org/10.1152/ajplung.1996.270.3.l459.
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Fibronectin and laminin have been implicated in regulating lung morphogenesis. In the present study, the cell surface receptors involved in fetal lung cell binding to laminin and fibronectin were identified. Messages for alpha5- and beta1-integrin subunits were detected in both fetal lung epithelial cells and fibroblasts. The presence of alpha5 beta1 -integrin on both cell types was demonstrated by immunocytochemistry and confirmed by cell adhesion experiments with fibronectin and RGD-containing peptides. Epithelial cells adhered more readily to laminin than fibroblasts. The alpha4 beta1-integrin, and RGD-independent fibronectin receptor, was weakly expressed on either cell type. Both cell types expressed alpha6-integrin subunit mRNA and stained immunopositive for the alpha6-subunit. Although either cell type expressed nonintegrin 67-kDa laminin-elastin receptor mRNA, no positive immunoreactivity for this laminin-elastin binding protein was detected. None of these findings explain the enhanced attachment of distal fetal lung epithelial cells to laminin compared with fibroblasts. Previously, we have reported that epithelial cells were enriched in alpha3-integrin subunit mRNA and protein expression. Herein, we found that epithelial cell attachment to laminin was nearly completely inhibited by alpha3- but only partially by alpha6 -monoclonal antibodies. A peptide near the globular region at the long arm of the laminin A-chain, which contained the IKVAV sequence, and the laminin A-chain amino acid sequence representing the alpha3 beta1 -integrin binding site, inhibited the adherence of epithelial cells to laminin. Fetal lung epithelial cells attached to substrata coated with the alpha3 beta1-integrin binding site peptide and the peptide containing the IKVAV sequence. These data suggest that both fetal lung cell types bind to fibronectin via the fibronectin receptor, alpha5 beta1, and fetal lung epithelial cells interact with laminin via alpha3 beta1 and proteins that recognize the IKVAV-containing sequence on the laminin A-chain.
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Chabot, V., T. Magallon, C. Taragnat, and Y. Combarnous. "Two free isoforms of ovine glycoprotein hormone alpha-subunit strongly differ in their ability to stimulate prolactin release from foetal pituitaries." Journal of Endocrinology 164, no. 3 (March 1, 2000): 287–97. http://dx.doi.org/10.1677/joe.0.1640287.
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alpha-Subunit dissociated from glycoprotein hormones has been previously shown to stimulate rat pituitary lactotroph differentiation and proliferation. However, whether the free form of the alpha-subunit (free alpha) can also play such a role is not known. To test whether free alpha may act on prolactin (PRL) release from ovine foetal pituitaries, this molecule was purified and two major isoforms, alphaA and alphaB were isolated. Free alphaA was found to be more acidic and more hydrophobic than both free alphaB and ovine LH alpha-subunit (oLHalpha). Free alphaA and oLHalpha exhibited a molecular mass of 14 kDa as determined by mass spectrometry, whereas free alphaB displayed a molecular mass of only 13.5 kDa because of its truncated N-terminus. All three alpha molecules bear mature-type N-linked saccharide chains including Nacetyl galactosamine residues but none of them contains O-linked oligosaccharide. The free alphaA isoform, more than the oLHalpha, was able to stimulate PRL release from ovine foetal pituitary explants in culture, whereas the free alphaB isoform displayed no activity. Moreover, the free alphaA and alphaB isoforms were able to recombine with the ovine LH beta-subunit (oLHbeta). The free alphaB/oLHbeta, and the oLHalpha/oLHbeta dimer were 4-fold more active than the free alphaA/oLHbeta dimer in a specific LH radioreceptor assay and in the stimulation of testosterone release from rat Leydig cells. The present study demonstrates that the two free alpha isoforms of ovine glycoprotein hormones exhibit distinct efficiencies in stimulating PRL release from ovine foetal pituitaries. Moreover, despite their identical ability to recombine with the oLHbeta, the free alpha isoform, which is the most efficient on PRL release, is the least efficient in conferring LH activity on the alpha/beta dimer.
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Leivo, I., T. Tani, L. Laitinen, R. Bruns, E. Kivilaakso, V. P. Lehto, R. E. Burgeson, and I. Virtanen. "Anchoring complex components laminin-5 and type VII collagen in intestine: association with migrating and differentiating enterocytes." Journal of Histochemistry & Cytochemistry 44, no. 11 (November 1996): 1267–77. http://dx.doi.org/10.1177/44.11.8918902.
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Anchoring complex component laminin-5 and its subunits laminin (Ln)-alpha3 and Ln-beta3 chains, Type VII collagen, and integrin chains alpha3, alpha6, and beta4 were studied in developing and adult human intestine and compared with findings on Ln-alpha1 and Ln-alpha2 chains. In adult human duodenum, jejunum, and ileum, Ln-5 detected with a polyclonal antiserum and Ln-alpha3 and Ln-beta3 chains, detected with monoclonal antibodies (MAbs), were restricted to the epithelial basement membranes (BMs) of villi, whereas Ln-alpha2 chain was seen only focally in crypt bottoms. In double labeling experiments, the stretch of crypt BM corresponding to the proliferative cell compartment was found to be devoid of both Ln-alpha3 and Ln-alpha2 chains. Double labeling for Ln-5 and proliferating cell nuclear antigen also showed an abrupt onset of Ln-5 expression exactly at the upper edge of the proliferative cell compartment. Type VII collagen was negligible in duodenum and showed a rising duodenal-ileal gradient localizing to villar BMs. Double labeling for Ln-5 and Type VII collagen, however, indicated only partial co-distribution in the intestine. Electron microscopy of ileum revealed both anchoring filaments and anchoring fibrils but no hemidesmosomal plaques. Our results demonstrate the expression of Ln-5 in BMs outside of stratified epithelia and indicate that Ln-5 in the intestine is associated with the compartment of migrating and differentiating enterocytes. Absence of hemidesmosomes and the presence of other anchoring complex components, such as Ln-5, Type VII collagen, and integrin chains alpha3, alpha6, and beta4, suggests unique properties for epithelial cell attachment in the intestine.
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Sastry, S. K., M. Lakonishok, D. A. Thomas, J. Muschler, and A. F. Horwitz. "Integrin alpha subunit ratios, cytoplasmic domains, and growth factor synergy regulate muscle proliferation and differentiation." Journal of Cell Biology 133, no. 1 (April 1, 1996): 169–84. http://dx.doi.org/10.1083/jcb.133.1.169.
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The role of integrins in muscle differentiation was addressed by ectopic expression of integrin alpha subunits in primary quail skeletal muscle, a culture system particularly amenable to efficient transfection and expression of exogenous genes. Ectopic expression of either the human alpha5 subunit or the chicken alpha6 subunit produced contrasting phenotypes. The alpha5-transfected myoblasts remain in the proliferative phase and are differentiation inhibited even in confluent cultures. In contrast, myoblasts that overexpress the alpha6 subunit exhibit inhibited proliferation and substantial differentiation. Antisense suppression of endogenous quail alpha6 expression inhibits myoblast differentiation resulting in sustained proliferation. These effects of ectopic alpha subunit expression are mediated, to a large extent, by the cytoplasmic domains. Ectopic expression of chimeric alpha subunits, alpha5ex/6cyto and alpha6ex/5cyto, produced phenotypes opposite to those observed with ectopic alpha5 or alpha6 expression. Myoblasts that express alpha5ex/6cyto show decreased proliferation while differentiation is partially restored. In contrast, the alpha6ex/5cyto transfectants remain in the proliferative phase unless allowed to become confluent for at least 24 h. Furthermore, expression of human alpha5 subunit cytoplasmic domain truncations, before and after the conserved GFFKR motif, shows that this sequence is important in alpha5 regulation of differentiation. Ectopic alpha5 and alpha6 expression also results in contrasting responses to the mitogenic effects of serum growth factors. Myoblasts expressing the human alpha5 subunit differentiate only in the absence of serum while differentiation of untransfected and alpha6-transfected myoblasts is insensitive to serum concentration. Addition of individual, exogenous growth factors to alpha5-transfected myoblasts results in unique responses that differ from their effects on untransfected cells. Both bFGF or TGFbeta inhibit the serum-free differentiation of alpha5-transfected myoblasts, but differ in that bFGF stimulates proliferation whereas TGF-beta inhibits it. Insulin or TGF-alpha promote proliferation and differentiation of alpha5-transfected myoblasts; however, insulin alters myotube morphology. TGF-alpha or PDGF-BB enhance muscle alpha-actinin organization into myofibrils, which is impaired in differentiated alpha5 cultures. With the exception of TGF-alpha, these growth factor effects are not apparent in untransfected myoblasts. Finally, myoblast survival under serum-free conditions is enhanced by ectopic alpha5 expression only in the presence of bFGF and insulin while TGF-alpha and TGF-beta promote survival of untransfected myoblasts. Our observations demonstrate (1) a specificity for integrin alpha subunits in regulating myoblast proliferation and differentiation; (2) that the ratio of integrin expression can affect the decision to proliferate or differentiate; (3) a role for the alpha subunit cytoplasmic domain in mediating proliferative and differentiative signals; and (4) the regulation of proliferation, differentiation, cytoskeletal assembly, and cell survival depend critically on the expression levels of different integrins and the growth factor environment in which the cells reside.
