Готові списки джерел за темами / Alpha4 integrins

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Добірка наукової літератури з теми "Alpha4 integrins"

Автор: Grafiati
Опубліковано: 11 березня 2023

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Статті в журналах з теми "Alpha4 integrins"

1

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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Анотація:
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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2

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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Анотація:
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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3

Kawamoto, Eiji, Susumu Nakahashi, Takayuki Okamoto, Hiroshi Imai, and Motomu Shimaoka. "Anti-Integrin Therapy for Multiple Sclerosis." Autoimmune Diseases 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/357101.

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Анотація:
Integrins are the foremost family of cell adhesion molecules that regulate immune cell trafficking in health and diseases. Integrin alpha4 mediates organ-specific migration of immune cells to the inflamed brain, thereby playing the critical role in the pathogenesis of multiple sclerosis. Anti-alpha4 integrin therapy aiming to block infiltration of autoreactive lymphocytes to the inflamed brain has been validated in several clinical trials for the treatment of multiple sclerosis. This paper provides readers with an overview of the molecular and structural bases of integrin activation as well as rationale for using anti-alpha4 integrin therapy for multiple sclerosis and then chronicles the rise and fall of this treatment strategy using natalizumab, a humanized anti-alpha4 integrin.
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4

Rose, David M., Jaewon Han, and Mark H. Ginsberg. "alpha4 integrins and the immune response." Immunological Reviews 186, no. 1 (August 2002): 118–24. http://dx.doi.org/10.1034/j.1600-065x.2002.18611.x.

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5

Escudero, E., M. Nieto, A. Martín, A. Molina, R. R. Lobb, F. Sanchez-Madrid, and F. Mampaso. "Differential effects of antibodies to vascular cell adhesion molecule-1 and distinct epitopes of the alpha4 integrin in HgCl2-induced nephritis in Brown Norway rats." Journal of the American Society of Nephrology 9, no. 10 (October 1998): 1881–91. http://dx.doi.org/10.1681/asn.v9101881.

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Анотація:
Four distinct epitopes (A, B1, B2, and C) have been functionally defined on the human alpha4 integrin. In this study, two cross-reactive antihuman alpha4 monoclonal antibodies (mAb) (HP2/1 and HP2/4 specific for epitopes B1 and B2, respectively) were used to functionally characterize the rat VLA-4 subunit and to define similar functional epitopes in this rodent species. It was found that B1 and B2 anti-alpha4 mAb completely block adhesion to fibronectin, but the inhibition of adhesion to vascular cell adhesion molecule-1 (VCAM-1) with HP2/1 mAb was lower than with HP2/4 mAb. It was also observed that epitope B2 HP2/4 mAb induced homotypic aggregation in rat lymphocytes, whereas epitope B1 HP2/1 mAb did not. Using the HgCl2 model of nephritis, this study shows the protective effect of both anti-alpha4 mAb against infiltration of the renal interstitium by leukocytes. Nevertheless, HP2/1 mAb, but not HP2/4 mAb, virtually abolished the anti-glomerular basement membrane antibody synthesis and glomerular deposits. These findings indicate the dual but independent role played by alpha4 integrins in both extravasation of leukocytes and in the production of antibodies. Finally, this study demonstrates that anti-rat VCAM-1 mAb showed a positive reactivity of the renal vascular endothelium and, most importantly, that administration of anti-VCAM-1 antibodies completely abrogated the interstitial cell infiltrates without affecting anti-glomerular basement membrane antibody production. These results confirm the important role played by VLA-4/VCAM-1 pathway in leukocyte infiltration, and further support the dual and independent role of alpha4 integrins in both renal infiltration and autoantibody synthesis in this model of renal disease.
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6

Hauzenberger, D., J. Klominek, J. Holgersson, S. E. Bergström, and K. G. Sundqvist. "Triggering of motile behavior in T lymphocytes via cross-linking of alpha 4 beta 1 and alpha L beta 2." Journal of Immunology 158, no. 1 (January 1, 1997): 76–84. http://dx.doi.org/10.4049/jimmunol.158.1.76.

