Relevant bibliographies by topics / Integrin alpha6

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Academic literature on the topic 'Integrin alpha6'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 February 2022

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Journal articles on the topic "Integrin alpha6"

1

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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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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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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De Arcangelis, A., M. Mark, J. Kreidberg, L. Sorokin, and E. Georges-Labouesse. "Synergistic activities of alpha3 and alpha6 integrins are required during apical ectodermal ridge formation and organogenesis in the mouse." Development 126, no. 17 (September 1, 1999): 3957–68. http://dx.doi.org/10.1242/dev.126.17.3957.

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Integrins alpha6beta1 and alpha6beta4 are cell surface receptors for laminins. Integrin alpha6-null mice die at birth with severe skin blistering and defects in the cerebral cortex and in the retina. Integrin alpha3beta1 can associate with laminins and other ligands. Integrin alpha3-null mice also die at birth, with kidney and lung defects at late stages of development, and moderate skin blistering. To investigate possible overlapping functions between alpha3 and alpha6 integrins, we analyzed the phenotype of compound alpha3−/−/alpha6−/− mutant embryos. Double homozygous mutant embryos were growth-retarded and displayed several developmental defects not observed in the single mutant animals. First, limb abnormalities characterized by an absence of digit separation and the fusion of preskeletal elements were observed. Further analyses indicated a defect in the apical ectodermal ridge, an essential limb organizing center. In the double mutant, the ridge appeared flattened, and ridge cells did not show a columnar morphology. A strong reduction in ridge cell proliferation and alterations of the basal lamina underlying the ectoderm were observed. These results suggest that alpha3 and alpha6 integrins are required for the organization or compaction of presumptive apical ectodermal ridge cells into a distinct differentiated structure. Additional defects were present: an absence of neural tube closure, bilateral lung hypoplasia, and several abnormalities in the urogenital tract. Finally, an aggravation of brain and eye lamination defects was observed. The presence of novel phenotypes in double mutant embryos demonstrates the synergism between alpha3 and alpha6 integrins and their essential roles in multiple processes during embryogenesis.
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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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Anderson, R., R. Fassler, E. Georges-Labouesse, R. O. Hynes, B. L. Bader, J. A. Kreidberg, K. Schaible, J. Heasman, and C. Wylie. "Mouse primordial germ cells lacking beta1 integrins enter the germline but fail to migrate normally to the gonads." Development 126, no. 8 (April 15, 1999): 1655–64. http://dx.doi.org/10.1242/dev.126.8.1655.

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Primordial germ cells are the founder cells of the gametes. They are set aside at the initial stages of gastrulation in mammals, become embedded in the hind-gut endoderm, then actively migrate to the sites of gonad formation. The molecular basis of this migration is poorly understood. Here we sought to determine if members of the integrin family of cell surface receptors are required for primordial germ cell migration, as integrins have been implicated in the migration of several other motile cell types. We have established a line of mice which express green fluorescent protein in germline cells that has enabled us to efficiently purify primordial germ cells at different stages by flow cytometry. We have catalogued the spectrum of integrin subunit expression by primordial germ cells during and after migration, using flow cytometry, immunocytochemistry and RT-PCR. Through analysis of integrin beta1(−/−)-->wild-type chimeras, we show that embryonic cells lacking beta1 integrins can enter the germline. However, integrin beta1(−/−) primordial germ cells do not colonize the gonad efficiently. Embryos with targeted deletion of integrin subunit alpha3, alpha6, or alphaV show no major defects in primordial germ cell migration. These results demonstrate a role for beta1-containing integrins in the development of the germline, although an equivalent role for * integrin subunit(s) has yet to be established.
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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.

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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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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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Niessen, C. M., E. H. Hulsman, L. C. Oomen, I. Kuikman, and A. Sonnenberg. "A minimal region on the integrin beta4 subunit that is critical to its localization in hemidesmosomes regulates the distribution of HD1/plectin in COS-7 cells." Journal of Cell Science 110, no. 15 (August 1, 1997): 1705–16. http://dx.doi.org/10.1242/jcs.110.15.1705.