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Li, Jifen, and Glenn L. Radice. "A New Perspective on Intercalated Disc Organization: Implications for Heart Disease." Dermatology Research and Practice 2010 (2010): 1–5. http://dx.doi.org/10.1155/2010/207835.
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Adherens junctions and desmosomes are intercellular adhesive junctions and essential for the morphogenesis, differentiation, and maintenance of tissues that are subjected to high mechanical stress, including heart and skin. The different junction complexes are organized at the termini of the cardiomyocyte called the intercalated disc. Disruption of adhesive integrity via mutations in genes encoding desmosomal proteins causes an inherited heart disease, arrhythmogenic right ventricular cardiomyopathy (ARVC). Besides plakoglobin, which is shared by adherens junctions and desmosomes, other desmosomal components, desmoglein-2, desmocollin-2, plakophilin-2, and desmoplakin are also present in ultrastructurally defined fascia adherens junctions of heart muscle, but not other tissues. This mixed-type of junctional structure is termed hybrid adhering junction or area composita. Desmosomal plakophilin-2 directly interacts with adherens junction protein alphaT-catenin, providing a new molecular link between the cadherin-catenin complex and desmosome. The area composita only exists in the cardiac intercalated disc of mammalian species suggesting that it evolved to strengthen mechanical coupling in the heart of higher vertebrates. The cross-talk among different junctions and their implication in the pathogenesis of ARVC are discussed in this review.
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Chung, Fa-Po, Yenn-Jiang Lin, Shih-Lin Chang, Li-Wei Lo, Yu-feng Hu, Ta-Chuan Tuan, Tze-Fan Chao, Jo-Nan Liao, and Shih-Ann Chen. "B-PO03-134 DECREASED EXPRESSION OF PLAKOPHILIN-2 AND ALPHAT-CATENIN IN ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY: POTENTIAL MARKERS FOR EARLY DIAGNOSIS." Heart Rhythm 18, no. 8 (August 2021): S243—S244. http://dx.doi.org/10.1016/j.hrthm.2021.06.608.
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Moretti, D. V., A. Prestia, G. Binetti, O. Zanetti, and G. B. Frisoni. "Alpha and Theta EEG Rhythms Activity Reveal Deep Changes in Resting Brain State in Subjects with Prodromal Alzheimer's Disease." Journal of Aging and Gerontology 2, no. 1 (February 5, 2014): 13–23. http://dx.doi.org/10.12974/2309-6128.2014.02.01.3.
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The increase of EEG alpha3/alpha2 frequency power ratio has been associated with AD-converters subjects with mild cognitive impairment (MCI) as well as a reduction in the regional cerebral blood flow (rCBF). In this study, the association between alpha3/alpha2 frequency power ratio with rCBF changes in subjects with MCI was evaluated. The alpha3/alpha2 frequency power ratio was computed in 27 subjects with MCI. Two groups were obtained according to the median values of alpha3/alpha2, at a cut-off of 1.17. In the groups so obtained, the correlation between brain perfusion and EEG markers were detected. In the MCI group with the alpha3/alpha2 frequency power ratio above 1,17 as compared to the group with alpha3/alpha2 frequency power ratio below 1.17 there was: 1) a constant trend to lower rCBF values; 2) smaller hippocampal volumes; 3) higher theta frequency power. The higher EEG alpha3 /alpha2 frequency power ratio individuates two different group of MCI subjects. A complex interplay between alpha and theta rhythms activity MCI patients is suggested in patients with prodromal Alzheimer's disease.
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Moretti, D. V., O. Zanetti, G. Binetti, and G. B. Frisoni. "Quantitative EEG Markers in Mild Cognitive Impairment: Degenerative versus Vascular Brain Impairment." International Journal of Alzheimer's Disease 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/917537.
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We evaluated the relationship between brain rhythmicity and both the cerebrovascular damage (CVD) and amygdalohippocampal complex (AHC) atrophy, as revealed by scalp electroencephalography (EEG) in a cohort of subjects with mild cognitive impairment (MCI). All MCI subjects underwent EEG recording and magnetic resonance imaging. EEGs were recorded at rest. Relative power was separately computed for delta, theta, alpha1, alpha2, and alpha3 frequency bands. In the spectral band power the severity of CVD was associated with increased delta power and decreased alpha2 power. No association of vascular damage was observed with alpha3 power. Moreover, the theta/alpha1 ratio could be a reliable index for the estimation of the individual extent of CV damage. On the other side, the group with moderate hippocampal atrophy showed the highest increase of alpha2 and alpha3 power. Moreover, when the amygdalar and hippocampal volumes are separately considered, within amygdalohippocampal complex (AHC), the increase of theta/gamma ratio is best associated with amygdalar atrophy whereas alpha3/alpha2 ratio is best associated with hippocampal atrophy. CVD and AHC damages are associated with specific EEG markers. So far, these EEG markers could have a prospective value in differential diagnosis between vascular and degenerative MCI.
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Buenafe, A. C., R. C. Tsu, B. Bebo, A. C. Bakke, A. A. Vandenbark, and H. Offner. "A TCR V alpha CDR3-specific motif associated with Lewis rat autoimmune encephalomyelitis and basic protein-specific T cell clones." Journal of Immunology 158, no. 11 (June 1, 1997): 5472–83. http://dx.doi.org/10.4049/jimmunol.158.11.5472.
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Abstract To investigate TCR V alpha gene expression in the Lewis rat model of experimental autoimmune encephalomyelitis, we obtained V alpha chain sequences from two V beta8.2+-encephalitogenic, BP72-89-specific T cell clones. Two different V alpha genes, a V alpha2 gene and a V alpha23 gene, are utilized, but both were found to contain an asparagine repeat (Asn3+) sequence present in the V alpha CDR3 region. This Asn3+ motif is also present in the previously reported sequence of a BP68-88-specific hybridoma, 510, which utilizes a different V alpha2 gene family member. In further experiments, spinal cord T cells were isolated at the onset of basic protein (BP)-induced disease and sorted for the OX-40 activation marker, which we have previously used to enrich for specifically activated T cells. Analysis of V alpha expression in the OX-40+ population revealed the biased use of three V alpha genes, V alpha1, V alpha2, and V alpha23. The Asn3+ motif was present in the V alpha CDR3 region of V alpha1, V alpha2, and V alpha23 cDNA derived from OX-40+ spinal cord T cells but found to be generally absent in the OX-40- spinal cord population. Since these Asn3+ motif-bearing V alpha chain sequences are nearly identical to those utilized by the BP-specific encephalitogenic clones described, it is likely that these V alpha sequences are derived from disease-associated T cells in the spinal cord. Thus, we demonstrate that the Asn3+ V alpha CDR3 motif is strongly associated with experimental autoimmune encephalomyelitis in the Lewis rat and propose that it plays a role in TCR recognition of a specific BP peptide/MHC complex.
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Bealer, S. L. "Preoptic recess alpha-adrenoceptors control cardiovascular responses to hyperosmolality." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 4 (April 1, 1997): R1283—R1289. http://dx.doi.org/10.1152/ajpregu.1997.272.4.r1283.
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The roles of alpha-adrenoceptors in the anteroventral third ventricle (AV3V) and diagonal band of Broca (DBB) in cardiovascular responses to peripheral hypertonicity were investigated in conscious rats. Normal artificial cerebrospinal fluid (aCSF) or aCSF containing phentolamine (alpha1- and alpha2-antagonist), yohimbine (alpha2-antagonist), or prazosin (alpha1-antagonist) was perfused through microdialysis probes in the DBB, AV3V, or lateral ventricle during a 30-min infusion of isotonic (0.17 M; 0.1 or 1.7 ml x kg(-1) x min(-1) i.v.) or hypertonic (2.5 M; 0.1 ml x kg(-1) x min(-1) i.v.) NaCl. Hypertonic infusion increased blood pressure [mean arterial blood pressure (MAP); 17 +/- 2 mmHg] and decreased heart rate (HR; 36 +/- 6 beats/min). Both responses were abolished by AV3V administration of phentolamine or yohimbine, whereas prazosin selectively prevented the bradycardia. Phentolamine in the DBB or lateral ventricle did not alter either response. Stimulation of AV3V alpha1-adrenoceptors (phenylephrine) decreased HR and MAP, whereas alpha2-adrenoceptor stimulation (clonidine) produced bradycardia but increased MAP. Data suggest that alpha-adrenoceptors in the AV3V, but not the DBB, regulate cardiovascular responses to hyperosmolality.
