Focal Adhesion Kinase
Mostrando 13-24 de 241 artigos, teses e dissertações.
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13. Expression of focal adhesion kinase is increased and correlates with fibrosis in failing human myocardium / Expressão da quinase de adesão focal e correlação com fibrose no miocardio humano exposto a sobrecarga volumetrica por insuficiencia da valvula mitral
A insuficiência cardíaca é um dos maiores problemas de saúde pública da atualidade. Esforços têm sido feitos para a obtenção do entendimento dos mecanismos que resultam no comprometimento funcional e estrutural do miocárdio, responsáveis, em última instância, pela síndrome clínica. Doenças das válvulas constituem importante contingente dentr
Publicado em: 2006
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14. Mechanisms of focal adhesion quinase for mechanical stimulation in cardiac myocytes : importance of ty / Mecanismos de ativação da quinase de adesão focal por estimulo mecanico em miocitos cardiacos : importancia da tirosino-fosfatase SHP-2
Arrazoado. A Quinase de Adesão Focal (FAK) é ativada e contribui para a regulação da sinalização que determina as alterações fenotípicas de cardiomiócitos estimulados mecanicamente. A regulação da atividade da FAK é complexa e depende de mecanismos intramoleculares e da cooperação com a tirosino-quinase Src. Há evidências de que a tirosino-f
Publicado em: 2006
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15. Disintegrins: integrin selective ligands which activate integrin-coupled signaling and modulate leukocyte functions
Extracellular matrix proteins and cell adhesion receptors (integrins) play essential roles in the regulation of cell adhesion and migration. Interactions of integrins with the extracellular matrix proteins lead to phosphorylation of several intracellular proteins such as focal adhesion kinase, activating different signaling pathways responsible for the regul
Brazilian Journal of Medical and Biological Research. Publicado em: 2005-10
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16. Avaliação das interações proteicas da quinase de adesão focal (FAK) em miocitos cardiacos : caracterização estrutural e funcional da interação da FAK com a cadeia pesada de miosina sarcomerica
Mechanical stress is a major factor involved in the development of myocardial adaptive and maladaptive changes in heart diseases. Local mechanical forces activate signaling mechanisms in cardiac myocytes inducing the expression of specific genetic programs linked to myocardial structural and functional remodeling. Although mechanical forces might directly tr
Publicado em: 2005
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17. Dimensions and dynamics in integrin function
Integrins play crucial roles in cell adhesion, migration, and signaling by providing transmembrane links between the extracellular matrix and the cytoskeleton. Integrins cluster in macromolecular complexes to generate cell-matrix adhesions such as focal adhesions. In this mini-review, we compare certain integrin-based biological responses and signaling durin
Brazilian Journal of Medical and Biological Research. Publicado em: 2003-08
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18. Sinalização celular durante aumento de tensão no coração : implicações no desenvolvimento de hipertrofia cardiaca : estudos em corações isolados
The mechanical input plays a major role in cardiac adaptive responses to hemodynamic overload. In addition of triggering the force-Iength mechanism and the homeometric autoregulation, the mechanical input activates signaling mechanisms involved on hypertrophic growth of cardiac myocytes, the hal1mark of themyocardial structural adaptation in response to sust
Publicado em: 2002
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19. Paxillin Binding Is Not the Sole Determinant of Focal Adhesion Localization or Dominant-Negative Activity of Focal Adhesion Kinase/Focal Adhesion Kinase-related Nonkinase
The carboxy-terminal 150 residues of the focal adhesion kinase (FAK) comprise the focal adhesion-targeting sequence, which is responsible for its subcellular localization. The mechanism of focal adhesion targeting has not been fully elucidated. We describe a mutational analysis of the focal adhesion-targeting sequence of FAK to further examine the mecha
The American Society for Cell Biology.
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20. Inhibition of focal adhesion kinase (FAK) signaling in focal adhesions decreases cell motility and proliferation.
It has been proposed that the focal adhesion kinase (FAK) mediates focal adhesion formation through tyrosine phosphorylation during cell adhesion. We investigated the role of FAK in focal adhesion structure and function. Loading cells with a glutathione-S-transferase fusion protein (GST-Cterm) containing the FAK focal adhesion targeting sequence, but not the
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21. Structural Insight into the Mechanisms of Targeting and Signaling of Focal Adhesion Kinase
Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase whose focal adhesion targeting (FAT) domain interacts with other focal adhesion molecules in integrin-mediated signaling. Localization of activated FAK to focal adhesions is indispensable for its function. Here we describe a solution structure of the FAT domain bound to a peptide derived from paxil
American Society for Microbiology.
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22. Csk enhances insulin-stimulated dephosphorylation of focal adhesion proteins.
Insulin has pleiotropic effects on the regulation of cell physiology through binding to its receptor. The wide variety of tyrosine phosphorylation motifs of insulin receptor substrate 1 (IRS-1), a substrate for the activated insulin receptor tyrosine kinase, may account for the multiple functions of insulin. Recent studies have shown that activation of the i
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23. Focal adhesion kinase phosphorylation in flow-activation of endothelial NF-κB. Focus on “Focal adhesion kinase modulates activation of NF-κB by flow in endothelial cells”
American Physiological Society.
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24. Active ERK/MAP kinase is targeted to newly forming cell–matrix adhesions by integrin engagement and v-Src
Integrin engagement generates cellular signals leading to the recruitment of structural and signalling molecules which, in concert with rearrangements of the actin cytoskeleton, leads to the formation of focal adhesion complexes. Using antisera reactive either with total ERK or with phosphorylated/activated forms of ERK, in rat embryo fibroblasts and embryon
Oxford University Press.