Relevant bibliographies by topics / Β4

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Β4'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 February 2022

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Journal articles on the topic "Β4"

1

Soung, Young, Shane Ford, Cecilia Yan, and Jun Chung. "The Role of Arrestin Domain-Containing 3 in Regulating Endocytic Recycling and Extracellular Vesicle Sorting of Integrin β4 in Breast Cancer." Cancers 10, no. 12 (December 11, 2018): 507. http://dx.doi.org/10.3390/cancers10120507.

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Despite the established role of integrin β4 (ITG β4) in breast cancer progression, the importance of endocytic recycling of ITG β4 and its regulatory mechanism are poorly understood. Here, we found that a sub-population of ITG β4 is sorted into early endosomes, recycled back to the plasma membrane, and secreted in the form of extracellular vesicles (EVs) upon EGF treatment in triple negative breast cancer (TNBC) cells. A metastasis suppressor, ARRDC3 (arrestin domain-containing 3) prevents EGF-driven endocytic recycling of ITG β4 by inducing NEDD4-dependent ubiquitination of ITG β4 and targeting endosomal ITG β4 into lysosomes. Endocytic recycling of ITG β4 is linked to sorting of ITG β4 into EVs (ITG β4+ EVs). ITG β4+ EVs are mainly detectable from supernatants of TNBC cells and their production is inhibited by ARRDC3 expression. ARRDC3 reduces the metastatic potentials of breast cancer cell-derived EVs by reducing ITG β4 levels in EVs. Overall, current studies provide novel mechanistic insights on the regulatory mechanism of ITG β4 recycling, and its importance in invasive potentials of TNBC EVs, thus providing the basis for therapeutic targeting of the ARRDC3/ITG β4 pathway in TNBC.
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2

Geuijen, Cecile A. W., and Arnoud Sonnenberg. "Dynamics of the α6β4 Integrin in Keratinocytes." Molecular Biology of the Cell 13, no. 11 (November 2002): 3845–58. http://dx.doi.org/10.1091/mbc.02-01-0601.

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The integrin α6β4 has been implicated in two apparently contrasting processes, i.e., the formation of stable adhesions, and cell migration and invasion. To study the dynamic properties of α6β4 in live cells two different β4-chimeras were stably expressed in β4-deficient PA-JEB keratinocytes. One chimera consisted of full-length β4 fused to EGFP at its carboxy terminus (β4-EGFP). In a second chimera the extracellular part of β4 was replaced by EGFP (EGFP-β4), thereby rendering it incapable of associating with α6 and thus of binding to laminin-5. Both chimeras induce the formation of hemidesmosome-like structures, which contain plectin and often also BP180 and BP230. During cell migration and division, the β4-EGFP and EGFP-β4 hemidesmosomes disappear, and a proportion of the β4-EGFP, but not of the EGFP-β4 molecules, become part of retraction fibers, which are occasionally ripped from the cell membrane, thereby leaving “footprints” of the migrating cell. PA-JEB cells expressing β4-EGFP migrate considerably more slowly than those that express EGFP-β4. Studies with a β4-EGFP mutant that is unable to interact with plectin and thus with the cytoskeleton (β4R1281W-EGFP) suggest that the stabilization of the interaction between α6β4 and LN-5, rather than the increased adhesion to LN-5, is responsible for the inhibition of migration. Consistent with this, photobleaching and recovery experiments revealed that the interaction of β4 with plectin renders the bond between α6β4 and laminin-5 more stable, i.e., β4-EGFP is less dynamic than β4R1281W-EGFP. On the other hand, when α6β4 is bound to laminin-5, the binding dynamics of β4 to plectin are increased, i.e., β4-EGFP is more dynamic than EGFP-β4. We suggest that the stability of the interaction between α6β4 and laminin-5 is influenced by the clustering of α6β4 through the deposition of laminin-5 underneath the cells. This clustering ultimately determines whether α6β4 will inhibit cell migration or not.
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Ivanova, V. P. "THE EFFECT OF THYMOSIN β4 ON THE FUNCTIONAL ACTIVITY OF THE IMMUNE AND NERVOUS SYSTEM COMPONENTS." Medical academic journal 19, no. 1S (December 15, 2019): 164–66. http://dx.doi.org/10.17816/maj191s1164-166.