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Donson, D., H. Borrero, M. Rutman, R. Pergolizzi, N. Malhado, and S. Macphail. "Gene transfer directly demonstrates a role for TCR V alpha elements in superantigen recognition." Journal of Immunology 158, no. 11 (June 1, 1997): 5229–36. http://dx.doi.org/10.4049/jimmunol.158.11.5229.
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Abstract Recent structure-function studies of ours and others indicating that regions of the TCR other than V beta are involved in the TCR-superantigen (SAg)-MHC class II trimolecular interaction were correlative; thus, while the conclusions were persuasive, they were not unequivocal. The transfection experiments described in this report show that 1) responsiveness to staphylococcal enterotoxin B in V beta6 T cells was transferred by a V alpha4- but not by V alpha8- and V alpha10-containing alpha-chain cDNA constructs, 2) responsiveness was not transferred by a chimeric alpha-chain construct containing the N and J regions from a responsive T hybrid clone and the V alpha10 V alpha region from a nonresponsive clone, and 3) responsiveness was transferred by a chimeric alpha-chain construct in which most of the V alpha region (from the N terminus to the C-terminal end of the complementarity-determining region 2) was derived from the V alpha4 alpha-chain of a responsive T hybrid and the rest (framework 3, N, and J) from the V alpha8 alpha-chain of a nonresponsive T hybrid. Thus, these data provide the first direct evidence for a specific SAg response facilitating activity in a defined V alpha segment and map this activity N-terminal of framework region 3. Furthermore, the diversity in the alpha- and beta-chain junctional regions of a panel of staphylococcal enterotoxin B-responsive V beta6 T hybrid clones excludes a stringent corequirement for a particular junctional region for the V alpha4 segment to mediate its facilitating activity. Finally, a model postulating a universal role for V alpha elements in TCR recognition of SAg is presented.
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Williams, M. W., W. G. Resneck, T. Kaysser, J. A. Ursitti, C. S. Birkenmeier, J. E. Barker, and R. J. Bloch. "Na,K-ATPase in skeletal muscle: two populations of beta-spectrin control localization in the sarcolemma but not partitioning between the sarcolemma and the transverse tubules." Journal of Cell Science 114, no. 4 (February 15, 2001): 751–62. http://dx.doi.org/10.1242/jcs.114.4.751.
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We used immunological approaches to study the factors controlling the distribution of the Na,K-ATPase in fast twitch skeletal muscle of the rat. Both alpha subunits of the Na,K-ATPase colocalize with beta-spectrin and ankyrin 3 in costameres, structures at the sarcolemma that lie over Z and M-lines and in longitudinal strands. In immunoprecipitates, the alpha1 and alpha2 subunits of the Na,K-ATPase as well as ankyrin 3 associate with beta-spectrin/alpha- fodrin heteromers and with a pool of beta-spectrin at the sarcolemma that does not contain alpha-fodrin. Myofibers of mutant mice lacking beta-spectrin (ja/ja) have a more uniform distribution of both the alpha1 and alpha2 subunits of the Na,K-ATPase in the sarcolemma, supporting the idea that the rectilinear sarcomeric pattern assumed by the Na,K-ATPase in wild-type muscle requires beta-spectrin. The Na,K-ATPase and beta-spectrin are distributed normally in muscle fibers of the nb/nb mouse, which lacks ankyrin 1, suggesting that this isoform of ankyrin is not necessary to link the Na,K-ATPase to the spectrin-based membrane skeleton. In immunofluorescence and subcellular fractionation experiments, the alpha2 but not the alpha1 subunit of the Na,K-ATPase is present in transverse (t-) tubules. The alpha1 subunit of the pump is not detected in increased amounts in the t-tubules of muscle from the ja/ja mouse, however. Our results suggest that the spectrin-based membrane skeleton, including ankyrin 3, concentrates both isoforms of the Na,K-ATPase in costameres, but that it does not play a significant role in restricting the entry of the alpha1 subunit into the t-tubules.
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Hiki, Yutaka, Ken-ichi Iyama, Junji Tsuruta, Hiroshi Egami, Takihiro Kamio, Shuji Suko, Ichiro Naito, Yoshikazu Sado, Yoshifumi Ninomiya, and Michio Ogawa. "Differential distribution of basement membrane type IV collagen alpha1(IV), alpha2(IV), alpha5(IV) and alpha6(IV) chains in colorectal epithelial tumors." Pathology International 52, no. 3 (March 2002): 224–33. http://dx.doi.org/10.1046/j.1440-1827.2002.01341.x.
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McDonough, A. A., Y. Zhang, V. Shin, and J. S. Frank. "Subcellular distribution of sodium pump isoform subunits in mammalian cardiac myocytes." American Journal of Physiology-Cell Physiology 270, no. 4 (April 1, 1996): C1221—C1227. http://dx.doi.org/10.1152/ajpcell.1996.270.4.c1221.
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The cardiac Na+ pump (Na+ -K+ -ATPase) provides the driving force for the Na+/Ca2+ exchanger, a determinant of intracellular Ca2+ stores. Three Na+ pump alpha-catalytic subunit isoforms are expressed in human heart, alpha1 and alpha2 are expressed in rat heart, and only alpha1 is expressed in guinea pig heart. The objective of this study was to determine whether there are isoform-specific patterns of expression in the transverse tubules (T tubules) vs. the peripheral sarcolemma. In adult rat cardiomyocytes, anti-alpha1-specific antibodies labeled the T tubules more intensely than the peripheral sarcolemma, in which labeling was patchy, the same pattern reported for distribution of the Na+/Ca2+ exchanger (J. S. Frank, G. Mottino, D. Reid, R. S. Molday, and K. D. Philipson, J. Cell Biol. 117: 337-345, 1992), whereas anti-alpha2- and anti-beta1-antibodies uniformly labeled T tubules and peripheral sarcolemma. In guinea pig cardiomyocytes, an anti-alpha-antibody against an extracellular epitope evenly labeled the peripheral sarcolemma and T tubules, and immunogold labeling demonstrated coincidence of alpha-subunits and intramembranous particles in sarcolemma. In summary, Na+ pumps are located in both peripheral sarcolemma and T tubules of cardiomyocytes expressing either multiple or single Na+ pump isoforms.
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Harashima, S., A. M. Miller, K. Tanaka, K. Kusumoto, K. Tanaka, Y. Mukai, K. Nasmyth, and Y. Oshima. "Mating-type control in Saccharomyces cerevisiae: isolation and characterization of mutants defective in repression by a1-alpha 2." Molecular and Cellular Biology 9, no. 10 (October 1989): 4523–30. http://dx.doi.org/10.1128/mcb.9.10.4523-4530.1989.
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The alpha 2 protein, the product of the MAT alpha 2 cistron, represses various genes specific to the a mating type (alpha 2 repression), and when combined with the MATa1 gene product, it represses MAT alpha 1 and various haploid-specific genes (a1-alpha 2 repression). One target of a1-alpha 2 repression is RME1, which is a negative regulator of a/alpha-specific genes. We have isolated 13 recessive mutants whose a1-alpha 2 repression is defective but which retain alpha 2 repression in a genetic background of ho MATa HML alpha HMRa sir3 or ho MAT alpha HMRa HMRa sir3. These mutations can be divided into three different classes. One class contains a missense mutation, designated hml alpha 2-102, in the alpha 2 cistron of HML, and another class contains two mat alpha 2-202, in the MAT alpha locus. These three mutants each have an amino acid substitution of tyrosine or acid substitution of tyrosine or phenylalanine for cysteine at the 33rd codon from the translation initiation codon in the alpha 2 cistron of HML alpha or MAT alpha. The remaining 10 mutants make up the third class and form a single complementation group, having mutations designated aar1 (a1-alpha 2 repression), at a gene other than MAT, HML, HMR, RME1, or the four SIR genes. Although a diploid cell homozygous for the aarl and sir3 mutations and for the MATa, HML alpha, and HMRa alleles showed alpha mating type, it could sporulate and gave rise to asci containing four alpha mating-type spores. These facts indicate that the domain for alpha2 repression is separable from that for a1-alpha2 protein interaction or complex formation in the alpha2 protein and that an additional regulation gene, AAR1, is associated with the a1-alpha2 repression of the alpha1 cistron and haploid-specific genes.