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Abstract The mechanisms by which T lymphocytes are transformed from passively transported cells during circulation in the vascular system to actively migrating cells during extravasation are unknown. Therefore, the possibility that lymphocyte receptors are capable of inducing motility was investigated using a modified Boyden chamber assay. Cross-linking of alphaL beta2 and alpha4 beta1 on human T lymphocytes (T cell line and peripheral blood T cells) with immobilized mAbs induced motile behavior on fibronectin, laminin, collagen type IV, and poly-L-lysine. This induction of T cell migration was very potent and in most cases more efficient than pretreatment of the cells with phorbol esters. In contrast, control Abs to several other integrin- and non-integrin molecules present on T lymphocytes did not induce T cell migration. Anti-CD3 Abs themselves did not trigger motile behavior. However, anti-CD3 promoted T cell migration in the Boyden chamber system if present simultaneously with 40-kDa alpha4 beta1 binding fibronectin fragments or alphaL beta2 binding intercellular adhesion molecule-1/hIgG1Fc fusion proteins on the upper side of the filter. Abs to other surface components on T cells did not trigger motility when presented together with the 40-kDa fibronectin fragments or the intercellular adhesion molecule-1/hIgG1Fc fusion proteins. The induction of motile behavior could be blocked if the T cells were pretreated with Genistein and Calphostin C, indicating the involvement of a protein tyrosine kinase and protein kinase C-dependent signaling pathway in triggering of T cell motility via integrins. These results indicate that alphaL beta2 and alpha4 beta1 on T lymphocytes can selectively trigger motile behavior when cross-linked by their endothelial or extracellular matrix ligands. Furthermore, these data indicate that cross-linking of CD3 facilitates ligand binding and subsequent triggering of a motile phenotype by alphaL beta2 and alpha4 beta1.
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7

Ulyanova, Tatiana, Ena R. Banerjee, Gregory V. Priestley, Linda Scott, and Thalia Papayannopoulou. "Migration Defects of Leukocytes from Alpha4 or Beta2 Integrin-Deficient Mice during Aseptic Peritonitis." Blood 104, no. 11 (November 16, 2004): 2387. http://dx.doi.org/10.1182/blood.v104.11.2387.2387.

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Анотація:
Abstract Leukocyte migration to the inflammatory sites involves a dynamic and coordinated sequence of adhesion/ migration events, in which the α4 and β2 integrins in leukocytes play critical roles. In a model of aseptic peritonitis, normal mice respond with an initial influx of neutrophils followed by later recruitment of mononuclear cells. Previous studies used antibodies to inhibit α4 integrins in this model and provided only early observations (up to 24 hrs). Events at later stages were not addressed. To clarify the role of α4 integrins in this process, we induced aseptic peritonitis in α4-ablated (α4−/ −) mice and compared the results to similarly treated wild type (WT), and β2 integrin-deficient (β2−/ −) animals. A 4, 16 and 96 hrs post thioglycollate injection, leukocytes, harvested from the peritoneal cavity, were counted and evaluated by FACS and by differentials in smears. 3-5 animals per time point per genotype were analyzed. Early neutrophil accumulation in the peritoneum was similar in WT and α4−/ − mice (Table 1). β2−/ − mice were slow to accumulate neutrophils, but at 16 hrs the peaks were not different from α4−/ − or WT animals. However at later times in both α4−/ − and β2−/ − mice neutrophils persisted longer, suggesting either increased survival or prolonged recruitment. At 16 hrs large numbers of monocyte/ macrophages accumulated in the peritoneum and they were similar in all groups of mice up to 96 hours. The cumulative number of leukocytes in the peritoneum was compared to the concurrent circulating pool of leukocytes in each mouse group. At the peak time (16 hrs) the fraction recovered in the WT represented 394±148%, while in the α4−/ − mice it was 98±33% and in the β2−/ − mice it was 40±19%. Thus, although sufficient numbers of leukocytes accumulated in the peritoneum of both integrin-deficient mice, migration in the WT mice was significantly higher than that observed in the other two genetic models, suggesting impairment in animals with either integrin deficiency. Furthermore, lymphocyte accumulation was dramatically decreased at all time points in the α4−/ − mice (Table 2). Preliminary data in a model of combined, α4- and β2-integrin deficiency, generated in our laboratory, showed that only 3±2% of circulating leukocytes migrated into the peritoneum. Taken together, our results indicate that (1) for migration into peritoneum, neutrophils and monocyte/ macrophages can use α4 and β2 integrins interchangeably, (2) for optimal migration both integrins are needed, and (3) lymphocytes have an absolute requirement of α4 integrins for migration. These data extend previous knowledge on kinetic changes of leukocytes accumulating in the aseptic peritonitis model. Whether different kinetic changes are seen in other inflammatory models using our integrin-deficient animals requires further studies. Accumulation of myeloid cells in peritoneum Neutrophils Monocyte/macrophages 4 hrs 16 hrs 96 hrs 4 hrs 16 hrs 96 hrs WT 5.5±0.5 9.8±7.4 0.2±0.04 3.1±0.6 17.7±3.9 11.0±5.2 β2−/ − 2.5±0.8 10.5±5.3 3.7±1.6 4.7±1.3 12.8±5.2 11.0±4.0 α4−/ − 5.2±2.1 9.8±7.4 0.8±0.4 4.6±1.1 11.0±5.2 12.6±5.1 Lymphocyte accumulation in peritoneum 4 hrs 16 hrs 96 hrs Cell number (x106) in peritoneum at various time points; in bold are the numbers that significantly differ from the WT for each time point (p<0.05) WT 2.7±1.2 2.5±0.3 3.1±0.5 β2−/ − 6.7±1.7 4.7±1.2 3.3±1.0 α4−/ − 0.5±0.1 0.4±0.1 0.6±0.1
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8