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The data on properties of thymosin β4, a conserved multifunctional polypeptide of mammals is summarized. Attention has been focused on regulatory activity of thymosin β4 in regard to immune and nervous system components. In these systems thymosin β4 is present in different cell types both stationary and mobile ones. Besides intracellular localization thymosin β4 is also located in extracellular fluids. Inside cells, thymosin β4 has been postulated to regulate actin polymerization as a G-actin-sequestering molecule. But molecular mechanisms of thymosin β4 located extra cells on cell functions remain unclear. The structural-functional organization of thymosin β4 is also discussed. Thymosin β4 is a perspective medicine preparation for the therapy of diseases related to immune and neurological disturbances in patients.
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Rima, Mohamad, Marwa Daghsni, Anaïs Lopez, Ziad Fajloun, Lydie Lefrancois, Mireia Dunach, Yasuo Mori, et al. "Down-regulation of the Wnt/β-catenin signaling pathway by Cacnb4." Molecular Biology of the Cell 28, no. 25 (December 2017): 3699–708. http://dx.doi.org/10.1091/mbc.e17-01-0076.

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The β4 isoform of the β-subunits of voltage-gated calcium channel regulates cell proliferation and cell cycle progression. Herein we show that coexpression of the β4-subunit with actors of the canonical Wnt/β-catenin signaling pathway in a hepatoma cell line inhibits Wnt-responsive gene transcription and decreases cell division, in agreement with the role of the Wnt pathway in cell proliferation. β4-subunit–mediated inhibition of Wnt signaling is observed in the presence of LiCl, an inhibitor of glycogen synthase kinase (GSK3) that promotes β-catenin translocation to the nucleus. Expression of β4-subunit mutants that lost the ability to translocate to the nucleus has no effect on Wnt signaling, suggesting that β4-subunit inhibition of Wnt signaling occurs downstream from GSK3 and requires targeting of β4-subunit to the nucleus. β4-subunit coimmunoprecipitates with the TCF4 transcription factor and overexpression of TCF4 reverses the effect of β4-subunit on the Wnt pathway. We thus propose that the interaction of nuclear β4-subunit with TCF4 prevents β-catenin binding to TCF4 and leads to the inhibition of the Wnt-responsive gene transcription. Thereby, our results show that β4-subunit is a TCF4 repressor and therefore appears as an interesting candidate for the regulation of this pathway in neurons where β4-subunit is specifically expressed.
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5

Pullar, Christine E., Brian S. Baier, Yoshinobu Kariya, Alan J. Russell, Basil A. J. Horst, M. Peter Marinkovich, and R. Rivkah Isseroff. "β4 Integrin and Epidermal Growth Factor Coordinately Regulate Electric Field-mediated Directional Migration via Rac1." Molecular Biology of the Cell 17, no. 11 (November 2006): 4925–35. http://dx.doi.org/10.1091/mbc.e06-05-0433.

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Endogenous DC electric fields (EF) are present during embryogenesis and are generated in vivo upon wounding, providing guidance cues for directional cell migration (galvanotaxis) required in these processes. To understand the role of beta (β)4 integrin in directional migration, the migratory paths of either primary human keratinocytes (NHK), β4 integrin-null human keratinocytes (β4−), or those in which β4 integrin was reexpressed (β4+), were tracked during exposure to EFs of physiological magnitude (100 mV/mm). Although the expression of β4 integrin had no effect on the rate of cell movement, it was essential for directional (cathodal) migration in the absence of epidermal growth factor (EGF). The addition of EGF potentiated the directional response, suggesting that at least two distinct but synergistic signaling pathways coordinate galvanotaxis. Expression of either a ligand binding–defective β4 (β4+AD) or β4 with a truncated cytoplasmic tail (β4+CT) resulted in loss of directionality in the absence of EGF, whereas inhibition of Rac1 blinded the cells to the EF even in the presence of EGF. In summary, both the β4 integrin ligand–binding and cytoplasmic domains together with EGF were required for the synergistic activation of a Rac-dependent signaling pathway that was essential for keratinocyte directional migration in response to a galvanotactic stimulus.
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Schaapveld, Roel Q. J., Luca Borradori, Dirk Geerts, Manuel R. van Leusden, Ingrid Kuikman, Mirjam G. Nievers, Carien M. Niessen, Renske D. M. Steenbergen, Peter J. F. Snijders, and Arnoud Sonnenberg. "Hemidesmosome Formation Is Initiated by the β4 Integrin Subunit, Requires Complex Formation of β4 and HD1/Plectin, and Involves a Direct Interaction between β4 and the Bullous Pemphigoid Antigen 180." Journal of Cell Biology 142, no. 1 (July 13, 1998): 271–84. http://dx.doi.org/10.1083/jcb.142.1.271.