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Harashima, S., A. M. Miller, K. Tanaka, K. Kusumoto, K. Tanaka, Y. Mukai, K. Nasmyth, and Y. Oshima. "Mating-type control in Saccharomyces cerevisiae: isolation and characterization of mutants defective in repression by a1-alpha 2." Molecular and Cellular Biology 9, no. 10 (October 1989): 4523–30. http://dx.doi.org/10.1128/mcb.9.10.4523.
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The alpha 2 protein, the product of the MAT alpha 2 cistron, represses various genes specific to the a mating type (alpha 2 repression), and when combined with the MATa1 gene product, it represses MAT alpha 1 and various haploid-specific genes (a1-alpha 2 repression). One target of a1-alpha 2 repression is RME1, which is a negative regulator of a/alpha-specific genes. We have isolated 13 recessive mutants whose a1-alpha 2 repression is defective but which retain alpha 2 repression in a genetic background of ho MATa HML alpha HMRa sir3 or ho MAT alpha HMRa HMRa sir3. These mutations can be divided into three different classes. One class contains a missense mutation, designated hml alpha 2-102, in the alpha 2 cistron of HML, and another class contains two mat alpha 2-202, in the MAT alpha locus. These three mutants each have an amino acid substitution of tyrosine or acid substitution of tyrosine or phenylalanine for cysteine at the 33rd codon from the translation initiation codon in the alpha 2 cistron of HML alpha or MAT alpha. The remaining 10 mutants make up the third class and form a single complementation group, having mutations designated aar1 (a1-alpha 2 repression), at a gene other than MAT, HML, HMR, RME1, or the four SIR genes. Although a diploid cell homozygous for the aarl and sir3 mutations and for the MATa, HML alpha, and HMRa alleles showed alpha mating type, it could sporulate and gave rise to asci containing four alpha mating-type spores. These facts indicate that the domain for alpha2 repression is separable from that for a1-alpha2 protein interaction or complex formation in the alpha2 protein and that an additional regulation gene, AAR1, is associated with the a1-alpha2 repression of the alpha1 cistron and haploid-specific genes.
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Hadwiger, J. A., K. Natarajan, and R. A. Firtel. "Mutations in the Dictyostelium heterotrimeric G protein alpha subunit G alpha5 alter the kinetics of tip morphogenesis." Development 122, no. 4 (April 1, 1996): 1215–24. http://dx.doi.org/10.1242/dev.122.4.1215.
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Tip morphogenesis during the Dictyostelium developmental life cycle is a process by which prestalk cells sort to form the anterior region of the multicellular organism. We show that the temporal regulation of this morphological process is dependent on the copy number of the Dictyostelium G alpha5 gene. Tip formation is delayed in aggregates of g alpha5 null mutant cells and accelerated in aggregates overexpressing the G alpha5 gene compared to tip formation in wild-type cells. The onset of cell-type-specific gene expression associated with mound formation and tip morphogenesis is also temporally altered in G alpha5 mutants. Tip morphogenesis in chimeric organisms of G alpha5 mutants and wild-type cells is dependent on the copy number of the G alpha5 gene, indicating that G alpha5 function plays an integral role in the intercellular signaling of this stage of development. The G alpha5 gene encodes a G alpha subunit that has 51% identity to the Dictyostelium G alpha4 subunit. Like the G alpha4 gene, the G alpha5 gene is expressed in a subset of cells distributed throughout the multicellular organism, with a distribution that is similar to the anterior-like cell population. Amino acid substitutions in the G alpha5 subunit analogous to substitutions altering guanine nucleotide binding and hydrolysis in other G alpha subunits had no apparent effect on the rate of tip formation when a single copy of the mutant gene was used to replace the wild-type gene. Overexpression of these mutant G alpha5 genes by increased gene dosage resulted in cell death, suggesting that high levels of the altered subunits have detrimental effects during vegetative growth.
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Laidler, P., D. Gil, A. Pituch-Noworolska, D. Ciołczyk, D. Ksiazek, M. Przybyło, and A. Lityńska. "Expression of beta1-integrins and N-cadherin in bladder cancer and melanoma cell lines." Acta Biochimica Polonica 47, no. 4 (December 31, 2000): 1159–70. http://dx.doi.org/10.18388/abp.2000_3968.
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Changes in the expression of integrins and cadherins might contribute to the progression, invasion and metastasis of transitional cell cancer of the bladder and of melanomas. The expression of alpha5 (P < 0.001), alpha2 and beta1 (P < 0.05 - P < 0.001) integrin subunits in melanoma cells from noncutaneous metastatic sites (WM9, A375) were significantly increased as compared to cutaneous primary tumor (WM35) and metastatic (WM239) cell lines. These differences might be ascribed to the invasive character of melanoma cells and their metastasis to the noncutaneous locations. The significantly heterogeneous expression of beta1 integrin subunit in two malignant bladder cancer cell lines (T24 and Hu456) and nonsignificant differences in the expression of alpha2, alpha3, and alpha5 subunits between malignant and non-malignant human bladder cell lines do not allow an unanimous conclusion on the role of these intergrin subunits in the progression of transitional cancer of bladder. The adhesion molecule, expressed in all studied melanoma and bladder cell lines, that reacted with anti-Pan cadherin monoclonal antibodies was identified as N-cadherin except in the HCV29 non-malignant ureter cell line. However, neither this nor any other bladder or melanoma cell line expressed E-cadherin. The obtained results imply that the replacement of E-cadherin by N-cadherin accompanied by a simultaneous increase in expression of alpha2, alpha3 and alpha5 integrin subunits clearly indicates an increase of invasiveness of melanoma and, to a lesser extent, of transitional cell cancer of bladder. High expression of N-cadherin and alpha5 integrin subunit seems to be associated with the most invasive melanoma phenotype.
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Nishikawa, Koichi, and Neil L. Harrison. "The Actions of Sevoflurane and Desflurane on the γ-Aminobutyric Acid Receptor Type A." Anesthesiology 99, no. 3 (September 1, 2003): 678–84. http://dx.doi.org/10.1097/00000542-200309000-00024.
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Background Previous studies have shown that specific amino acid residues in the putative second transmembrane segment (TM2) of the gamma-aminobutyric acid receptor type A (GABAA) receptor play a critical role in the enhancement of GABAA receptor function by halothane, enflurane, and isoflurane. However, very little is known about the actions of sevoflurane and desflurane on recombinant GABAA receptors. The aim of this study was to examine the effects of sevoflurane and desflurane on potentiation of GABA-induced responses in the wild-type GABAA receptor and in receptors mutated in TM2 of the alpha1, alpha 2, or beta 2 subunits. Methods GABAA receptor alpha 1 or alpha 2, beta 2 or beta 3, and gamma 2s subunit cDNAs were expressed for pharmacologic study by transfection of human embryonic kidney 293 cells and assayed using the whole cell voltage clamp technique. Concentration-response curves and EC50 values for agonist were determined in the wild-type alpha 1 beta 2 gamma 2s and alpha 2 beta 3 gamma 2s receptors, and in receptors harboring mutations in TM2, such as alpha1(S270W)beta 2 gamma 2s, alpha 1 beta 2(N265W)gamma 2s, and alpha2(S270I)beta 3 gamma 2s. The actions of clinically relevant concentration of volatile anesthetics (isoflurane, sevoflurane, and desflurane) on GABA activated Cl- currents were compared in the wild-type and mutant GABAA receptors. Results Both sevoflurane and desflurane potentiated submaximal GABA currents in the wild-type GABAA alpha 1 beta 2 gamma 2s receptor and alpha 2 beta 3 gamma 2s receptor. Substitution of Ser270 in TM2 of the alpha subunit by a larger amino acid, tryptophan (W) or isoleucine (I), as in alpha1(S270W)beta 2 gamma 2s and alpha 2(S270I)beta 3 gamma 2s, completely abolished the potentiation of GABA-induced currents by these anesthetic agents. In contrast, mutation of Asn265 in TM2 of the beta subunit to tryptophan (W) did not prevent potentiation of GABA-induced responses. The actions of sevoflurane and desflurane in the wild-type receptor and in mutated receptors were qualitatively and quantitatively similar to those observed for isoflurane. Conclusions Positions Ser270 of the GABAA alpha1 and alpha2 subunits, but not Asn265 in the TM2 of the beta2 subunit, are critical for regulation of the GABAA receptor by sevoflurane and desflurane, as well as isoflurane, consistent with the idea that these three volatile anesthetics share a common site of actions on the alpha subunit of the GABAA receptor.
