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1 ns were mainly mediated by activation of the c-Src kinase.
2 sp90 does not influence the almost identical c-Src kinase.
3 es the tyrosine phosphorylation of villin by c-Src kinase.
4 sine kinase but not of the highly homologous c-Src kinase.
5 ced death by suppressing early activation of c-Src kinase.
6 inic receptor couples to Ca(2+) channels via c-src kinase.
7 st precursors, is tyrosine-phosphorylated by c-Src kinase.
8 essing glutamate-induced early activation of c-Src kinase.
9 pstream elements, such as p38 MAP kinase and c-Src kinase.
10 cted a specific interaction between CD44 and c-Src kinase.
11 c, G6G is a potent inhibitor of both Abl and c-Src kinases.
12 ediated formation of Shc.c-Src complexes and c-Src kinase activation are early events in Ras-dependen
14 sion kinase phosphorylation was dependent on c-Src kinase activation, for which caveolin-1 was requir
15 ts indicate that HA binding to CD44 promotes c-Src kinase activation, which, in turn, increases Twist
16 xpressing clones exhibited increased Akt and c-Src kinase activities, as well as higher levels of mat
19 tTG function (monodansylcadaverine; MDC) or c-Src kinase activity (PP2) disrupted the formation of t
20 Agonists of the CaR can stimulate increased c-SRC kinase activity and increased extracellular signal
22 phorylation of FAK in the liver, we measured c-Src kinase activity and the abundance of 3 major prote
23 t osteoclastic bone resorption requires both c-Src kinase activity and the targeting of Src kinase by
25 d levels of Bcl-x(L.) However, inhibition of c-Src kinase activity by PP2 in vector control cells did
27 on, in the presence of EGFR TKIs, inhibiting c-Src kinase activity decreased cell growth in SUM229 ce
28 n Rat-2 cells transiently stimulated Hck and c-Src kinase activity in the absence of extracellular si
29 nism of c-Src regulation have suggested that c-Src kinase activity is downregulated by phosphorylatio
30 nd sufficient to induce IGF-IR upregulation, c-Src kinase activity is necessary, but alone is insuffi
33 rast, pharmacologic inhibition of endogenous c-Src kinase activity or small interfering RNA-mediated
37 tantly, erbB2:EGFr heterodimer formation and c-src kinase activity were also elevated in TPA-treated
38 In one such cell line, SUM229, inhibiting c-Src kinase activity with either a dominant-negative c-
39 wer c-Src phosphotyrosine 527 level, greater c-Src kinase activity, and increased tyrosine phosphoryl
41 as accompanied by an EGF-induced increase in c-Src kinase activity, relocalisation of c-Src to the ce
42 cortactin was found uncoupled of endogenous c-Src kinase activity, thus further supporting the hypot
43 with its receptor leads to the activation of c-Src kinase activity, which in turn facilitates the bin
44 rc kinase recruitment to CD44 and stimulates c-Src kinase activity, which, in turn, increases tyrosin
49 e swelling, which triggers via integrins and c-Src kinase an activation of the epidermal growth facto
50 ine-rich sequence) as negative regulators of c-Src kinase and demonstrate a new function for these ph
54 D44 (a primary HA receptor) interaction with c-Src kinase and the transcriptional factor, Twist, in b
55 that activate the focal-adhesion kinase and c-Src kinase and their downstream MAP-ERK kinase/extrace
58 e assessed the involvement of protein kinase C, Src kinases, and proline-rich tyrosine kinase 2 in th
60 Epidermal growth factor receptor-kinase, c-src kinase, and focal adhesion kinase were phosphoryla
61 by the expression of a constitutively active c-Src kinase, and repressed by the expression of dominan
62 both CD44 (the hyaluronan (HA) receptor) and c-Src kinase are expressed in human ovarian tumor cells
65 ion site of FAK, which is a reported site of c-Src kinase binding, is required for bacterial internal
66 TCDD appears to be limited to activation of c-Src kinase, but not kinases associated with activation
67 nonphagocytic NAD(P)H oxidases (NOX-1), and c-Src kinases (c-Src) were colocalized in the caveolae o
68 stimulates tyrosine kinases, including pp60(c-src) kinase (c-Src), focal adhesion kinase (FAK), and
69 Met cells treated with inhibitors of MEK1 or c-Src kinases, completely blocked by expression of a cat
70 hat the expression of these genes in src- or c-src kinase-deficient cells did not differ from wild-ty
71 ormed complexes that included an active pp60(c-src) kinase, demonstrating that PP2A activity is not e
72 ulated kinase (Erk) MAPK, an event requiring c-Src kinase-dependent epidermal growth factor receptor
75 lso enhanced the transformation potential of c-Src kinase in focus formation assays, and PELP1 overex
80 rexpression of a dominant-negative mutant of c-Src kinase (K295R) in SK-OV-3.ipl cells impairs the tu
81 olo-like kinase 1 (Plk1) kinase by enhancing c-Src kinase-mediated tyrosine phosphorylation of Plk1.
85 ific effects were prevented by deletion of a c-Src kinase phosphorylation DYD motif, identified in si
86 strongly suggest that CD44 interaction with c-Src kinase plays a pivotal role in initiating cortacti
87 binding of HA to SK-OV-3.ipl cells promotes c-Src kinase recruitment to CD44 and stimulates c-Src ki
89 s show for the first time that Rap1 mediates c-Src kinase signaling and reveal mechanistic difference
90 ther, these data demonstrate the role of the c-src kinase/STAT3 pathway in Ox-PAPC-mediated IL-8 expr
91 ol did not influence activity of recombinant c-Src kinase suggesting that its mechanism of action may
93 r402, which mediates the binding of RAFTK to c-Src kinase, was required for the phosphorylation of th
95 tion, pyk2(K457A) blocked acid activation of c-Src kinase, which is also required for acid regulation
96 tive conformation of the catalytic domain of c-Src kinase while the tyrosine 416 in the activation lo
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