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Hemidesmosomes (HDs) are stable anchoring structures that mediate the link between the intermediate filament cytoskeleton and the cell substratum. We investigated the contribution of various segments of the β4 integrin cytoplasmic domain in the formation of HDs in transient transfection studies using immortalized keratinocytes derived from an epidermolysis bullosa patient deficient in β4 expression. We found that the expression of wild-type β4 restored the ability of the β4-deficient cells to form HDs and that distinct domains in the NH2- and COOH-terminal regions of the β4 cytoplasmic domain are required for the localization of HD1/plectin and the bullous pemphigoid antigens 180 (BP180) and 230 (BP230) in these HDs. The tyrosine activation motif located in the connecting segment (CS) of the β4 cytoplasmic domain was dispensable for HD formation, although it may be involved in the efficient localization of BP180. Using the yeast two-hybrid system, we could demonstrate a direct interaction between β4 and BP180 which involves sequences within the COOH-terminal part of the CS and the third fibronectin type III (FNIII) repeat. Immunoprecipitation studies using COS-7 cells transfected with cDNAs for α6 and β4 and a mutant BP180 which lacks the collagenous extracellular domain confirmed the interaction of β4 with BP180. Nevertheless, β4 mutants which contained the BP180-binding region, but lacked sequences required for the localization of HD1/plectin, failed to localize BP180 in HDs. Additional yeast two- hybrid assays indicated that the 85 COOH-terminal residues of β4 can interact with the first NH2-terminal pair of FNIII repeats and the CS, suggesting that the cytoplasmic domain of β4 is folded back upon itself. Unfolding of the cytoplasmic domain may be part of a mechanism by which the interaction of β4 with other hemidesmosomal components, e.g., BP180, is regulated.
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Litjens, Sandy H. M., Jan Koster, Ingrid Kuikman, Sandra van Wilpe, José M. de Pereda, and Arnoud Sonnenberg. "Specificity of Binding of the Plectin Actin-binding Domain to β4 Integrin." Molecular Biology of the Cell 14, no. 10 (October 2003): 4039–50. http://dx.doi.org/10.1091/mbc.e03-05-0268.

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Plectin is a major component of the cytoskeleton and links the intermediate filament system to hemidesmosomes by binding to the integrin β4 subunit. Previously, a binding site for β4 was mapped on the actin-binding domain (ABD) of plectin and binding of β4 and F-actin to plectin was shown to be mutually exclusive. Here we show that only the ABDs of plectin and dystonin bind to β4, whereas those of other actin-binding proteins do not. Mutations of the ABD of plectin-1C show that Q131, R138, and N149 are critical for tight binding of the ABD to β4. These residues form a small cavity, occupied by a well-ordered water molecule in the crystal structure. The β4 binding pocket partly overlaps with the actin-binding sequence 2 (ABS2), previously shown to be essential for actin binding. Therefore, steric interference may render binding of β4 and F-actin to plectin mutually exclusive. Finally, we provide evidence indicating that the residues preceding the ABD in plectin-1A and -1C, although unable to mediate binding to β4 themselves, modulate the binding activity of the ABD for β4. These studies demonstrate the unique property of the plectin-ABD to bind to both F-actin and β4, and explain why several other ABD-containing proteins that are expressed in basal keratinocytes are not recruited into hemidesmosomes.
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Bertotti, Andrea, Paolo M. Comoglio, and Livio Trusolino. "β4 integrin activates a Shp2–Src signaling pathway that sustains HGF-induced anchorage-independent growth." Journal of Cell Biology 175, no. 6 (December 11, 2006): 993–1003. http://dx.doi.org/10.1083/jcb.200605114.

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Despite being a cell–matrix adhesion molecule, β4 integrin can prompt the multiplication of neoplastic cells dislodged from their substrates (anchorage-independent growth). However, the molecular events underlying this atypical behavior remain partly unexplored. We found that activation of the Met receptor for hepatocyte growth factor results in the tyrosine phosphorylation of β4, which is instrumental for integrin-mediated recruitment of the tyrosine phosphatase Shp2. Shp2 binding to β4 enhances the activation of Src, which, in turn, phosphorylates the multiadaptor Gab1 predominantly on consensus sites for Grb2 association, leading to privileged stimulation of the Ras–extracellular signal-regulated kinase (ERK) cascade. This signaling axis can be inhibited by small interfering RNA–mediated β4 depletion, by a β4 mutant unable to bind Shp2, and by pharmacological and genetic inhibition of Shp2 or Src. Preservation of the β4 docking sites for Shp2 as well as the integrity of Shp2, Src, or ERK activity are required for the β4-mediated induction of anchorage-independent growth. These results unravel a novel pathway whereby β4 directs tyrosine kinase–based signals toward adhesion-unrelated outcomes.
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Grimm, P. Richard, Ruth M. Foutz, Robert Brenner, and Steven C. Sansom. "Identification and localization of BK-β subunits in the distal nephron of the mouse kidney." American Journal of Physiology-Renal Physiology 293, no. 1 (July 2007): F350—F359. http://dx.doi.org/10.1152/ajprenal.00018.2007.