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Milinkovic, M. M., M. M. Savic, S. Huang, R. Furtmüller, S. Majumder, J. Samardic, J. M. Divljakovic, B. L. Roth, W. Sieghart, and J. M. Cook. "P.1.d.016 Jy-xhe-053, a benzodiazepine ligand less efficacious at GABAA receptors containing alphal and alpha5 than alpha2 and alpha3 subunits." European Neuropsychopharmacology 19 (September 2009): S296. http://dx.doi.org/10.1016/s0924-977x(09)70438-9.
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Moretti, D. V., A. Prestia, C. Fracassi, C. Geroldi, G. Binetti, P. M. Rossini, O. Zanetti, and G. B. Frisoni. "Volumetric Differences in Mapped Hippocampal Regions Correlate with Increase of High Alpha Rhythm in Alzheimer's Disease." International Journal of Alzheimer's Disease 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/208218.
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Objective. The increase of high alpha relative to low alpha power has been recently demonstrated as a reliable EEG marker of hippocampal atrophy conversion of patients with mild cognitive impairment (MCI) in Alzheimer's disease (AD). In the present study we test the reliability of this EEG index in subjects with AD.Methods. Correlation between EEG markers and volumetric differences in mapped hippocampal regions was estimated in AD patients.Results. Results show that the increase of alpha3/alpha2 power ratio is correlated with atrophy of mapped hippocampal regions in Alzheimer's disease.Conclusions. The findings confirm the possible diagnostic role of EEG markers.
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Saleque, S., M. Singh, R. D. Little, S. L. Giannini, J. S. Michaelson, and B. K. Birshtein. "Dyad symmetry within the mouse 3' IgH regulatory region includes two virtually identical enhancers (C alpha3'E and hs3)." Journal of Immunology 158, no. 10 (May 15, 1997): 4780–87. http://dx.doi.org/10.4049/jimmunol.158.10.4780.
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Abstract The transcription of the murine Ig heavy chain locus is regulated not only by the intronic enhancer, E mu, but also by a 3' regulatory region located downstream of the C alpha membrane exon. Several DNase I-hypersensitive sites (hs1-4) and enhancer elements (e.g., C alpha3'E) have been identified in this 3' regulatory region, and some of these were suggested to comprise a locus control region. However, little is known about the coordinate regulation or function of these individual elements. Here we provide evidence that C alpha3'E and hs3 are virtually mirror images of each other and demarcate the edges of an approximately 25-kb region of quasi-dyad symmetry with 3'alphaE(hs1,2) at its center. Flanking 3'alphaE(hs1,2) are inverted repeats and families of repetitive sequences uniquely located in this region. We have observed that, like 3'alphaE(hs1,2) and hs3, C alpha3'E is DNase I hypersensitive in plasma cell lines, but not in a pre-B cell line. Additionally, we found that C alpha3'E and hs3 show significant transcriptional synergy in transfection assays only in a plasma cell line. The DNA topology of the 3' regulatory region coupled with new and existing data on the activity of its individual enhancers during B cell differentiation lead us to propose a biphasic model for the activity of this region. According to our model, one unit, consisting of the 3'-most enhancer, hs4, is active early and throughout B cell development. The second unit, which comprises C alpha3'E, 3'alphaE(hs1,2), and hs3, becomes active later in development, when it contributes to such processes as class switching and increased levels of Ig heavy chain gene transcription in plasma cells.
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Wischhusen, Jörg, Jingjing Wu, Fadhil Ahsan, McFleder Rhonda, Ann-Kathrin Karl, Shriya Mamatha Jayaram, Heike Wecklein, et al. "alpha-synuclein peptides presented on chimeric MHC class Ib molecules prevent loss of substantia nigra neurons in an animal model for Parkinson’s disease." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 60.16. http://dx.doi.org/10.4049/jimmunol.208.supp.60.16.
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Abstract Aim An accumulating body of evidence suggests the involvement of alpha-synuclein (aSyn) specific autoreactive T cells in Parkinson’s disease (PD). Here, we investigate whether novel antigen-specific tolerance-inducing biomolecules, that present peptide antigens on MHC class Ib-related molecules, can inhibit neurodegeneration and prevent PD in vivo. Methods The alpha3 domain of the human MHC class Ib molecule HLA-G inhibits T cells via the human ILT-2 or the murine PIRB receptor. We fused this HLA-G alpha3 domain to MHC class I alpha1-alpha2 antigen presenting domains, antigenic peptides and beta2-microglobulin. These single-chain AutoImmunity Modifying Biologicals (AIM Bios) induce antigen-specific tolerogenic CD8+ Treg cells in human cells in vitro and in mice in vivo. We used this platform to prevent autoimmune disease symptoms in mouse models for autoimmune diseases, including an aSynA53T-AAV driven model for PD. Results Single-chain model AIM Bios with MHC-derived antigen-presenting domains and antigenic peptides polarize cognate CD8+ T cells towards a CD8+CD122+ IL-10 secreting Treg phenotype. Such antigen-specific Treg can also be induced in mice in vivo. Disease-associated aSyn CD8+ epitopes were identified in aSynA53T-AAV PD mice. Corresponding AIM Bios prevented mobility impairments. Post mortem histopathological assessment confirmed the induction a favorable in-situ immune cell composition and the rescue of substantia nigra neurons. The translational potential of this approach deserves further exploration. Supported by grants from the IZKF Wuerzburg A421 and by Aeterna Zentaris Inc.
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Capmany, G. "Distribution of alpha3, alpha5 and alpha(v) integrin subunits in mature and immature human oocytes." Molecular Human Reproduction 4, no. 10 (October 1, 1998): 951–56. http://dx.doi.org/10.1093/molehr/4.10.951.
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Ljubimov, A. V., R. E. Burgeson, R. J. Butkowski, J. R. Couchman, L. Zardi, Y. Ninomiya, Y. Sado, Z. S. Huang, A. B. Nesburn, and M. C. Kenney. "Basement membrane abnormalities in human eyes with diabetic retinopathy." Journal of Histochemistry & Cytochemistry 44, no. 12 (December 1996): 1469–79. http://dx.doi.org/10.1177/44.12.8985139.
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Vascular and parenchymal basement membranes (BMs) are thickened in diabetes, but alterations in individual BM components in diabetic eyes, especially in diabetic retinopathy (DR), are obscure. To identify abnormalities in the distribution of specific constituents, we analyzed cryostat sections of human eyes obtained at autopsy (seven normal, five diabetic without DR, and 13 diabetic with DR) by immunofluorescence with antibodies to 30 BM and extracellular matrix components. In non-DR eyes, no qualitative changes of ocular BM components were seen. In some DR corneas, epithelial BM was stained discontinuously for laminin-1, entactin/nidogen, and alpha3-alpha4 Type IV collagen, in contrast to non-DR corneas. Major BM alterations were found in DR retinas compared to normals and non-DR diabetics. The inner limiting membrane (retinal BM) of DR eyes had accumulations of fibronectin (including cellular) and Types I, III, IV (alpha1-alpha2), and V collagen. The BM zone of new retinal blood vessels in neovascularized areas accumulated tenascin and Type XII collagen, whereas normal, diabetic, and adjacent DR retinas showed only weak and irregular staining. In preretinal membranes, perlecan, bamacan, and Types VI, VIII, XII, and XIV collagen were newly identified. Diabetic BM thickening appears to involve qualitative alterations of specific BM markers at an advanced disease stage, with the appearance of DR.
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Morohoshi, Kazunori, Ryo Mochinaga, Tsukasa Watanabe, Ryojun Nakajima, and Toshio Harigaya. "16 kDa vasoinhibin binds to integrin alpha5 beta1 on endothelial cells to induce apoptosis." Endocrine Connections 7, no. 5 (May 2018): 630–36. http://dx.doi.org/10.1530/ec-18-0116.
