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1 to explore the conformational landscape of a c-Src kinase.
2 ormations near the inhibitor binding site in c-Src kinase.
3 ns were mainly mediated by activation of the c-Src kinase.
4 es the tyrosine phosphorylation of villin by c-Src kinase.
5 sp90 does not influence the almost identical c-Src kinase.
6 ced death by suppressing early activation of c-Src kinase.
7 inic receptor couples to Ca(2+) channels via c-src kinase.
8 st precursors, is tyrosine-phosphorylated by c-Src kinase.
9 essing glutamate-induced early activation of c-Src kinase.
10 pstream elements, such as p38 MAP kinase and c-Src kinase.
11 sine kinase but not of the highly homologous c-Src kinase.
12 cted a specific interaction between CD44 and c-Src kinase.
13 c, G6G is a potent inhibitor of both Abl and c-Src kinases.
15 ediated formation of Shc.c-Src complexes and c-Src kinase activation are early events in Ras-dependen
17 sion kinase phosphorylation was dependent on c-Src kinase activation, for which caveolin-1 was requir
18 ts indicate that HA binding to CD44 promotes c-Src kinase activation, which, in turn, increases Twist
19 xpressing clones exhibited increased Akt and c-Src kinase activities, as well as higher levels of mat
22 tTG function (monodansylcadaverine; MDC) or c-Src kinase activity (PP2) disrupted the formation of t
23 Agonists of the CaR can stimulate increased c-SRC kinase activity and increased extracellular signal
25 phorylation of FAK in the liver, we measured c-Src kinase activity and the abundance of 3 major prote
26 t osteoclastic bone resorption requires both c-Src kinase activity and the targeting of Src kinase by
28 d levels of Bcl-x(L.) However, inhibition of c-Src kinase activity by PP2 in vector control cells did
30 on, in the presence of EGFR TKIs, inhibiting c-Src kinase activity decreased cell growth in SUM229 ce
31 n Rat-2 cells transiently stimulated Hck and c-Src kinase activity in the absence of extracellular si
32 nism of c-Src regulation have suggested that c-Src kinase activity is downregulated by phosphorylatio
33 nd sufficient to induce IGF-IR upregulation, c-Src kinase activity is necessary, but alone is insuffi
36 rast, pharmacologic inhibition of endogenous c-Src kinase activity or small interfering RNA-mediated
40 tantly, erbB2:EGFr heterodimer formation and c-src kinase activity were also elevated in TPA-treated
41 In one such cell line, SUM229, inhibiting c-Src kinase activity with either a dominant-negative c-
42 wer c-Src phosphotyrosine 527 level, greater c-Src kinase activity, and increased tyrosine phosphoryl
44 as accompanied by an EGF-induced increase in c-Src kinase activity, relocalisation of c-Src to the ce
45 cortactin was found uncoupled of endogenous c-Src kinase activity, thus further supporting the hypot
46 with its receptor leads to the activation of c-Src kinase activity, which in turn facilitates the bin
47 rc kinase recruitment to CD44 and stimulates c-Src kinase activity, which, in turn, increases tyrosin
52 e swelling, which triggers via integrins and c-Src kinase an activation of the epidermal growth facto
53 ine-rich sequence) as negative regulators of c-Src kinase and demonstrate a new function for these ph
57 D44 (a primary HA receptor) interaction with c-Src kinase and the transcriptional factor, Twist, in b
58 that activate the focal-adhesion kinase and c-Src kinase and their downstream MAP-ERK kinase/extrace
61 e assessed the involvement of protein kinase C, Src kinases, and proline-rich tyrosine kinase 2 in th
63 Epidermal growth factor receptor-kinase, c-src kinase, and focal adhesion kinase were phosphoryla
64 by the expression of a constitutively active c-Src kinase, and repressed by the expression of dominan
65 both CD44 (the hyaluronan (HA) receptor) and c-Src kinase are expressed in human ovarian tumor cells
66 PP1), in bulk solution and on the surface of c-Src kinase are reduced as the concentration of crowder
70 ion site of FAK, which is a reported site of c-Src kinase binding, is required for bacterial internal
71 TCDD appears to be limited to activation of c-Src kinase, but not kinases associated with activation
72 nonphagocytic NAD(P)H oxidases (NOX-1), and c-Src kinases (c-Src) were colocalized in the caveolae o
73 stimulates tyrosine kinases, including pp60(c-src) kinase (c-Src), focal adhesion kinase (FAK), and
75 Met cells treated with inhibitors of MEK1 or c-Src kinases, completely blocked by expression of a cat
76 hat the expression of these genes in src- or c-src kinase-deficient cells did not differ from wild-ty
77 ormed complexes that included an active pp60(c-src) kinase, demonstrating that PP2A activity is not e
78 ulated kinase (Erk) MAPK, an event requiring c-Src kinase-dependent epidermal growth factor receptor
81 lso enhanced the transformation potential of c-Src kinase in focus formation assays, and PELP1 overex
86 rexpression of a dominant-negative mutant of c-Src kinase (K295R) in SK-OV-3.ipl cells impairs the tu
87 olo-like kinase 1 (Plk1) kinase by enhancing c-Src kinase-mediated tyrosine phosphorylation of Plk1.
91 ific effects were prevented by deletion of a c-Src kinase phosphorylation DYD motif, identified in si
92 strongly suggest that CD44 interaction with c-Src kinase plays a pivotal role in initiating cortacti
93 binding of HA to SK-OV-3.ipl cells promotes c-Src kinase recruitment to CD44 and stimulates c-Src ki
95 s show for the first time that Rap1 mediates c-Src kinase signaling and reveal mechanistic difference
96 ut virtual screening hits for three targets: c-SRC kinase, Smoothened receptor, and dopamine D1 recep
97 ther, these data demonstrate the role of the c-src kinase/STAT3 pathway in Ox-PAPC-mediated IL-8 expr
98 ol did not influence activity of recombinant c-Src kinase suggesting that its mechanism of action may
99 re, we investigate an inhibitor binding with c-Src kinase using atomistic molecular dynamics (MD) sim
101 r402, which mediates the binding of RAFTK to c-Src kinase, was required for the phosphorylation of th
103 tion, pyk2(K457A) blocked acid activation of c-Src kinase, which is also required for acid regulation
104 tive conformation of the catalytic domain of c-Src kinase while the tyrosine 416 in the activation lo
106 ifts of the disordered N terminal (SH4UD) of c-Src kinase without reweighting or constraining the sim