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Large-conductance, Ca2+-activated K+ channels (BK), comprised of pore-forming α- and accessory β-subunits, secrete K+ in the distal nephron under high-flow and high-K+ diet conditions. BK channels are detected by electrophysiology in many nephron segments; however, the accessory β-subunit associated with these channels has not been determined. We performed RT-PCR, Western blotting, and immunohistochemical staining to determine whether BK-β1 is localized to the connecting tubule's principal-like cells (CNT) or intercalated cells (ICs), and whether BK-β2-4 are present in other distal nephron segments. RT-PCR and Western blots revealed that the mouse kidney expresses BK-β1, BK-β2, and BK-β4. Available antibodies in conjunction with BK-β1−/− and BK-β4−/− mice allowed the specific localization of BK-β1 and BK-β4 in distal nephron segments. Immunohistochemical staining showed that BK-β1 is localized in the CNT but not ICs of the connecting tubule. The localization of BK-β4 was discerned using an anti-BK-β4 antibody on wild-type tissue and anti-GFP on GFP-replaced BK-β4 mouse (BK-β4−/−) tissue. Both antibodies (anti-BK-β4 and anti-GFP) localized BK-β4 to the thick ascending limb (TAL), distal convoluted tubule (DCT), and ICs of the distal nephron. It is concluded that BK-β1 is narrowly confined to the apical membrane of CNTs in the mouse, whereas BK-β4 is expressed in the TAL, DCT, and ICs.
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Yang, Xiuwei, Oleg V. Kovalenko, Wei Tang, Christoph Claas, Christopher S. Stipp, and Martin E. Hemler. "Palmitoylation supports assembly and function of integrin–tetraspanin complexes." Journal of Cell Biology 167, no. 6 (December 20, 2004): 1231–40. http://dx.doi.org/10.1083/jcb.200404100.

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As observed previously, tetraspanin palmitoylation promotes tetraspanin microdomain assembly. Here, we show that palmitoylated integrins (α3, α6, and β4 subunits) and tetraspanins (CD9, CD81, and CD63) coexist in substantially overlapping complexes. Removal of β4 palmitoylation sites markedly impaired cell spreading and signaling through p130Cas on laminin substrate. Also in palmitoylation-deficient β4, secondary associations with tetraspanins (CD9, CD81, and CD63) were diminished and cell surface CD9 clustering was decreased, whereas core α6β4–CD151 complex formation was unaltered. There is also a functional connection between CD9 and β4 integrins, as evidenced by anti-CD9 antibody effects on β4-dependent cell spreading. Notably, β4 palmitoylation neither increased localization into “light membrane” fractions of sucrose gradients nor decreased solubility in nonionic detergents—hence it does not promote lipid raft association. Instead, palmitoylation of β4 (and of the closely associated tetraspanin CD151) promotes CD151–α6β4 incorporation into a network of secondary tetraspanin interactions (with CD9, CD81, CD63, etc.), which provides a novel framework for functional regulation.
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Dissertations / Theses on the topic "Β4"

1

Rossdeutsch, A. "The role of thymosin β4 in vascular development." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1333963/.

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Thymosin β4 (Tβ4) is a 43 amino acid peptide encoded by the Tmsb4x gene located on the X-chromosome. It has previously been shown to act as a secreted factor from the myocardium to the overlying epicardium of the developing murine heart, to mediate transformation of epicardial derived progenitor cells (EPDCs) into the coronary vasculature. This PhD project seeks to build on these studies and characterises the function of Tβ4 in the developing systemic vasculature, using the mouse as a model system. Expression analyses demonstrated specific localisation of Tβ4/Tβ4 in the endothelial cells of the embryonic vasculature. In order to ascertain the function of vascular Tβ4, global and endothelial cell specific in vivo Tβ4 loss of function models were examined. Both global and endothelial-specific Tβ4 mutant embryos displayed a reduced recruitment of vascular mural cells to developing blood vessels. Detailed phenotypic examination revealed that the mural cell deficit could be attributed to impaired differentiation of mature mural cells from undifferentiated mesoderm. This process was modelled in vitro, and it was discovered that treatment of the mural progenitor cell lines 10T1/2 and A404 with exogenous Tβ4 could promote their differentiation into mural cells. This process correlated with an increase in Smad phosphorylation and increased activity of the TGF-β pathway. Decreased levels of TGF-β target genes in vivo in Tβ4β null embryos indicated that TGF-β signalling was perturbed in the absence of Tβ4. These findings suggest a model whereby Tβ4 is secreted by the developing endothelium to stimulate the differentiation of uncommitted mesoderm into mature peri-vascular mural cells, via activation of the TGF-β pathway in the target cell population. As a consequence, Tb4 plays an essential role in vascular stability through mural cell support which has implications for vascular dysfunction in disease.
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2