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Many functions of vasoinhibins have been reported, but its receptor has not been clarified yet. Vasoinhibins, 11–18 kDa N-terminal fragments of prolactin, have anti-angiogenic activity and act on endothelial cells to induce apoptosis and to inhibit migration and proliferation, which are opposite to the effects of prolactin. Although vasoinhibins bind to the prolactin receptor, its binding activity is very weak compared to prolactin. Therefore, in this study, we evaluated the binding activity between 16 kDa vasoinhibin and integrin beta1, alpha5 beta1, alpha1 beta1 and alphaV beta3 to identify a specific receptor for vasoinhibins. Moreover, we examined whether 16 kDa vasoinhibin induced apoptosis through integrin beta1 and alpha5 beta1 in endothelial cells. In this study, binding assays and co-immunoprecipitation experiments demonstrated that 16 kDa vasoinhibin could bind strongly to integrin beta1 and alpha5 beta1. Moreover, neutralizing with integrin beta1 and alpha5 beta1 antibody could inhibit 16 kDa vasoinhibin-induced apoptosis in endothelial cells. These findings suggest that vasoinhibins can act on endothelial cells through integrin alpha5 beta1 to induce apoptosis.
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Maciag, Monika, Danuta Plochocka, Ewa Jablonska-Skwiecinska, Ewa Mendek-Czajkowska, Ewa Golaszewska, Wojciech Strojny, Walentyna Balwierz, Ewa Zdebska, and Beata Burzynska. "Molecular analysis of three novel G6PD variants: G6PD Pedoplis-Ckaro, G6PD Piotrkow and G6PD Krakow." Acta Biochimica Polonica 54, no. 4 (December 8, 2007): 877–81. http://dx.doi.org/10.18388/abp.2007_3192.
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We present three novel mutations in the G6PD gene and discuss the changes they cause in the 3-dimensional structure of the enzyme: 573C-->G substitution that predicts Phe to Leu at position 191 in the C-terminus of helix alphae, 851T-->C mutation which results in the substitution 284Val--> -->Ala in the beta+alpha domain close to the C-terminal part of helix alphaj, and 1175T-->C substitution that predicts Ile to Thr change at position 392.
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Kingery, Wade S., Geeta S. Agashe, Tian Z. Guo, Shigehito Sawamura, M. Frances Davies, J. David Clark, Brian K. Kobilka, and Mervyn Maze. "Isoflurane and Nociception." Anesthesiology 96, no. 2 (February 1, 2002): 367–74. http://dx.doi.org/10.1097/00000542-200202000-00023.
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Background The authors recently established that the analgesic actions of the inhalation anesthetic nitrous oxide were mediated by noradrenergic bulbospinal neurons and spinal alpha2B adrenoceptors. They now determined whether noradrenergic brainstem nuclei and descending spinal pathways are responsible for the antinociceptive actions of the inhalation anesthetic isoflurane, and which alpha adrenoceptors mediate this effect. Methods After selective lesioning of noradrenergic nuclei by intracerebroventricular application of the mitochondrial toxin saporin coupled to the antibody directed against dopamine beta hydroxylase (DbetaH-saporin), the antinociceptive action of isoflurane was determined. Antagonists for the alpha1 and alpha2 adrenoceptors were injected at spinal and supraspinal sites in intact and spinally transected rats to identify the noradrenergic pathways mediating isoflurane antinociception. Null mice for each of the three alpha2-adrenoceptor subtypes (alpha2A, alpha2B, and alpha2C) and their wild-type cohorts were tested for their antinociceptive response to isoflurane. Results Both DbetaH-saporin treatment and chronic spinal transection enhanced the antinociceptive effects of isoflurane. The alpha1-adrenoceptor antagonist prazosin also enhanced isoflurane antinociception at a supraspinal site of action. The alpha2-adrenoceptor antagonist yohimbine inhibited isoflurane antinociception, and this effect was mediated by spinal alpha2 adrenoceptors. Null mice for the alpha2A-adrenoceptor subtype showed a reduced antinociceptive response to isoflurane. Conclusions The authors suggest that, at clinically effective concentrations, isoflurane can modulate nociception via three different mechanisms: (1) a pronociceptive effect requiring descending spinal pathways, brainstem noradrenergic nuclei, and supraspinal alpha1 adrenoceptors; (2) an antinociceptive effect requiring descending noradrenergic neurons and spinal alpha2A adrenoceptors; and (3) an antinociceptive effect mediated within the spinal cord for which no role for adrenergic mechanism has been found.
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Modolo, F., MT Martins, SVL Loducca, and VC de Araujo. "Expression of integrin subunits alpha2, alpha3, alpha5, alphav, beta1, beta3 and beta4 in different histological types of ameloblastoma compared with dental germ, dental lamina and adult lining epithelium." Oral Diseases 10, no. 5 (September 2004): 277–82. http://dx.doi.org/10.1111/j.1601-0825.2004.01028.x.
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COLOMBATTI, Alfonso, Paolo BONALDO, and Francesco BUCCIOTTI. "Stable expression of chicken type-VI collagen alpha1, alpha2 and alpha3 cDNAs in murine NIH/3T3 cells." European Journal of Biochemistry 209, no. 2 (October 1992): 785–92. http://dx.doi.org/10.1111/j.1432-1033.1992.tb17349.x.
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Franchi, Alessandro, Roberto Santoro, Milena Paglierani, and Roberto Bondi. "Immunolocalization of alpha2, alpha5, and alpha6 integrin subunits in salivary tissue and adenomas of the parotid gland." Journal of Oral Pathology and Medicine 23, no. 10 (November 1994): 457–60. http://dx.doi.org/10.1111/j.1600-0714.1994.tb00444.x.
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Yao, C. C., J. Breuss, R. Pytela, and R. H. Kramer. "Functional expression of the alpha 7 integrin receptor in differentiated smooth muscle cells." Journal of Cell Science 110, no. 13 (July 1, 1997): 1477–87. http://dx.doi.org/10.1242/jcs.110.13.1477.
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Expression of the alpha7 integrin is developmentally regulated and is thought to be tissue-specific for both skeletal and cardiac muscles. We now report that alpha7 is also strongly and ubiquitously expressed by various types of smooth muscle, including vascular, gastrointestinal and genitourinary smooth muscles. In addition, alpha7 was surface-expressed by a number of smooth muscle cell lines that maintained their differentiated phenotype following adaptation to culture. Studies with the mouse 9E11G smooth muscle cell line showed that the alpha7 integrin mediated both adhesion and motility of these cells on laminin 1 substrates. Alpha7 expression appears to correlate with the smooth-muscle-differentiated phenotype. The multipotential P19 mouse embryonic stem cell line lacks alpha7 but uses the alpha6 integrin to adhere to laminin 1. Following retinoic acid-induced P19 differentiation predominantly to the smooth muscle cell lineage, high expression of alpha7 was detected along with partial dependence on alpha7 for binding to laminin. The expression of alpha7 paralleled the induction of smooth-muscle-specific alpha-actin, as revealed by dual-labeling flow cytometry. In contrast, alpha7, which initially was highly expressed on the surface of vascular smooth muscle cell explants, was rapidly downregulated in smooth muscle cell outgrowths as they dedifferentiated into their synthetic phenotype. The results indicate that the expression of alpha7 integrin in smooth muscle cells is associated with their differentiated phenotype and mediates their interaction with laminins.
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Desban, N., and J. L. Duband. "Avian neural crest cell migration on laminin: interaction of the alpha1beta1 integrin with distinct laminin-1 domains mediates different adhesive responses." Journal of Cell Science 110, no. 21 (November 1, 1997): 2729–44. http://dx.doi.org/10.1242/jcs.110.21.2729.
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In the present study, to further elucidate the molecular events that control neural crest cell migration, we have analyzed in vitro the adhesive and locomotory response of avian trunk neural crest cells to laminin-1 and searched for the integrin receptors involved in this process. Adhesion of crest cells on laminin-1 was comparable to that found on fibronectin or vitronectin. By contrast, migration was significantly greater on laminin-1 than on the other substrate molecules. Interaction of crest cells with laminin-1 involved two major cell-binding domains situated in different portions of the molecule, namely the E1′ and E8 fragments, which elicited different cellular responses. Cells were poorly spread on the E1′ fragment whereas, on E8, they were extremely flattened and cohesive. Either fragment supported cell locomotion, albeit not as efficiently as laminin-1. Immunoprecipitation and immunocytochemistry analyses revealed that crest cells expressed the alpha1beta1, alpha3beta1, alpha6beta1 and alpha vbeta3 integrins, as well as beta8 integrins, as presumptive laminin-1 receptors, but not alpha6beta4 and alpha2beta1. Immunofluorescence labeling of cultured cells showed that the alpha1, alpha v, beta1 and beta3 subunits were diffuse on the cell surface and in focal contacts. In contrast, alpha3 and beta8 were diffuse, while alpha6 was mostly intracytoplasmic and, secondarily, in focal contacts. Inhibition assays of cell adhesion and migration with function-perturbing antibodies demonstrated that alpha1beta1 played a predominant role in both adhesion and migration on laminin-1 and interacted with either binding sites in the E1′ and E8 fragments. Alpha vbeta3 was also implicated in neural crest cell migration. In contrast, alpha3beta1, alpha6beta1 and the beta8 integrins appeared to play only subsidiary roles in cell adhesion and migration. Finally, the ability of neural crest cells to interact with laminin-1 was found to increase with time in culture, possibly in correlation with changes in alpha3 distribution on the cell surface. In conclusion, our study indicates that (1) the preferential migration of neural crest cells along basal laminae can be accounted for by the ability of laminin-1 to promote migration with great efficiency; (2) interaction with laminin-1 involves two major cell binding domains that are both recognized by the alpha1beta1 integrin; (3) alpha1beta1 integrin can elicit different cellular responses depending on the laminin-1 domains with which it interacts; and (4) changes in the repertoire of integrins expressed by neural crest cells are consistent with the modulations of cell-substratum adhesion occurring throughout migration.