Rabinowich, H., M. Manciulea, R. B. Herberman, and T. L. Whiteside. "Beta1 integrin-mediated activation of focal adhesion kinase and its association with Fyn and Zap-70 in human NK cells." Journal of Immunology 157, no. 9 (November 1, 1996): 3860–68. http://dx.doi.org/10.4049/jimmunol.157.9.3860.

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Анотація:
Abstract Adhesive interactions mediated by cell surface receptors have been shown to induce signal transduction pathways that regulate changes in cellular function. We have reported recently that fibronectin (FN) receptors, alpha4beta1 and alpha5beta1 integrins, on NK cells transduce transmembrane signals leading to tyrosine phosphorylation of 60-, 70-, and 120-kDa proteins. In the current study, we have identified a 120-kDa phosphoprotein as the focal adhesion kinase (p125FAK), a structurally unique nonreceptor protein tyrosine kinase that localizes to focal adhesions. Activity of p125FAK was induced by adhesion of NK cells to plastic-immobilized FN, by cross-linking of cell surface-bound FN or FN fragments, FN120 or FN40, with anti-FN mAb, or by cross-linking of alpha4beta1 or alpha5beta1 integrins with alpha-chain-specific Abs. We also observed that enhanced in vitro kinase activity was associated with immunoprecipitates of alpha4beta1 or alpha5beta1 integrins from lysates of FN-adherent NK cells as compared with BSA-treated NK cells. In addition to p125FAK activity, FN-induced kinase activity was also found to be mediated by Fyn, Lyn, and Zap-70, as assessed by in vitro phosphorylation of the immunoprecipitated kinases in the presence of [gamma-32P]ATP. Clustering of FN receptors on NK cells by agonists such as immobilized FN or alpha4- or alpha5-specific Abs also induced association of Fyn and Zap-70 with p125FAK. Our observations indicate that activation and phosphorylation of p125FAK as well as Zap-70 and certain kinases of the src family play an important role in formation of active signaling complexes in response to triggering via beta1 integrins on NK cells. These results also suggest the existence of cross-talk or points of convergence between the beta1 integrin-mediated and other receptor-signaling pathways.
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9

Palecanda, A., M. J. Briskin, and T. B. Issekutz. "Rat mast cell lines bind to the vascular cell adhesion molecule-1 (VCAM-1) and the mucosal addressin cell adhesion molecule-1 (MAdCAM-1)." Journal of Immunology 158, no. 6 (March 15, 1997): 2904–10. http://dx.doi.org/10.4049/jimmunol.158.6.2904.