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The integrin alpha6 beta4 is a major component of hemidesmosomes, in which it mediates firm adhesion to laminin 5. Previous studies have shown that the incorporation of alpha6 beta4 into hemidesmosomes requires a 303 amino acid stretch of the cytoplasmic domain of beta4, comprising part of the first fibronectin type III (FNIII) repeat, the second FNIII repeat and the segment that connects the second to the third FNIII repeat (connecting segment). Now, we have further defined sequences within beta4 that are critical for its localization in hemidesmosomes and we demonstrate that these sequences also induce the redistribution of HD1/plectin into junctional complexes containing the integrin alpha6 beta4 in COS-7 cells, transfected with cDNAs encoding alpha6A and beta4. Truncation of the cytoplasmic domain of beta4 after amino acids 1,382 or 1,355 in the connecting segment, by which a potential tyrosine activation motif (TAM) is removed, does not prevent the localization of alpha6 beta4 in hemidesmosomes in the rat bladder carcinoma cell line 804G and neither did it eliminate the ability of alpha6 beta4 to change the subcellular distribution of HD1/plectin in COS-7 cells. In contrast, beta4 subunits in which the entire connecting segment had been deleted or which were truncated after amino acid 1,328, which removes almost the complete segment, had lost both of these functions. Furthermore, when beta4 subunits with either a deletion of the second FNIII repeat or a small deletion in this repeat were co-expressed with alpha6, the integrins were not localized in hemidesmosomes and did not induce the redistribution of HD1/plectin in COS-7 cells. Finally, the fourth FNIII repeat of beta4 could not replace the second in either of these activities. These findings establish that a region in beta4, which encompasses the second FNIII repeat and a stretch of 27 amino acids (1,329-1,355) of the connecting segment, is critical for the localization of alpha6beta4 in hemidesmosomes and that it regulates the distribution of HD1/plectin.
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Dissertations / Theses on the topic "Integrin alpha6"

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Kacsinta, Apollo Daniel. "Determining Biological Effectors of alpha6 Integrin Cleavage." Diss., The University of Arizona, 2010. http://hdl.handle.net/10150/193604.

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Cancer metastasis is a multi–step process that initiates with a tumor cell obtaining the ability to migrate. A multitude of changes occur in such a cell including changes to cell adhesion molecules such as integrins. In cancer cells, integrins are known to be involved in migration, invasion and metastasis. Investigation by our group of the α6 integrin led to the discovery of a cleaved form of the integrin lacking the ligand binding domain, called α6p. While it is known that the integrin is cleaved by urokinase plasminogen activator (uPA) little is known about how this process is regulated. There is a need to better understand the players involved in regulation of α6 cleavage as inhibiting this event from occurring may contribute to prolonged or increased patient survival or ultimately a cure.The existence of the integrin–actin complex has been known for many years. In this study actin was identified as a potential regulator of α6 cleavage. Using a diverse set of tumor cell lines (DU145, PC3 and MDA–MB–231) and a number of actin modifing compounds (latrunculin A, jasplakinolide and siRNA) it is reported here that disassembling actin filaments leads to an increase in α6p production. Although the increase in cleavage product did not always correlate with an increase in uPA receptor, an increase in uPAR was observed when actin was complexed by small molecule inhibitors. Taken together the results demonstrate a potential role for actin filaments to protect α6 integrin from uPA–uPAR induced cleavage via a multi–protein complex.
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Nollet, Eric A. "Integrin alpha6 Activity in Castration-Resistant Prostate Cancer." Thesis, Van Andel Research Institute, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10289534.

