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1. |
Results indicate that Wnt5a/Ror2 signaling involves the activation of a SFK, leading to MMP-13 expression, and that constitutively active Wnt5a/Ror2 signaling confers invasive properties on osteosarcoma cells in a cell-autonomous manner. |
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2. |
The structural and conformational changes upon phosphorylation were monitored through chemical shift perturbations and residual dipolar couplings, indicating that modifications occur at local level and no global rearrangements were apparent. |
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3. |
Observational study of gene-disease association. (HuGE Navigator) |
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4. |
Insulin promotes the interaction of Hsp90 with the IP(3)R to dampen its Ca(2+) release activity by a complex mechanism involving mammalian target of rapamycin and the Src kinase. |
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5. |
Oncogenic potential of c-Src tyrosine kinase is controled by lipid rafts. (review) |
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6. |
A comparative sequence analysis of cDNAs for Csk tyrosine kinase of normal lymphocytes and lymphocytes of patients with choroidal melanoma revealed a nucleotide substitution in dexon 10 of the gene, which appears to be of diagnostic significance |
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7. |
activated Src within the nucleus of ER-positive tumours predicts an improved outcome. In ER/PgR-positive disease |
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8. |
Absolute requirement for c-Src in villin-induced regulation of cell migration of intestinal tumor cells. |
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9. |
Csk serves to maintain the constancy of baseline excitatory synaptic transmission by inhibiting Src kinase-dependent synaptic plasticity in the hippocampus |
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10. |
Small interference RNAs specific for Csk, was identified that reproducibly reduce viral RNA and viral protein levels in hepatitis C virus replicon-bearing cells |
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11. |
PRL3 has a role in the gene-specific translational control of Csk expression |
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12. |
Neph1 but not nephrin specifically binds to adaptor protein Grb2 and tyrosine kinase Csk in a phosphorylation-dependent manner. |
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13. |
Collectively, our experiments implicate a novel signaling pathway involving calpain 2, PTP1B, and Src in the regulation of invadopodia and breast cancer invasion. |
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14. |
c-Src is recruited by AF-6 to cell-cell contact sites, suggesting that c-Src is regulated by a PDZ protein in special cellular locations. |
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15. |
C terminus of c-Src via its Gly-Glu-Asn-Leu sequence presents a mechanism that restricts c-Src in epithelia and prevents progression toward an invasive phenotype |
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16. |
The interaction of c-Src with LNX1 depends on the C-terminal PDZ ligand of c-Src. |
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17. |
Thus, these results suggest that endogenous c-Src, c-Yes, and Lyn are differentially activated through Cdc2 activation during M phase. |
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18. |
A full-length encoding cDNA of the tyrosine kinase csk gene of human lymphocytes was cloned. |
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19. |
These results demonstrate that the chimeric strategy is useful for detailed dissection of the mechanistic basis of substrate specificity and regulation of protein tyrosine kinases. |
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20. |
Csk is activated by increase of p140Cap which leads to inhibition of Src and downstream signalling as well as of cell motility and invasion |
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21. |
functions of the activation loop in phosphorylation of its physiological substrate Src probed by extensive site-specific mutagenesis and kinetic studies |
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22. |
this study reveals a mechanism by which Src family kinases may control PDGF-mediated responses both at transcriptional and translational levels. |
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23. |
Csk tyrosine kinase interacts with G3BP, a new player in T-cell-antigen receptor signaling, which reduces the amount of Csk in the immune synapse. |
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24. |
Csk Phe183 stabilizes the movement of the alphaC-helix of the protein tyrosine kinase |
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25. |
Study shows EGF-stimulation-induced Csk-binding protein (Cbp) tyrosine phosphorylation followed by Cbp-Csk association, in a SFK-dependent manner.[Csk-binding protein] |
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26. |
Tyrosine kinase c-Src constitutes a bridge between cystic fibrosis transmembrane regulator channel failure and MUC1 overexpression in cystic fibrosis |
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27. |
Upon platelet interaction with fibrinogen, cholesterol accumulated at the tips of filopodia and at the leading edge of spreading cells; cholesterol-rich raft aggregation was accompanied by concentration of c-Src and CD63 in these cell domains |
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28. |
model of substrate-docking site which provides the structural basis of substrate specificity in Csk |