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Abstract Mast cells are key mediators of allergy and inflammation. Increased mast cell numbers are observed in the gut during helminth infestation and at many sites of inflammation. To determine whether mast cells express functional receptors for endothelial cell adhesion molecules, we studied the adhesion of two rat mucosal-type mast cell lines RBL-1 and RCMC-1 to transfected mucosal addressin cell adhesion molecule-1 (MAdCAM-1) and VCAM-1. Both mast cell lines expressed high levels of alpha4 integrins on their surface and bound to CHO cells transfected with VCAM-1. Anti-alpha4 mAbs, TA-2 and L25, inhibited the specific adhesion of the mast cells to VCAM-1 by about 92 and 63%, respectively. Both of the mast cell lines also demonstrated an increased adhesion to CHO cells transfected with MAdCAM-1. The adhesion of RBL-1 to MAdCAM-1 was also significantly inhibited by the anti-alpha4 mAbs TA-2, L25, and HP2/1 by 39, 76, and 42%, respectively. In addition, RBL-1 cells adhered to both VCAM-1 and MAdCAM-1 under both static and nonstatic (shear) conditions, and this was also inhibited by the anti-alpha4 mAb TA-2. Thus, mucosal-type mast cell lines express functional alpha4 integrins that can mediate adhesion to VCAM-1 and MAdCAM-1. These results suggest a mechanism for mast cell accumulation at sites of inflammation and in the gut.
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10

McIntyre, B. W., D. G. Woodside, D. A. Caruso, D. K. Wooten, S. I. Simon, S. Neelamegham, J. K. Revelle, and P. Vanderslice. "Regulation of human T lymphocyte coactivation with an alpha4 integrin antagonist peptide." Journal of Immunology 158, no. 9 (May 1, 1997): 4180–86. http://dx.doi.org/10.4049/jimmunol.158.9.4180.

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Abstract The cyclic hexapeptide CWLDVC (TBC 772) is an antagonist of alpha4 integrins and a potent inhibitor of lymphocyte interactions with fibronectin, vascular cell adhesion molecule-1, and muscosal vascular addressin cell adhesion molecule-1 (MAdCAM-1). As such, peptide TBC 772 effectively inhibits the activation of freshly isolated human T lymphocytes stimulated with purified vascular cell adhesion molecule-1 coimmobilized with anti-CD3 mAb. The influence of peptide binding on distinct sites of the alpha4beta1 complex was determined by flow cytometry and cellular adhesion assays employing a panel of mAbs. Binding of the alpha4-specific mAb L25 and the beta1-specific mAb 33B6 was not altered by the peptide; however, binding of mAb 19H8, which is specific for a combinatorial epitope of alpha4beta1, was dramatically inhibited. Treatment of lymphocytes with the peptide caused an increase in a ligand-induced epitope on beta1 integrin defined by mAb 15/7. In T cell activation studies using coimmobilized anti-CD3 mAb and the anti-integrin mAbs, the peptide had broader inhibitory activity, suppressing costimulation induced by all the integrin mAbs. The peptide was not generally toxic and was integrin selective in its suppressive activity, as coactivation by ligation of CD3 in conjunction with CD28 or CD26 was not affected. These results suggest that the antagonist peptide CWLDVC can effectively neutralize integrin coactivation systems by a mechanism independent of competitive binding.
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Більше джерел

Дисертації з теми "Alpha4 integrins"

1

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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2

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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3

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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Анотація:
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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4

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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5

Chakraborty, Arup R. "Differential expression of integrin [alpha]₃[beta]₁ and [alpha]₆[beta]₄ molecules on a panel of rat esophageal cell lines." Connect to this title online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=bgsu1131345357.

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6

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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7

Parks, William. "Force activation of I domain containing and lacking integrins on live cells." Thesis, Georgia Institute of Technology, 2010. http://hdl.handle.net/1853/42695.

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Анотація:
Cellular adhesion plays a crucial role in the biological function of cells, allowing them to communicate and signal, as well as physically anchor, by enabling them to adhere to either other cells or the extra cellular matrix (ECM). This process is regulated by several factors including intrinsic bond kinetics, internal cellular signaling, environment, force exerted on the bond, and force history of the bond. Concerning the force and force history dependence, the observation of catch bonds in integrin binding has asked as more questions than it has answered. To explore the force and force history dependence this process, each bond was loaded to a peak force before relaxing to a much lower force that was held for the duration of the measurement. Two different integrins were studied, both of which have in previous works exhibited a catch bond. Furthermore, the effects of different metal ion conditions and an allosteric antagonist were also studied to elucidate the conformational effects on force priming of integrin. What was observed was that I domain, or αA domain, possessing integrin, whether tested against its more active or less active binding state, changed very little in terms of off rate once the priming force was applied. However in the I domain, or αA domain, lacking integrin, the observed off rate changed as well. It seems that force priming is capable of causing integrin to bind in a stronger manner regardless of the other conditions used to either activate or inhibit binding. However the way in which the binding is strengthened depends on the receptors structure.
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8

Laplantine, Emmanuel. "Interactions au niveau des domaines intracellulaires des sous-unites alpha3a, alpha6a et beta1a des integrines." Paris 6, 2000. http://www.theses.fr/2000PA066262.