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Although castration-resistant prostate cancers no longer respond to anti-androgen therapies, the androgen receptor (AR) is still required to promote tumor survival. However, the signaling pathways downstream of AR that promote this survival are not well known. We recently identified an AR-dependent survival pathway whereby AR induction of integrin α6β1 and adhesion to laminin activates NF-κB/RelA signaling and Bcl-xL. This pathway acts in parallel with the PI3K/Akt pathway in Pten-null tumor cells such that combined inhibition of both PI3K and integrin α6β1 is required to effectively kill tumor cells adherent to laminin. However, PTEN-null castration-resistant tumors were not effectively killed by this combination. I discovered that BNIP3, a hypoxia-induced BH3-only, pro-mitophagic Bcl-2 family member, is induced by androgen in castration-resistant cells through integrin α6β1 and HIF1α. Furthermore, castration-resistant cells adherent to laminin were much more efficient at inducing autophagy in response to androgen. Androgen blocked the ability of the PI3K inhibitor PX866 to kill castration-resistant tumors, but this was reversed by loss of BNIP3. Although BNIP3 was dispensable for androgen-induced autophagy, its mitophagy function was required for BNIP3 to promote resistance to PX866. Thus, enhanced hypoxia signaling in cooperation with AR/α6β1/HIF1α signaling on laminin in castration-resistant cells drives the expression of BNIP3 and enhances autophagy, both of which contribute to PX866 resistance through induction of mitophagy.

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Chang, Cheng. "Function and Regulation of the α6 Integrins in Mammary Epithelial Biology and Breast Cancer: A Dissertation." eScholarship@UMMS, 2015. http://escholarship.umassmed.edu/gsbs_diss/734.

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Integrins have the ability to impact major aspects of epithelial biology including adhesion, migration, invasion, signaling and differentiation, as well as the formation and progression of cancer (Hynes 2002; Srichai and Zent 2010; Anderson et al. 2014). This thesis focuses on how integrins are regulated and function in the context of mammary epithelial biology and breast cancer with a specific focus on the α6 integrin heterodimers (α6β1 and α6β4). These integrins function primarily as receptors for the laminin family of extracellular matrix (ECM) proteins and they have been implicated in mammary gland biology and breast cancer (Friedrichs et al. 1995; Wewer et al. 1997; Mercurio et al. 2001; Margadant and Sonnenberg 2010; Muschler and Streuli 2010; Nistico et al. 2014). The first project investigates how alternative splicing of the α6 subunit impacts the genesis and function of breast cancer stem cells (CSCs). This work revealed that the α6Bβ1 splice variant, but not α6Aβ1, is necessary for the function of breast CSCs because it activates the Hippo transducer TAZ (Zhao et al. 2008a), which is known to be essential for breast CSCs (Cordenonsi et al. 2011). My work also led to the discovery that laminin (LM) 511 is the specific ligand for α6Bβ1 and that autocrine LM511, which is mediated by TAZ, is needed to sustain breast CSCs by functioning as a ‘ECM niche’. An important aspect of this study is the finding that surface-bound LM511 characterizes a small population of cells in human breast tumors with CSC properties. The second project of my thesis concentrated on identifying transcription factors that regulate expression of the β4 subunit. The expression of the α6β4 integrin is repressed during the epithelial-mesenchymal transition (EMT) (Yang et al. 2009) but the contribution of specific transcription factors to this repression is poorly understood. This study revealed that Snai1 is a transcriptional repressor of β4, which is responsible for establishing the PRC2 (Polycomb complex 2)- associated repressive histone mark H3K27Me3. However, I also found that the ability of Snai1 to repress transcription is abrogated by its interaction with Id2. Specifically, I identified the biochemical mechanism for how Id2 regulates Snai1. Id2 binds the SNAG domain of Snai1 that is the docking site for several corepressors (Peinado et al. 2004; Lin et al. 2010b; Dong et al. 2012a). One important consequence of Id2 interacting with Snai1 on the β4 promoter is that it prevents repressive epigenetic modifications. This finding may explain why some epithelial cells express Snai1 and β4 because they also express Id2 (Vincent et al. 2009; Bastea et al. 2012). The repression of the α6β4 integrin during the EMT is consistent with data indicating that this integrin is not expressed in CSCs (Mani et al. 2008; Goel et al. 2012; Goel et al. 2013; Goel et al. 2014). An important question going forward is to understand how the α6β4 integrin contributes to tumor formation. In summary, my thesis provides novel insights into the biology of the α6 integrins that has important implications for the function of these integrins in mammary gland biology and breast cancer, especially our understanding of breast CSCs.
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Hamade, Hussein. "Analyse des mécanismes moléculaires et cellulaires conduisant à une inflammation dans l'intestin et une progression tumorale induits par la perte de la sous-unité d'intégrine Alpha6 chez la souris." Thesis, Strasbourg, 2014. http://www.theses.fr/2014STRAJ062/document.

