ライフサイエンスコーパス: Src kinase

1 t position 32 within the switch I region via Src kinase.

2 ne kinase but not of the highly homologous c-Src kinase.

3 ular cleavage of the beta3 chain, talin, and Src kinase.

4 ays, including MAPK, Smad, beta-catenin, and Src kinase.

5 ts were noted with siRNA targeting Smad2 and Src kinase.

6 were mainly mediated by activation of the c-Src kinase.

7 lex consisting of Na,K-ATPase, caveolin, and Src kinase.

8 re detected between Na,K-ATPase and purified Src kinase.

9 atients show similar increased activation of SRC kinase.

10 90 does not influence the almost identical c-Src kinase.

11 hondria to the cytosol during HI through the Src kinase.

12 G6G is a potent inhibitor of both Abl and c-Src kinases.

13 ide, activated neutrophils, or inhibition of Src kinases.

14 ggers phosphorylation of mammalian Robo3 via Src kinases.

15 tase Shp-2, and this process is dependent on Src kinases.

16 eposition via neutrophil FcgammaRIIA and Abl/Src kinases.

17 satinib inhibits tyrosine kinases, including Src kinases.

18 SH2, and catalytic domains seen in mammalian Src kinases.

19 phosphatidylinositol-3-OH kinase (PI3-K), or Src kinases.

20 clude a role as an anti-adhesive effector of Src kinases.

21 ar tyrosine kinase evolutionarily related to Src kinases.

22 daptor protein that controls the activity of Src kinases.

23 We also found that rhodopsin-regulated Src kinase activation in retina leads to the phosphoryla

24 tested for their ability to directly inhibit Src kinase activation in vitro.

25 Furthermore, increased Src kinase activation promoted migration, invasion, and

26 ted, reactive oxygen species (ROS)-dependent Src kinase activation, was required for beta-catenin to

27 n in p66(shc) reduced its ability to inhibit Src kinase activation.

28 o a lack of CD45, a phosphatase required for Src kinase activation.

29 TG function (monodansylcadaverine; MDC) or c-Src kinase activity (PP2) disrupted the formation of thi

30 cts as a biomechanical sensor that regulates Src kinase activity and stress fiber formation.

31 MIM knockdown results in increased Src kinase activity and subsequent hyperphosphorylation

32 We conclude that K6 negatively regulates Src kinase activity and the migratory potential of skin

33 Our study suggests that Src kinase activity determines NEDD9 exchange at focal a

34 ts in increased cholesterol biosynthesis and Src kinase activity in breast cancer cells and suggest t

35 These data suggest that increased Src kinase activity is a mechanism of lapatinib resistan

36 In this study, we demonstrate that increased Src kinase activity is associated with high-fat diet-acc

37 ocalization of SHIP, whereas neither PI3K or Src kinase activity is essential.

38 Pharmacological activation of Src kinase activity mimicked the effects of VEGF on P-gl

39 Inhibition of Src kinase activity prevented the increase in phosphoryl

40 AhR-complex-associated Src kinase activity promoted IDO1 phosphorylation and si

41 Our data show that Src kinase activity regulates IL-13-induced p38 MAPK tyr

42 eductions in the protein kinase C, Pyk 2 and Src kinase activity that in tandem can decrease GluN2 ac

43 Further, inhibition of Src kinase activity using caveolin-1 scaffolding domain

44 CD45 also enriched in AISs but to modulate Src kinase activity, because localization of CD45 at the

45 egrin and that this transactivation requires Src kinase activity.

46 rylation between SRC and AURKA that enhanced SRC kinase activity.

47 sphorylation of Src Tyr-418 and an increased Src kinase activity.

48 the E2F1 transcription factor; this required Src kinase activity.

49 between Src kinase specific activity (total Src kinase activity/total Src content) and metastatic ag

50 nous CD44 rolled on E-selectin and activated Src kinases after binding anti-CD44 antibody.

51 Moreover, the activity of Src kinases, along with oxidative stress, were significa

52 swelling, which triggers via integrins and c-Src kinase an activation of the epidermal growth factor

53 FGFR1 proteins lose their ability to recruit Src kinase, an important mediator of FGFR1 signaling, as

54 lated PAG serves as an anchor for C-terminal SRC kinase, an inhibitor of SRC-family kinases.