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Les adhesions focales (af) constituent un lien essentiel entre la matrice extracellulaire et le cytosquelette, ainsi que le site de transmission de signaux par les integrines. Les integrines 31 et 61, recepteurs des laminines, different dans leur specificite de reconnaissance : la laminine 1 se lie a l'integrine 61 seulement et l'adherence des cellules a ce substrat entraine la formation d'af distinctes de celles formees sur d'autres isoformes de laminine liant a la fois 31 et 61. L'integrine 31 pourrait donc reguler de maniere transdominante l'integrine 61. Afin de tester cette hypothese, des peptides representant le domaine intracellulaire des sous-unites 3a ou 6a d'integrines ont ete injectes dans des fibroblastes vivants adheres a la laminine 1. Seule la microinjection du peptide 3a entraine une reorganisation specifique des af, rappelant celles formees lors de l'activation du recepteur 31 par ses ligands. De plus, des etudes par resonance plasmonique de surface (spr) permettent de detecter une interaction directe entre les peptides correspondant aux domaines intracellulaires des sous-unites 3a et 1a d'integrine. Enfin, un criblage de banque d'adnc avec le domaine intracellulaire de la sous-unite 3a comme amorce dans le systeme double hybride chez la levure, a permis l'identification de plusieurs partenaires d'interaction. Parmi ceux-ci, la proteine dral/fhl2 interagit avec l'integrine 31 in vivo. En conclusion, differentes interactions specifiques au domaine intracellulaire de la sous-unite 3a, contribuent a la regulation de l'organisation des af par l'integrine 31. Par ailleurs, nous avons examine la contribution du domaine intracellulaire de la sous-unite 1a dans le phenomene de clustering des integrines. Des analyses en spr revelent une affinite du domaine intracellulaire de 1a pour lui-meme. Des experiences en gel filtration et en sds-page montrent que ce domaine forme des multimeres qui, d'apres des mesures en dichroisme circulaire, adoptent une structure en helice. L'oligomerisation et le changement de structure secondaire du domaine intracellulaire de la sous-unite 1a pourraient intervenir de maniere active dans l'agregation des integrines et la formation des af.
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9

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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Weiken, Claudia. "Kollagenrezeptor [alpha]2[beta]1-Integrin [Alpha-2-Beta-1-Integrin] auf humanen und tierischen Thrombozyten Heterogenität und ihre Bedeutung /." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=976077981.

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Книги з теми "Alpha4 integrins"

1

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

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2

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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3

Schwab, Esther Irene. Immunhistochemische Expressionsanalyse von Hirntumorgewebe mit Integrin alpha-v-beta spezifischen Antikörpern und ihren Liganden. [S.l: s.n.], 2013.

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4

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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5

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

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6

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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7

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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Частини книг з теми "Alpha4 integrins"

1

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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2

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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3

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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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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5

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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6

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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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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8

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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9

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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10

Mittelbrunn, Maria, and Francisco Sánchez-Madrid. "Integrin Alpha 4 (Itga 4)." In Encyclopedia of Signaling Molecules, 2630–34. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_143.

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Тези доповідей конференцій з теми "Alpha4 integrins"

1

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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2

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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3

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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4

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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5

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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6

Singh, Amrita, Carmine Fedele, Renato V. Iozzo, and Lucia R. Languino. "Abstract 357: Exosome-mediated transfer of alphaV integrins promotes prostate cancer cell-cell communication." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-357.

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7

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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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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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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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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Звіти організацій з теми "Alpha4 integrins"

1

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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2

Shaw, Leslie M., and A. Mercurio. Regulation of Breast Carcinoma Progression by the Alpha-6 Integrins. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada404843.

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3

Shaw, Leslie M. Regulation of Breast Carcinoma Progression by the Alpha-6 Integrins. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada383962.

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4

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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5

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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7

Cardo-Vila, Marina. Isolation of Signaling Molecules Involved in Angiogenic Pathways Mediated Alpha v Integrins. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada435432.

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8

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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9

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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10

Gilcrease, Michael Z. Investigation of Alpha6 Integrins and Their Signaling Intermediate as Prognostic Markers for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada407363.

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