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Le laboratoire a établi un modèle de souris α6ΔIEC qui développe une inflammation chronique intestinale associée à la formation d’adénocarcinomes colorectaux. Ce modèle correspond à une délétion ciblée à l’épithélium intestinal de l’intégrine α6β4. Mon projet de thèse a consisté à définir les mécanismes qui influencent la transformation de lésions inflammatoires en adénocarcinomes. La caractérisation du modèle α6ΔIEC a permis de mettre en évidence plusieurs altérations : détachement de l’épithélium, régénération du tissu, prolifération, augmentation de la perméabilité intestinale, hypersécrétion du mucus, ségrégation anormale des bactéries, inflammation chronique et formation de tumeurs.Pour étudier la séquence et la cinétique des mécanismes, j’ai développé un modèle de souris inductible (α6ΔIECTAM). Cette lignée présente, deux semaines après l’invalidation de l’intégrine α6,les mêmes signes d’inflammation que les souris α6ΔIEC. Mon approche a consisté à dissocier les processus impliqués dans chacune des étapes-clés de la pathologie afin de définir la contribution respective de l’infection par les bactéries et du stress mécanique
We generated a new mouse model, α6ΔIEC, in which the genetic ablation of α6 integrin from intestinal epithelial cells triggered the development of spontaneous colitis and colorectal cancer. My main goal was to define the mechanisms by which inflamed lesions degenerate into infiltrating adenocarcinomas. Loss of α6 integrin in this model resulted in epithelial barrier damage, enhanced permeability, altered mucus layers, abnormal bacterial segregation, chronic inflammation and tumor development.In order to define the sequence of events and the mechanisms involved at each stage of the disease, from inflamed to tumor lesions, I developed an inducible mouse model, α6ΔIECTAM, in which α6 integrin ablation was induced by tamoxifen treatment. This line recapitulates all aspects of inflammation observed in the α6ΔIEC model, as early as two weeks after tamoxifen treatment. In particular, I tried to define the respective contribution of infection by bacteria and mechanical stress during disease progression
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Mutz, Diana. "Identifizierung von Bindungspartnern des cytosolischen Teils der [alpha]3-Integrin-Untereinheit [Alpha3-Integrin-Untereinheit] und die Aufklärung ihrer Rolle bei der Funktion des [alpha]3[beta]1-Integrins [Alpha3beta1-Integrins]." [S.l. : s.n.], 2004. http://www.diss.fu-berlin.de/2004/214/index.html.

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Schaff, Mathieu. "Etude des mécanismes d'adhérence et d'activation des plaquettes sanguines appliquée à l'identification de nouvelles cibles anti-thrombotiques plus sûres." Phd thesis, Université de Strasbourg, 2012. http://tel.archives-ouvertes.fr/tel-00867777.

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L'adhérence, l'activation et l'agrégation des plaquettes sanguines sont essentielles à l'hémostase mais peuvent également conduire à la thrombose artérielle sur plaque d'athérosclérose, aujourd'hui première cause de mortalité dans le monde. Les anti-thrombotiques actuels, dirigés contre l'activation et l'agrégation plaquettaires, ont une efficacité reconnue mais ont pour inconvénient d'augmenter le risque de saignement. L'objectif de cette thèse a été d'explorer de nouvelles stratégies réduisant la thrombose tout en préservant l'hémostase. L'utilisation de souris modifiées génétiquement a mis en évidence que l'intégrine alpha6 beta1, impliquée dans l'adhérence des plaquettes aux laminines, joue un rôle critique en thrombose expérimentale mais pas en hémostase. De plus, nous avons montré dans un système de perfusion de sang qu'une protéine préférentiellement exprimée dans les plaques d'athérosclérose, la ténascine-C, permet l'adhérence et l'activation des plaquettes. En revanche, la beta-arrestine-1, une protéine de signalisation, ne contribue que modestement aux fonctions plaquettaires et à la thrombose. En conclusion, ce travail a permis de dégager deux nouvelles pistes anti-thrombotiques potentiellement capables de préserver l'hémostase, basées sur le ciblage de l'intégrine alpha6 beta1 ou de l'interaction plaquette/ténascine-C.
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Bao, Wenjie. "Role of integrin signaling in cell proliferation and survival /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-394-9/.