Lowe, Martin David. "Functional characterisation of the cardiac putative β4-adrenergic receptor." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619730.

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Ruban, Emily L. "PLC-β4 signalling & function in human squamous cell carcinoma." Thesis, Queen Mary, University of London, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612569.

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Martin, R. K. "Exploring the role of centaurin β4 in a melanoma cell line." Thesis, University of Newcastle Upon Tyne, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501277.

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Melanoma is a cancer of the epidermal pigment cells, melanocytes. It is characterised by its metastatic ability and resistance to chemotherapy and radiotherapy. Centaurin β4 expression was recently shown to be upregulated in advanced stages of uveal melanoma and also in breast, colon and prostate cancer. Centaurin β4 is involved in the cyclic activation of ADP Ribosylation Factors (Arfs) which are activated at membranes. Arfs are involved in clathrin and COPI/Il vesicle formation and budding and therefore control protein trafficking between membranes. They are also involved in control of the actin cytoskeleton and their cyclic activation promotes protrusions such as invadopodia. Centaurin β4 is a multi-domain protein whose interaction with cortactin promotes invasion and metastasis specifically in tumour cells. Knock-down of centaurin β4 expression reduces invasion and motility of breast cancer cell lines sussesting an important role in carcinogenesis.
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Harrington, Lauriane. "The role of β4-containing nicotinic acetylcholine receptors in nicotine addiction." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066328/document.

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Le tabac est consommé par environ un milliard de personnes. D'après l'Organisation Mondiale de la Santé, le tabagisme est la première cause évitable de mortalité dans le monde, provocant six millions de morts par an. La nicotine est le composant neuro-actif principal dans le tabac, et exerce ses effets neurologiques via une activation directe des récepteurs nicotiniques de l’acétylcholine (nAChR). Ces récepteurs transmembranaires sont composés de sous-unités alpha, ou alpha plus beta, créant une variété de canaux ioniques ligand-dépendants activés par le neurotransmetteur ACh. Les études génétiques chez l’homme ont mis en évidence des variants dans le cluster génomique CHRNA5-CHRNA3-CHRNB4, codant pour les sous-unités α5, α3 et β4, comme facteurs influençant le tabagisme. Cette thèse a étudié le rôle des nAChRs contenant la sous-unité β4 (β4*) dans l’addiction à la nicotine. En collaboration, nous avons montré que les souris déficientes pour la sous-unité β4 (β4 KO), sont moins sensibles aux effets récompensant et aversifs de la nicotine. En générant un lentivirus exprimant la séquence murine d'ADN complémentaire de β4, j’ai pu restaurer son expression dans des régions d’intérêt du cerveau, sur un fond génétique β4KO. Ceci a permis de mettre en évidence le rôle du réseau habénulo-interpedonculaire dans la contribution des β4* nAChRs à la consommation de nicotine. Ceci a également démontré le rôle modulateur de ces récepteurs dans les réponses de la voie mésolimbique à la nicotine, voie centrale dans l'effet renforçant des drogues
Tobacco is consumed by an estimated 1 billion people world-wide. The World Health Organization names tobacco consumption the primary cause of preventable morbidity and mortality, causing six million deaths per year. Nicotine is the principal neuro-active compound in tobacco, and exerts neurological effects by binding to nicotinic acetylcholine receptors (nAChRs). These transmembrane receptors are composed of alpha or alpha plus beta subunits, forming a diverse variety of ligand-gated ion channels endogenously activated by ACh. Human genetic studies have highlighted variants in the CHRNA5-CHRNA3-CHRNB4 genomic cluster, coding for subunits α5, α3 and β4, as altering smoking behaviours. The present thesis investigated the role of β4-containing (β4*) nAChRs in nicotine addiction. In collaboration, we showed that β4 knockout (KO) mice are less sensitive to nicotine reward and nicotine aversion. Generating a lentivirus for the expression of mouse β4 nAChR subunit complementary DNA, I was able to restore receptor expression to brain regions of interest on a KO background, locating the role of β4* nAChR in nicotine reward and aversion to the habenulo-interpedunular pathway. This also demonstrated the receptor’s modulation of nicotinic responses of the mesolimbic system, central hub of drug reinforcement
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Knop, Jana [Verfasser], and Ewald [Akademischer Betreuer] Hannappel. "Die enzymatische und chemische Vernetzung von Thymosin β4 mit Proteinen. Charakterisierung der Vernetzung und Auswirkung auf die biologischen Funktionen von Thymosin β4 / Jana Knop. Betreuer: Ewald Hannappel." Erlangen : Universitätsbibliothek der Universität Erlangen-Nürnberg, 2013. http://d-nb.info/1036305317/34.