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BELL, S. C., M. W. HALES, S. R. PATEL, P. H. KIRWAN, J. O. DRIFE, and A. MILFORD-WARD. "Amniotic fluid concentrations of secreted pregnancy-associated endometrial alpha1 and alpha2-globulins (alpha1- and alpha2-PEG)." BJOG: An International Journal of Obstetrics and Gynaecology 93, no. 9 (September 1986): 909–15. http://dx.doi.org/10.1111/j.1471-0528.1986.tb08007.x.
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Sitnikova, Evgenia, Maria Pupikina, and Elizaveta Rutskova. "Alpha2 Adrenergic Modulation of Spike-Wave Epilepsy: Experimental Study of Pro-Epileptic and Sedative Effects of Dexmedetomidine." International Journal of Molecular Sciences 24, no. 11 (May 29, 2023): 9445. http://dx.doi.org/10.3390/ijms24119445.
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In the present report, we evaluated adrenergic mechanisms of generalized spike-wave epileptic discharges (SWDs), which are the encephalographic hallmarks of idiopathic generalized epilepsies. SWDs link to a hyper-synchronization in the thalamocortical neuronal activity. We unclosed some alpha2-adrenergic mechanisms of sedation and provocation of SWDs in rats with spontaneous spike-wave epilepsy (WAG/Rij and Wistar) and in control non-epileptic rats (NEW) of both sexes. Dexmedetomidine (Dex) was a highly selective alpha-2 agonist (0.003–0.049 mg/kg, i.p.). Injections of Dex did not elicit de novo SWDs in non-epileptic rats. Dex can be used to disclose the latent form of spike-wave epilepsy. Subjects with long-lasting SWDs at baseline were at high risk of absence status after activation of alpha2- adrenergic receptors. We create the concept of alpha1- and alpha2-ARs regulation of SWDs via modulation of thalamocortical network activity. Dex induced the specific abnormal state favorable for SWDs—“alpha2 wakefulness”. Dex is regularly used in clinical practice. EEG examination in patients using low doses of Dex might help to diagnose the latent forms of absence epilepsy (or pathology of cortico-thalamo-cortical circuitry).
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Chernii, Tatiana V., Volodymyr I. Cherniy, and Daria О. Fokina. "IMPLEMENTATION OF QUANTITATIVE ELECTROENCEPHALOGRAPHY TO IMPROVE EFFICACY OF DIAGNOSIS AND TREATMENT MANAGEMENT OF CHRONIC CEREBRAL ISCHEMIA." Wiadomości Lekarskie 75, no. 11 (2022): 2565–68. http://dx.doi.org/10.36740/wlek202211101.
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The aim: To improve the effectiveness of diagnosis and treatment of chronic cerebral ischemia through the use of quantitative electroencephalography in civil servants on the outpatient and hospital stage. Materials and methods: A total of 150 patients (59 males and 91 females) aged from 40 to 69 years were examined. The patients were divided into three groups statistically correlated with the main disease - chronic cerebral ischemia (CCI), degree of severity - CCI level 2, age and statistical status. Registration of brain biopotentials was performed using a computerized electroencephalograph of «TredexExpert» series. The total spectral power capacity - ASP (μV/√Hz), relative power capacity - RSP (%) were studied in the investigated frequency ranges. Results: The study of three groups of patients with CCI of different genesis, an increase in ASP of all studied ranges, but of varying degrees of severity, was found: first, delta and theta ranges, then beta ranges, and finally, to a lesser extent, ASP of the alpha1 range and alphaS range. Therefore, the RSP of alpha1- and alphaS-bands significantly decreased in all studied groups. Conclusions: 1. In all studied groups, the relative spectral power of the alpha 1 and alphaS bands decreased significantly. An increase in the relative spectral power of the beta-frequency rhythm in all leads was established. 2. The identified neurophysiological differences in the formation and course of dyscirculatory encephalopathy of various genesis are used to monitor the effectiveness of treatment of chronic brain ischemia.
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Chen, L., V. Shick, M. L. Matter, S. M. Laurie, R. C. Ogle, and G. W. Laurie. "Laminin E8 alveolarization site: heparin sensitivity, cell surface receptors, and role in cell spreading." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 3 (March 1, 1997): L494—L503. http://dx.doi.org/10.1152/ajplung.1997.272.3.l494.
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Cell adhesion to amino acids 2179-2198 (SN-peptide) of the laminin-1 alpha1-chain is required for lung alveolar formation in vitro (M. L. Matter and G. W. Laurie. J. Cell Biol. 124: 1083-1090, 1994). The nature of the SN-peptide receptor(s) was probed with neutralizing anti-integrin monoclonal antibodies (MAb), cells lacking integrin subunits, soluble heparin, and SN-peptide columns. Cell adhesion and spreading studies confirmed the specificity of SN-peptide and revealed adhesion to be unaffected by inclusion of anti-beta1-, anti-alpha(2-6)- or anti-alpha(V)beta5-integrin MAb. Cells lacking beta1- or alpha6-integrin subunits were fully adherent. Adhesion was heparin, but not chondroitin sulfate or heparinase, sensitive, much as is alpha-dystroglycan-laminin-1 binding. Heparin eluted approximately 155- and 180-kDa cell-surface proteins from SN-peptide columns. An additional approximately 91-kDa protein was eluted by EDTA. All were unrecognized by anti-beta1-integrin MAb. SN-peptide therefore interacts with three cell-surface proteins for which the identity remains to be determined.
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Kim, Jeong-Youn, Jae-Beom Son, Hyun-Sung Leem, and Seung-Hwan Lee. "Psychophysiological Alteration After Virtual Reality Experiences Using Smartphone-Assisted Head Mount Displays: An EEG-Based Source Localization Study." Applied Sciences 9, no. 12 (June 19, 2019): 2501. http://dx.doi.org/10.3390/app9122501.
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Brain functional changes could be observed in people after an experience of virtual reality (VR). The present study investigated cyber sickness and changes of brain regional activity using electroencephalogram (EEG)-based source localization, before and after a VR experience involving a smartphone-assisted head mount display. Thirty participants (mean age = 25 years old) were recruited. All were physically healthy and had no ophthalmological diseases. Their corrected vision was better than 20/20. Resting state EEG and the simulator sickness questionnaire (SSQ) were measured before and after the VR experience. Source activity of each frequency band was calculated using the sLORETA program. After the VR experience, the SSQ total score and sub scores (nausea, oculomotor symptoms, and disorientation) were significantly increased, and brain source activations were significantly increased: alpha1 activity in the cuneus and alpha2 activity in the cuneus and posterior cingulate gyrus (PCG). The change of SSQ score (after–before) showed significant negative correlation with the change of PCG activation (after–before) in the alpha2 band. The study demonstrated increased cyber sickness and increased alpha band power in the cuneus and PCG after the VR experience. Reduced PCG activation in alpha band may be associated with the symptom severity of cyber sickness.
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Manie, SN, A. Astier, D. Wang, JS Phifer, J. Chen, AI Lazarovits, C. Morimoto, and AS Freedman. "Stimulation of tyrosine phosphorylation after ligation of beta7 and beta1 integrins on human B cells." Blood 87, no. 5 (March 1, 1996): 1855–61. http://dx.doi.org/10.1182/blood.v87.5.1855.1855.