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Nadif, Raja. "The in vivo role of integrin alpha7 in heart integrity and function." Thesis, University of Manchester, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492878.

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Cardiovascular complications, including cardiac hypertrophy, arrhythmias and sudden death, are commonly associated with muscular dystrophies. Null mutations of the integrin alpha? gene, an essential mediator of cellular attachment to the extracellular matrix in cardiac and skeletal muscle, leads to progressive muscular dystrophy in humans, which is faithfully replicated in the integrin alpha? deficient (a7-/-) mouse model. In the latter, premature sudden death is not directly attributable to the dystrophic phenotype. We therefore analysed the cardiac phenotype in integrin a7-/- mice to determine whether their premature death is associated with altered cardiac structure and function and/or altered cardiac rhythm.
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Rahman, Abdul. "Neonatale Alloimmunthrombozytopenie die Entwicklung von rekombinanten [alpha]II-1tnb[beta]3-Integrin-Isoformen [Alpha-IIb-Beta-3-Integrin-Isoformen] (HPA-1 Antigene) und funktionelle Untersuchung einer seltenen Punktmutation auf [beta]3-Integrins [Beta-3-Integrins] (Oea-Antigen) /." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968380859.

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Zargham, Ramin. "[Alpha]8[beta]1 integrin and vascular injury : role of [alpha]8[beta]1 integrin in restenosis after balloon injury." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111876.

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Restenosis is the major cause of the failure of reconstruction methods to restore the blood flow in atherosclerotic arteries. Restenosis results from neointima formation and consequent constrictive remodelling. Vascular smooth muscle cell (VSMC) migration from the tunica media toward the intima is crucial in neointima genesis. The prerequisite for VSMC migratory activity is the modulation from the differentiated (contractile) to the de-differentiated (noncontractile) phenotype. VSMC phenotype change is associated with the altered expression of integrins. alpha8beta1 integrin is upregulated in cell types with contractile properties, including myofibroblasts and mesangial kidney cells. It is one of the integrins that is intensely expressed in mature VSMCs. alpha8beta1 integrin expression during vascular injury and its role in VSMC function have not been studied so far.
In this work, a rat model of carotid angioplasty was used to mimic vascular injury in humans. alpha8beta1 integrin was downregulated in the tunica media concomitantly with loss of the contractile phenotype. In vitro study revealed that it is a differentiation marker of VSMCs. To test the functional significance of the association between alpha8 integrin and the VSMC phenotype, short interference RNA was deployed to silence the alpha8 integrin gene. alpha8 integrin gene silencing heightened VSMC migratory activity as well as modulation of the VSMC phenotype in favour of the noncontractile state. In addition, alpha8 integrin overexpression induced re-differentiation of VSMCs and attenuated their migratory activity. It is, therefore, suggested that alpha8 integrin overexpression after vascular injury might control VSMC migration and neointima formation. On the other hand, alpha8 integrin gene silencing led to a reduced growth rate, which indicated a dichotomy between VSMC migration and proliferation.
In the later stages of neointima formation, constrictive remodeling plays a major role in late lumen loss. Our data demonstrated that alpha8 integrin is upregulated in the neointima during constrictive remodeling with concomitant luminal narrowing. The importance of this finding was highlighted by results showing that alpha8 integrin was required for the VSMC contractile phenotype evoked by transforming growth factor-beta (TFG-beta) and TFG-beta-induced myofibroblastic differentiation of Rat1 fibroblasts. Thus, it appears that alpha8 integrin expression blockade might reduce contractile remodeling and late lumen loss. Although the mechanism of alpha8 integrin signaling is not yet clear, our findings demonstrate that the alpha8 integrin-induced contractile phenotype is blocked by RhoA inhibitors. Furthermore, alpha8 integrin and RhoA are co-immunoprecipitated, and alpha8 integrin gene silencing reduces RhoA activity. Hence, it is postulated that alpha8-RhoA signaling might be closely intertwined.
Altogether, these studies indicate that alpha8 integrin is a contractile marker of VSMCs and a negative regulator of VSMC migration. Therefore, forced alpha8 integrin expression may be applied to reduce neointima formation. However, alpha8 integrin upregulation during constrictive remodeling concomitant with late lumen loss suggest that it could be involved in lumen narrowing. It seems likely that in therapeutic strategies to reduce restenosis the timeline of interference might be very important. Therefore, alpha8 integrin gene silencing in the later stages of neointima formation might be beneficial.
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Books on the topic "Integrin alpha6"