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Viltard, Mélanie. "Mise en évidence de nouveaux gènes impliqués dans la néphrogenèse : Thymosine β4 [Bêta 4]." Paris 6, 2005. http://www.theses.fr/2005PA066364.

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Zhao, Yanan. "The role of thymosin β4 during embryonic wound healing and tail regeneration in Xenopus." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-thymosin-4-during-embryonic-wound-healing-and-tail-regeneration-in-xenopus(7578b7d2-c63a-4a89-992c-16ab8bf1e24c).html.

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At the outset of my PhD, my aim was to investigate the mechanisms responsible for the directed migration of primitive myeloid cells (PMCs) to wounds in Xenopus embryos. PMCs are the first blood cells to differentiate and become functional in Xenopus embryos, and have a notable migratory ability to be recruited by embryonic wounds before a functional vasculature is established. To find the mechanism underlying PMCs migration toward embryonic wounds, I first performed a screen to identify candidate cytoskeleton related genes, which might be responsible for facilitating the inflammatory response to injury in embryos. In situ hybridization and RT-PCR showed that coronin1a and l-plastin were specifically expressed in PMCs. I carried out loss-of-function experiments for coronin 1a and l-plastin in Xenopus embryos. Unfortunately neither knockdown affected the ability for PMCs to migrate during embryonic development or during the wound healing process. Loss-of-function experiments on coronin 1a and l-plastin also did not affect epidermal wound closure speed. Thus, although coronin 1a and l- plastin are expressed specifically in PMCs, they do not appear to be necessary for the migration of PMCs during development and during wound healing in Xenopuos embryos. Since my initial aim failed to provide insight into the mechanisms that mediate 9the inflammatory response to embryonic wounds, I decided to investigate the function of a previously identified monomeric actin protein during embryonic wound healing and appendage regeneration: namely Thymosin beta4 (Tβ4). In situ hybridization experiments showed that Tβ4 is expressed exclusively in the epidermis of developing frog embryos. Tβ4 knockdown embryos resulted in a significantly delay in the speed of wound closure during the early phase of wound healing. This delay correlated with a decrease in the actin contractile ring at the wound margin. Furthermore I found that the cell shapes of epidermal cells in the Tβ4 knockdown embryos were different from epidermal cells in control embryos. I hypothesize that this reduction caused the actin filaments changes in the epidermal cells, and were responsible for the failure of the cells to form an actin contractile ring, thus delaying the initial speed of wound closure. I tried to confirm that most of these defects specific to Tβ4, by performing rescue experiments with Tβ4 mRNA injections. Furthermore, I discovered that Tβ4 knockdown embryos displayed defects in tail development, including the absence of blood vessel branching within the fin of the tail. Finally, I found that the tails in Tβ4 knocked-down tadpoles failed to regenerate, while tails in control embryos regenerated completely following amputation. Both in situ hybridization and real-time PCR showed that Tβ4 was up regulated in the regenerated part of the tail in Xenopus tadpoles. Together with the tail amputation results, Tβ4 might be important for tail development and regeneration. These findings suggest that Tβ4 might play an important roles in the modulation of the actin cytoskeleton, which are essential for the proper behavior of epidermal cells during wound healing and appendage regeneration.
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Lexow, Jonas Maximilian. "Inducible depletion of cardiac thymosin β4 : development and shortcomings of a popular technique in cardiac research." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/11091.