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29. |
NMR and site-directed mutagenesis reveal novel mechanism of enzyme regulation |
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30. |
Csk achieves a low K(m) for the substrate Src, not by stabilizing protein-protein interactions but rather by facilitating a fast phosphoryl transfer step |
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31. |
High c-Src activityis associated with ductal carcinoma in situ with high risk of recurrence or progression to invasive breast cancer. |
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32. |
in more advanced stages of colorectal carcinogenesis, increases in c-Src levels and activity are likely to have functions other than the direct promotion of tumor growth |
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33. |
striking functional differences between the Csk and Chk SH2 domains |
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34. |
These data implicate an important role of c-Src in phosphorylating RelA/p65 to promote the transcriptional activity of NF-kappaB and thereby ICAM-1 expression in endothelial cells. |
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35. |
in Caco-2 cells oxidative stress-induced disruption of tight junction is mediated by the activation of c-Src. |
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36. |
Csk suppression is an important early event in colorectal cancer pathogenesis. |
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37. |
C-terminal Src kinase is regulated by the leukocyte inhibitory receptor CD85j |
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38. |
c-Src may act as a global regulator of early proinflammatory host responses to group D adenovirus Ad19 infection of the human cornea, such as early IL-8 gene transcription. |
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39. |
These data demonstrate that LPXN forms a signaling complex with Pyk2, c-Src, and PTP-PEST to regulate migration of prostate cancer cells. |
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40. |
identification between c-Src and diacylglycerol kinase-zeta |
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41. |
c-Src is a novel localization and binding partner for histone deacetylase (HDAC) 3 and is implicated in HDAC3 regulation. |
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42. |
c-Src tyrosine kinase is activated by dsRNA in human monocyte-derived dendritic cells, is recruited to TLR3 in a double-stranded (ds)RNA-dependent manner, and plays a central role in antiviral immunity. |
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43. |
steps involving Src association, phosphorylation, and product release are fast, and a structural change in Csk participates in limiting the catalytic cycle |
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44. |
The data indicate that reversible cross-linking of two cysteine residues in the SH2 domain greatly impacts catalytic function and interdomain communication in Csk. |
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45. |
these observations support the hypothesis that there is a specific coordination between the activation of the cytosolic Ah receptor and the c-Src- and cdc37-containing HSP90 complex. |
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46. |
study elucidated a nongenomic extranuclear signal mediated by the RAR-SRC interaction that is negatively regulated by CSK and is required for RA-induced neuronal differentiation |
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47. |
Regulation of an ERG K+ current by Src tyrosine kinase. |
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48. |
cAMP regulates Csk via both spatial and enzymatic mechanisms, thereby inhibiting signaling through the T-cell receptor |
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49. |
activation of Csk and GSK-3beta by Galphaq may contribute to the physiological and pathological effects of Gq-coupled receptors |
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50. |
c-Src plays a critical role in IL-1-induced NF-kappa B activation through the IKK complex. |
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51. |
The SH2 domain moves in a cantilever fashion with respect to the small lobe of the kinase domain, ordering the active site for catalysis. Binding of a small Cbp-derived peptide to the SH2 domain of Csk modifies these motions, enhancing Src recognition. |
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52. |
activation by adaptor protein Shc |
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53. |
c-Src has been identified as the tyrosine kinase involved in TNF-alpha-inducing NF-kappa B transcriptional activation in the in vitro induction of COX-2 promoter activity. |
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54. |
beta3 integrin alters TGF-beta signaling in mammary epithelial cells via Src-mediated TbetaR-II tyrosine phosphorylation, which significantly enhanced the ability of TGF-beta to induce epithelial to mesenchymal transition and invasion. |
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55. |
These results suggest that dimerization of Src plays an important role in the regulation of Src tyrosine kinase activity. |
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56. |
role of elevated Src in human colon cancer cells is to modulate integrin-dependent cell-matrix attachment and formation of adhesion structures. |
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57. |
analysis of docking-based substrate recognition by the catalytic domain of Csk |
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58. |
EG-1 may be involved in signaling pathways including c-Src activation. |