1

Sheridan, Joseph Michael. Rational design of integrin [alpha]4[beta]1 antagonists. Manchester: University of Manchester, 1995.

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Makarem, Rima. Regulation and molecular basis of ligand recognition by the integrin [alpha]4[beta]1. Manchester: University of Manchester, 1993.

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Silva, Matthew. Implications of the presence of petroleum resources on the integrity of the WIPP. Albuquerque, N.M: Environmental Evaluation Group, 1994.

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Chan, Jason Randolph. Role [alpha]4 integrins in ealry stages of leukocyte recruitment. 2002.

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Efficient adenovirus-mediated transgene expression in human acute myeloid leukemia cells: The roles of the integrins [alpha]v[beta]3, [alpha]v[beta]3, and of the coxsackievirus and adenovirus receptor. Ottawa: National Library of Canada, 2002.

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Guest, Deryn. Judging Yhwh in the Book of Judges. Edited by Danna Nolan Fewell. Oxford University Press, 2015. http://dx.doi.org/10.1093/oxfordhb/9780199967728.013.14.

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Narrative approaches initiated a sea-change in Judges studies. Narrative approaches, however, require additional tools if they are to challenge the text’s ideology. While several narrative critics combined their expertise with feminist theory, scholars are yet to engage fully with the critical study of masculinities or with queer studies that offer a new, rich vein of research focused on how gender and sexuality is an integral aspect of character. YHWH has largely evaded the kind of attention given to other, more earthly, characters. This chapter discusses YHWH’s alpha-male qualities and how they create gender trouble for the cast of male characters in Judges; how YHWH is caught up with the cultural dictates of honor and shame; how object-relations theory can be fruitful in understanding the relationship dynamics between YHWH and Israel. Attention finally returns to the narrator and his stake in this representation of the deity.
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Badimon, Lina, Felix C. Tanner, Giovanni G. Camici, and Gemma Vilahur. Pathophysiology of thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0018.

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Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its ability to induce thrombin formation (a potent platelet agonist) and subsequent fibrin deposition at sites of vascular injury. Adhered platelets at the site of injury also play a crucial role in the pathophysiology of atherothrombosis. Platelet surface receptors (mainly glycoproteins) interact with vascular structures and/or Von Willebrand factor triggering platelet activation signalling events, including an increase in intracellular free Ca2+, exposure of a pro-coagulant surface, and secretion of platelet granule content. On top of this, interaction between soluble agonists and platelet G-coupled protein receptors further amplifies the platelet activation response favouring integrin alpha(IIb)beta(3) activation, an essential step for platelet aggregation. Blood-borne TF and microparticles have also been shown to contribute to thrombus formation and propagation. As thrombus evolves different circulating cells (red-blood cells and leukocytes, along with occasional undifferentiated cells) get recruited in a timely dependent manner to the growing thrombus and further entrapped by the formation of a fibrin mesh.
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Book chapters on the topic "Integrin alpha6"

1

Appleton, Kathryn M., Ian Cushman, Yuri K. Peterson, Balachandran Manavalan, Shaherin Basith, Sangdun Choi, Akihiro Kimura, et al. "Integrin Alpha 11." In Encyclopedia of Signaling Molecules, 941–45. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_118.