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In reference to recent studies highlighting the importance of Thymosin beta 4 (Tβ4) during embryonic development and its therapeutic potential, an inducible cardiac-specific knockdown of Tβ4 was established to investigate the outcomes of loss of function in adult mammalian hearts. Tβ4shRNAflox/MerCreMer mice were generated with the aim of depleting cardiac Tβ4 expression by RNA interference in a tamoxifen-dependent fashion. In vivo, in vitro and ex vivo approaches showed that tamoxifen treatment of Tβ4shRNAflox/MerCreMer mice does not result in significant down-regulation of Tβ4 mRNA or protein in the heart. Interestingly, higher levels of Tβ4 were identified in cardiac fibroblasts compared to cardiomyocytes. The above analyses suggest that an inducible knockout of Tβ4 would be a more direct, more reliable and more effective means to study loss of function in the adult mammalian heart. In the course of the study, an adverse cardiac phenotype was observed in tamoxifen-treated MerCreMer-positive animals, consisting of perivascular and interstitial fibrosis, decreased cardiac function, a marked inflammatory response and increased expression of factors involved in cardiac remodelling and hypertrophy. This was not related to MerCreMer gene copy number (homo/heterozygosity) but found to be associated with tamoxifen dose, mode of delivery and genetic background. A thorough analysis of related literature revealed that a number of recent publications have failed to include tamoxifen-treated αMHC/MerCreMer controls and some of the presented data may be affected by Cre toxicity. In conclusion, αMHC/MerCreMer mice should be included as controls in the analysis of future studies or alternative inducible systems considered. Recent analyses revealed that IGF-1Ea overexpression in the heart improves the outcome of myocardial infarction in mice. This process has been described on the molecular level but a comprehensive analysis of the subcellular structure of αMHC/IGF-1Ea hearts had not previously been performed. A detailed transmission electron microscope analysis of αMHC/IGF-1Ea hearts revealed previously not described large electron-dense structures inside αMHC/IGF-1Ea cardiomyocytes. The structures resembled large autophagolysosomes although markers of autophagy were neither found to be associated with the structures nor upregulated in the hearts of αMHC/IGF-1Ea mice. Intriguingly lysosomes were identified in the proximity of the structures potentially implying a role in turnover of intracellular material. These results provide further insights into the diverse roles of IGF-1Ea in the heart.
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Bon, Emeline. "Implication de la sous-unité B4 des canaux sodiques dépendants du voltage dans l'invasivité des cellules cancéreuses mammaires et régulation de son expression par l'acide docosahexaènoïque." Thesis, Tours, 2015. http://www.theses.fr/2015TOUR3310/document.

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La perte de l’expression de la sous-unité β4 des canaux sodiques dépendants du voltage NaV dans les tumeurs mammaires est associée à un grade cancéreux élevé et au développement des métastases. L’extinction de son expression dans les cellules MDA-MB-231 augmente de plus de deux fois leur invasivité. Au cours de cette thèse, nous avons montré que la sous-expression de β4 favorise la transition mésenchymato-amoeboïde et augmente l’invasion cancéreuse indépendante de NaV. Cette transition se caractérise par l’acquisition d’une morphologie plus arrondie, par la présence de blebs à la surface cellulaire et par une augmentation de l’activité RhoA-GTPase. Cette transition est inhibée par la surexpression du domaine intracellulaire C-terminal de la sousunité β4. L’expression de β4 peut être augmentée par un apport en acide docosahexaènoïque (22:6n-3), qui augmente l’activité du promoteur de son gène SCN4B. Le DHA augmente également l’expression de β4 en modulant l’expression des récepteurs nucléaires PPAR, sensibles aux lipides
The loss of voltage gated sodium channel NaVβ4 subunit expression in breast cancer biopsies is associated with high grade tumors and metastatic development. The inhibition of β4 expression in MDA-MB-231 breast cancer cells enhanced their invasiveness by two fold. During this thesis, we have shown that β4 underexpression promotes mesenchymal-amoeboid transition and increases NaV-independent invasion. This transition is characterized by rounded morphology, the presence of blebs at the cell surface and an increased RhoAGTPase activity. This transition is inhibited by β4 C-terminal intracellular domain overexpression. Expression of β4 can be enhanced by a DHA supplementation that increases the encoding SCN4B promoter activity. DHA also increases β4 expression through the modulation of PPARs lipid-sensitive nuclear receptors expression
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Book chapters on the topic "Β4"

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Shaper, Nancy L., and Joel H. Shaper. "β4-Galactosyltransferase-I." In Handbook of Glycosyltransferases and Related Genes, 11–19. Tokyo: Springer Japan, 2002. http://dx.doi.org/10.1007/978-4-431-67877-9_2.

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Furukawa, Koichi. "β4-N-Acetylgalactosaminyltransferase." In Handbook of Glycosyltransferases and Related Genes, 174–79. Tokyo: Springer Japan, 2002. http://dx.doi.org/10.1007/978-4-431-67877-9_23.