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Abstract B lymphocytes express several members of the integrin family of adhesion molecules that mediate cell-cell and cell-extracellular matrix interactions. In addition to beta1 integrins, predominantly alpha4 beta1, mature B cells also express alpha4 beta7, which is a receptor for vascular cell adhesion molecule-1 and fibronectin, and is also involved in the homing of B cells to mucosal sites through binding to a third ligand, mucosal address in cell adhesion molecule-1. Here we describe that crosslinking of alpha4 beta7 integrins on B cell lines and normal tonsillar B cells, induces tyrosine phosphorylation of multiple substrates of 105–130 kD, indicating that beta7 integrin plays a role as signaling molecule in B cells. This pattern of phosphorylated proteins was very similar to that induced following ligation of alpha4 beta1. Interestingly, ligation of alpha5 beta1 or alpha6 beta1 also stimulated the 105–125 kD group of phosphorylated proteins, whereas ligation of beta2 integrins did not. The focal adhesion tyrosine kinase p125FAK was identified as one of these substrates. Beta1 or beta7 mediated tyrosine phosphorylations were markedly decreased when the microfilament assembly was inhibited by cytochalasin B. These results suggest that intracellular signals initiated by different integrins in B cells may converge, to similar cytoskeleton-dependent tyrosine phosphorylated proteins.
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Manie, SN, A. Astier, D. Wang, JS Phifer, J. Chen, AI Lazarovits, C. Morimoto, and AS Freedman. "Stimulation of tyrosine phosphorylation after ligation of beta7 and beta1 integrins on human B cells." Blood 87, no. 5 (March 1, 1996): 1855–61. http://dx.doi.org/10.1182/blood.v87.5.1855.bloodjournal8751855.
Full textAbstract:
B lymphocytes express several members of the integrin family of adhesion molecules that mediate cell-cell and cell-extracellular matrix interactions. In addition to beta1 integrins, predominantly alpha4 beta1, mature B cells also express alpha4 beta7, which is a receptor for vascular cell adhesion molecule-1 and fibronectin, and is also involved in the homing of B cells to mucosal sites through binding to a third ligand, mucosal address in cell adhesion molecule-1. Here we describe that crosslinking of alpha4 beta7 integrins on B cell lines and normal tonsillar B cells, induces tyrosine phosphorylation of multiple substrates of 105–130 kD, indicating that beta7 integrin plays a role as signaling molecule in B cells. This pattern of phosphorylated proteins was very similar to that induced following ligation of alpha4 beta1. Interestingly, ligation of alpha5 beta1 or alpha6 beta1 also stimulated the 105–125 kD group of phosphorylated proteins, whereas ligation of beta2 integrins did not. The focal adhesion tyrosine kinase p125FAK was identified as one of these substrates. Beta1 or beta7 mediated tyrosine phosphorylations were markedly decreased when the microfilament assembly was inhibited by cytochalasin B. These results suggest that intracellular signals initiated by different integrins in B cells may converge, to similar cytoskeleton-dependent tyrosine phosphorylated proteins.
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Moretti, Davide V. "Increase of EEG Alpha3/Alpha2 Power Ratio Detects Inferior Parietal Lobule Atrophy in Mild Cognitive Impairment." Current Alzheimer Research 15, no. 5 (March 14, 2018): 443–51. http://dx.doi.org/10.2174/1567205014666171030105338.
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Objective: The inferior parietal lobule (IPL) has been implicate in many higher cognitive processes, as visuo-motor transformations, tool use or tool making. In subjects with mild cognitive impairment (MCI) at major risk to develop Alzheimer' Disease (AD) an impairment of subtle visuomotor or praxic abilities is a well-known clinical feature. Enhance of the ratio of EEG alpha3/alpha2 frequency power was detected in subjects with MCI who will transform in Alzheimer's disease (AD). Methods: We explored of the association of alpha3/alpha2 power ratio with cortical size of IPL in patients with MCI. 74 subjects with MCI undergone EEG recording and MRI scans. Alpha3/alpha2 power ratio in addition to cortical size had been computed for each patient. Three MCI groups had been acquired in keeping with growing tertile values of alpha3/alpha2 ratio. Huge difference of cortical thickness among the groups was calculated. Higher alpha3/alpha2 power ratio group had broader cortical loss compared to other teams on the IPL, particularly in the Supramarginal Gyrus, and Precuneus on both hemispheres. Results: Our results unveil the possible part that the IPL could play in determining the classic alterations of early Alzheimer's disease (AD). Conclusion: Finally, the rise of alpha3/alpha2 power ratio detected a focused anatomo-functional association that could be a reliable marker of incipient AD.
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Chandy, Mammen, Eunice E. Sindhuvi, R. V. Shaji, Vikram Mathews, Biju George, Auro Vishwabandya, and Alok Srivastava. "Surveyor™ Nuclease: A New Rapid and Effective Strategy for Detection of Single Nucleotide Changes in Alpha Globin Genes." Blood 106, no. 11 (November 16, 2005): 3653. http://dx.doi.org/10.1182/blood.v106.11.3653.3653.
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Abstract Alpha thalassemia is the most common globin gene disorder in the world and the disease is caused by mutations in either the alpha2 or alpha1 genes. Deletions of one (-α) or both (--) of these genes are the most common cause of alpha-thalassemia, while point mutations and small insertions/deletions are present but at a much lower frequency (5%). The number of point mutations described in these genes has been steadily increasing, with greater than 40 identified to date. Identifying these point mutations acquires importance as patients with non-deletional hemoglobin (Hb) H disease are more severely affected. Comprehensive evaluation of α globin genes is also essential while determining the molecular basis of the thalassemia intermedia phenotype. Mutations in the alpha globin gene can be detected either by direct DNA sequencing or by screening methods. Although small (about 1kb, 3 exons and 2 introns), the alpha-globin genes are duplicate and highly G-C rich, which makes them difficult to denature and therefore reducing sequencing efficiency and causing frequent artifacts. We have developed a simple and robust method based on mismatch-specific DNA endonuclease, SurveyorTM Nuclease. Genomic DNA control samples (n=21) harboring 12 different nucleotide changes characterized by direct DNA sequencing in either the alpha2 or alpha1 samples were used to validate this method. These samples were heterozygous or homozygous for each point mutation, or compound heterozygous for a deletion and the point mutation. Controls were amplified by gene specific primers designed by Primer3 software followed by digestion with SurveyorTM Nuclease. This endonuclease is a member of the CEL nuclease family of mismatch-specific nucleases derived from celery. It recognizes all insertions, deletions and base substitutions, and cleaves the mismatch of any heteroduplex DNA. After digestion, cleavage products are analyzed by agarose gel electrophoresis. The size of the digestion products indicates the location of the mutation, which is then confirmed and characterized by sequencing. All the 12 different nucleotide changes [α1 CD 14 TàC, α2 CD 104 TàG, α2 IVS II-55 TàG, α1 IVS II 141 TàC, α1 IVS I 117 GàT, α2 IVS I 1 GàA, Poly A (-AA), α1 CD 119 CàT, α2 IVS I 116, α2 CD 22 CàT, α2 CD 29 TàC, α2 +15 CàG] in the alpha globin genes were detected by this assay indicating a high sensitivity and specificity of this method. Mutation screening by SurveyorTM Nuclease is rapid (~ 5 hours), cost effective ($8/sample) and sensitive (100%). This assay in combination with the multiplex-PCR for screening the common alpha globin gene deletions will be the most comprehensive and economical approach for genetic diagnosis of alpha thalassaemia. Mismatch specific nucleases may have increasing application as a mutation detection strategy for human genetic diseases.
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Moretti, D. V., A. Prestia, C. Fracassi, G. Binetti, O. Zanetti, and G. B. Frisoni. "Specific EEG Changes Associated with Atrophy of Hippocampus in Subjects with Mild Cognitive Impairment and Alzheimer's Disease." International Journal of Alzheimer's Disease 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/253153.
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We evaluated the association between hippocampal atrophy and increase of the EEG markers alpha3/alpha2 relative power ratio in mild cognitive impairment (MCI) and Alzheimer's disease patients. Seventy-nine subjects with MCI and 11 patients with AD underwent EEG recording and MRI scan. The MCI group was subdivided in three subgroups according to growing hippocampal atrophy. The groups were characterized by alpha3/alpha2 relative power ratio. In AD patients group mapped hippocampal regions were computed and related with alpha3/alpha2 power ratio. Results show that the increase of alpha3/alpha2 power ratio is correlated with atrophy of hippocampus both in MCI and in Alzheimer's disease patients. This finding confirms the possible diagnostic role of EEG markers as diagnostic and prognostic factors in patient with prodromal and declared Alzheimer's disease.