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Biswas-Fiss, Esther E., Stephanie Affet, Malissa Ha, Takaya Satoh, Joe B. Blumer, Stephen M. Lanier, Ana Kasirer-Friede, et al. "Alpha E Integrin." In Encyclopedia of Signaling Molecules, 96–99. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_168.

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Biswas-Fiss, Esther E., Stephanie Affet, Malissa Ha, Takaya Satoh, Joe B. Blumer, Stephen M. Lanier, Ana Kasirer-Friede, et al. "Alpha v Integrin." In Encyclopedia of Signaling Molecules, 100. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100057.

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Appleton, Kathryn M., Ian Cushman, Yuri K. Peterson, Balachandran Manavalan, Shaherin Basith, Sangdun Choi, Akihiro Kimura, et al. "Integrin Alpha 4." In Encyclopedia of Signaling Molecules, 945. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100657.

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Anthony, Bryan A., and Gregg A. Hadley. "Alpha E Integrin." In Encyclopedia of Signaling Molecules, 280–85. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_168.

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Appleton, Kathryn M., Ian Cushman, Yuri K. Peterson, Balachandran Manavalan, Shaherin Basith, Sangdun Choi, Akihiro Kimura, et al. "Integrin Alpha V (ITGAV)." In Encyclopedia of Signaling Molecules, 949–59. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_619.

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Kerr, Bethany A., and Tatiana V. Byzova. "Integrin Alpha V (ITGAV)." In Encyclopedia of Signaling Molecules, 2634–45. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_619.

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Zeltz, Cédric, and Donald Gullberg. "Integrin Alpha11 (ITGA11)." In Encyclopedia of Signaling Molecules, 2645–52. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_118.

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Zeltz, Cédric, and Donald Gullberg. "Integrin Alpha11 (ITGA11)." In Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_118-1.

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Appleton, Kathryn M., Ian Cushman, Yuri K. Peterson, Balachandran Manavalan, Shaherin Basith, Sangdun Choi, Akihiro Kimura, et al. "Integrin Alpha 4 (Itga 4)." In Encyclopedia of Signaling Molecules, 945–49. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_143.

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Conference papers on the topic "Integrin alpha6"

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Mercier, MC, N. Fanny, LR Isabelle, S. Florence, and D. Monique. "PO-295 Heterogeneity of the alpha5 integrin subunit expression in glioblastoma." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.326.

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Cagle, L., L. Franzi, A. Linderholm, J. Last, N. J. Kenyon, and R. W. Harper. "Role of Dual Oxidase in Alpha-4 Integrin-Mediated Neutrophil Transmigration." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5253.

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Bhatia, Shreshtha Sailesh, H. Phillip Koeffler, and Sudhakar Jha. "Abstract 4670: TIP60 regulates alternative splicing of Integrin subunit alpha 6." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4670.

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Rondinella, V. V., T. Wiss, J. P. Hiernaut, and J. Cobos. "Studies on Spent Fuel Alterations During Storage and Radiolysis Effects on Corrosion Behaviour Using Alpha-Doped UO2." In ASME 2003 9th International Conference on Radioactive Waste Management and Environmental Remediation. ASMEDC, 2003. http://dx.doi.org/10.1115/icem2003-4593.