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Wang, S. S., B. S. H. Wang, and A. L. Goldstein. "Thymosin α1, thymosin β4 and analogs." In Peptides, 39–43. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-010-9069-8_9.

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Voelter, W., F. P. Armbruster, A. Kapurniotu, E. Livaniou, M. Mihelić, and C. Perrei. "Theoretical and experimental epitope mapping of thymosin β4." In Peptides, 895–96. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2264-1_364.

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Furukawa, Kiyoshi, and Henrik Clausen. "β4-Galactosyltransferase-II, -III, -IV, -V, -VI, and -VII." In Handbook of Glycosyltransferases and Related Genes, 20–26. Tokyo: Springer Japan, 2002. http://dx.doi.org/10.1007/978-4-431-67877-9_3.

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Sato, Takeshi, and Kiyoshi Furukawa. "Expression and Transcriptional Regulation of β4-Galactosyltransferase Genes in Cancer." In Glycoscience: Biology and Medicine, 1–5. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54836-2_73-1.

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Sato, Takeshi, and Kiyoshi Furukawa. "Expression and Transcriptional Regulation of β4-Galactosyltransferase Genes in Cancer." In Glycoscience: Biology and Medicine, 1135–39. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54841-6_73.

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Au, Joshua K., Mira Krendel, Daniel Safer, and Enrique M. De La Cruz. "The Roles of Thymosin β4 in Cell Migration and Cell-to-Cell Signaling in Disease." In Actin-Binding Proteins and Disease, 218–28. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-71749-4_9.

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Mihelić, Mirna, and Wolfgang Voelter. "Immunohistochemical localization of thymosin β4 with antibodies raised from a synthetic fragment with high antigenicity." In Peptides 1992, 905–6. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1470-7_415.

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Wise, T., J. Klindt, F. C. Buonomo, and J. T. Yen. "Effects of Porcine Somatotropin on Thymic Weight, Thymosin α1, and Thymosin β4 in Gilts and Barrows." In Growth Hormone II, 317–27. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4613-8372-7_24.

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Conference papers on the topic "Β4"

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Ruan, Shasha, Ming Lin, Yongshun Chen, Elaine Hurt, Alfred E. Chang, Max S. Wicha, and Qiao Li. "Abstract 375: Integrin β4-targeted cancer immunotherapies." 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.am2019-375.

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Ruan, Shasha, Ming Lin, Yongshun Chen, Elaine Hurt, Alfred E. Chang, Max S. Wicha, and Qiao Li. "Abstract 375: Integrin β4-targeted cancer immunotherapies." 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.sabcs18-375.

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Chen, W., S. Sammani, J. Zhao, J. Garcia, and J. Jacobson. "The Attenuation of Murine Acute Lung Injury by Simvastatin Is Mediated by Integrin β4." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5550.

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Provo, Richard, Stuart G. Murdoch, John D. Harvey, and David Méchin. "Experimental Demonstration of the Phase Matching Curve for Bragg Scattering in a Positive β4 Fiber." In Conference on Lasers and Electro-Optics. Washington, D.C.: OSA, 2010. http://dx.doi.org/10.1364/cleo.2010.ctui7.

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Lin, Li-Fang, Meei-Maan Wu, and Te-Chang Lee. "Abstract 1616: Galectin-4 interferes with the integrin β4/Src/FAK cascade and attenuates metastasis in urothelial carcinoma." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1616.

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Munshaw, Sonali, Susann Bruche, Jyoti Patel, Andia Redpath, Karina N. Dubé, Regent Lee, Ashok Handa, Keith M. Channon, and Nicola Smart. "B Thymosin β4 – a novel regulator of low density lipoprotein receptor related protein 1 (LRP1) in vascular disease." In British Cardiovascular Society Annual Conference ‘Digital Health Revolution’ 3–5 June 2019. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bcs.225.

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Masugi, Yohei, Ken Yamazaki, Katsura Emoto, Kathryn Effendi, Minoru Kitago, Osamu Itano, Yuko Kitagawa, and Michiie Sakamoto. "Abstract 1146: Up-regulation of integrin β4 promotes epithelial-mesenchymal transition and is a novel prognostic marker in pancreatic cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1146.

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Bhatia, Vandanajay, Ramanjaneya V. Mula, and Miriam A. Falzon. "Abstract 1969: Mapping the cross talk between parathyroid hormone related protein (PTHrP) and Integrins α6 and β4 in prostate cancer cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1969.

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Tai, Yu-Ling, and Tang-Long Shen. "Abstract C44: Activation of focal adhesion kinase by direct interaction with β4 integrin in an EGFR-Src-dependent pathway in tumor progression." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-c44.

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