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UO2 containing different fractions of short-lived alpha-emitters, the so-called alpha-doped UO2 simulates the level of activity of spent fuel after different storage times, and can be used to study the effects of radiolysis on the corrosion behaviour of aged spent fuel exposed to groundwater in a geologic repository. Furthermore, the integral over time of the alpha-decay in alpha-doped UO2 can simulate the decay damage accumulated in spent fuel during storage. This allows investigating property modifications occurring to the fuel during storage periods of interest (e.g. in view of spent fuel retrieval or in view of final disposal) within a laboratory-acceptable timescale. Periodical measurements of lattice parameter are performed on high activity alpha-doped UO2 to investigate the build-up of radiation damage and evaluate possible dose rate effects. Additionally, annealing tests combined with He-release measurements using a Knudsen cell and with microstructure examination using TEM are performed to establish a correlation among the annealing of damage in the microstructure (mainly characterized by dislocation loops) and the release behaviour of He. The effects on the microstructure due to the accumulation of He and α-decay damage are of interest as they may considerably affect the mechanical integrity of the fuel rods, by causing e.g. swelling or cracking in the fuel and/or overpressurization of the cladding. Alpha-doped UO2 with specific activities spanning over three orders of magnitude and undoped UO2 were used in static leaching experiments at room temperature in deionized water under nominally anoxic conditions. Under these experimental conditions (single effect studies) a clear dissolution enhancing effect of alpha-radiolysis was observed coupled with the establishment of higher redox potential due to the radiolytic process. An alpha-activity dependence of the dissolution behaviour was observed.
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Hruska, K. A., and M. A. Chellaiah. "THE CRITICAL FUNCTION OF OSTEOPONTIN IN [alpha]v[beta]3 SIGNALING." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.309.

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Joshi, Raghav, Wenying Ren, and Paul Mathew. "Abstract 1902: The comparative superiority of a bispecific antibody targeting alpha v and alpha 5 integrins is uniquely characterized by induced degradation of integrins." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1902.

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Joshi, Raghav, Wenying Ren, and Paul Mathew. "Abstract 1902: The comparative superiority of a bispecific antibody targeting alpha v and alpha 5 integrins is uniquely characterized by induced degradation of integrins." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1902.

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Hong, Ji Hyung, Jeong-Hun Lee, Na Ra Yoon, Suk Hee Hong, and Yoon Ho Ko. "Abstract 2340: Integrin subunit alpha 5: Potential prognostic biomarker in lung adenocarcinoma." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2340.

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Huang, YL, CY Liang, M. Konantz, M. Nunez Lopez, C. Lengerke, F. Jacob, and V. Heinzelmann-Schwarz. "PO-173 Sialylation of integrin alpha 2 promotes ovarian cancer cells metastasis." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.212.

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Chellaiah, Meenakshi A., Rajat S. Biswas, David A. Yuen, Susan R. Rittling, David T. Denhardt, and Keith A. Hruska. "MOLECULAR MECHANISMS OF INTERACTION BETWEEN [alpha]V[beta]3 AND CD44 SIGNALING." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.236.

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Reports on the topic "Integrin alpha6"

1

Kamata, Tetsuji. (ALPHA) 2 (BETA) 1 Integrin-Induced Breast Cancer Differentiation. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada398563.

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Huang, Shuang. Vitronectin and Integrin alpha(v)Beta3 in Ovarian Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada420884.

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Kamata, Tetsuji. (ALPHA)2(BETA)1 Integrin-Induced Breast Cancer Differentiation. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada377910.

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Huang, Shuang. Vitronectin and Integrin (alpha)v(beta)3 in Ovarian Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396886.

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Turner-Haenssen, Keneshia. Role of Integrin Alpha 5 in ErbB2-Mediated Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2009. http://dx.doi.org/10.21236/ada513289.

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Baxter, Ruth M. Defining the Role of Integrin Alpha 11 in Wound Healing and Fibrosis. Fort Belvoir, VA: Defense Technical Information Center, September 2010. http://dx.doi.org/10.21236/ada535357.

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Mercurio, Arthur M. Integrin-Mediated Stimulation of HIF-1 alpha and Angiogenesis in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada408072.

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O'Connor, Kathleen L. Regulation of Breast Carcinoma Chemotaxis By the Integrin (Alpha)6 (BETA)4. Fort Belvoir, VA: Defense Technical Information Center, April 1999. http://dx.doi.org/10.21236/ada368334.

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Baxter, Ruth M. Defining the Role of Integrin Alpha 11 in Wound Healing and Fibrosis. Fort Belvoir, VA: Defense Technical Information Center, September 2009. http://dx.doi.org/10.21236/ada541391.

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Shaw, Leslie M., and A. Mercurio. Regulation of Breast Carcinoma Progression by the Alpha-6 Integrins. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada394030.

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