55 We showed that proto-oncogene Src kinase and Akt are direct targets of miR-23b.

56 bility to directly inhibit the activation of Src kinase and by its binding to the scaffold protein Ci

57 FN-induced EMT depends on Src kinase and extracellular signal-regulated kinase/mit

58 This newly identified interaction between Src kinase and HNF4alpha has important implications for

59 ne alpha1D369Nbeta1FXYD1) and purified human Src kinase and human caveolin 1 or interactions between

60 Na,K-ATPase is proposed to bind Src kinase and inhibit its activity, whereas ouabain, th

61 ntracellular HMGB1, through associating with Src kinase and inhibiting interactions between Src and F

62 esent study supports that the interaction of Src Kinase and integrins plays a critical role in the de

63 found that Dyn2 is phosphorylated at FAs by Src kinase and is recruited to FAs by a direct interacti

64 w that this trait results from activation of Src kinase and key Src substrates that promote cell migr

65 ription factor-1 cascade, which requires Fyn-Src kinase and lipid rafts in human taste bud cells (TBC

66 Src kinase and MLCK inhibitors blocked this synergistic

67 chanism involving calcium, oxidative stress, Src kinase and MLCK.

68 Mechanisms were investigated with src kinase and other inhibitors.

69 8 to beta1 integrins is elucidated requiring Src kinase and potential implication of the C2beta isofo

70 showed that protein-tyrosine kinases such as Src kinase and PTPs such as PTPalpha and PTPepsilon modu

71 the coupling of FcgammaRI to FcgammaRIIB by Src kinase and resulting activation of SH2 domain-contai

72 in the plasma membrane cholesterol activated Src kinase and stimulated the endocytosis and degradatio

73 ate that integrin alpha v (alphaV) recruited Src kinase and that leads to subsequent Src activation i

74 hat activate the focal-adhesion kinase and c-Src kinase and their downstream MAP-ERK kinase/extracell

75 adhesion kinase and ERKs 1/2, and decreased Src kinases and aquaporins 3 and 4.

76 protein tyrosine phosphatase that regulates Src kinases and collagen-induced platelet activation.

77 ng an additional and unexpected link between Src kinases and MAPK signaling.

78 gical studies additionally support roles for Src kinases and MAPK/ERK downstream of beta-arrestin2 in

79 ess-activated GSK3beta acted upstream to the Src kinases and phosphorylated the Src kinases, leading

80 have previously been shown to interact with Src kinases and PLCgamma.

81 ractions with endothelial selectins activate Src kinases and spleen tyrosine kinase (Syk), leading to

82 plasma membrane and receptor association to Src-kinases and phosphatidylinositol-3-kinase signalling

83 ough PKC and interaction with beta-arrestin, Src kinase, and hence the mitogen-activated-protein-kina

84 axis consisting of the integrin alphavbeta3, Src kinase, and the transcription factor Slug suppresses

85 taining phosphatase-1 (Shp-1) and C-terminal Src kinase, and we use modeling of early TCR signaling t

86 complex, posttranslational modifications of Src kinases, and morphological changes consistent with t

87 ession, activating focal adhesion kinase and Src kinases, and promoting cell migration and invasion.

88 DJ-1 directly bound to Lyn but not to other Src kinases, and this interaction was specific for human

89 ents to healthy control levels, suggesting a Src kinase- and actin-dependent mechanism.

90 /mechanistic target of rapamycin complex 2-, Src kinase-, and mRNA binding-dependent manner.

91 Exactly how SRC kinases are activated and hippo signaling is lost in

92 show that, in the Drosophila embryonic CNS, Src kinases are dispensable for midline attraction of co

93 Because Src kinases are involved in bridging the membrane to the

94 n promoting angiogenesis during SK and since Src kinases are involved in signaling by many of them, t

95 Mammalian Src kinases are normally regulated in a reciprocal fashi

96 mmon early signaling mediators, we show that Src kinases are required for lytic granule convergence,

97 t on integrin-mediated adhesion, and because SRC kinases are the main regulators of this process, the

98 These findings reveal Src kinase as a critical oncogenic driver underlying JMM

99 hogenicity of LAM cells and they rationalize Src kinase as a novel therapeutic target for treatment o

100 enin specifically complexed to HIF1alpha and Src kinase as critically involved in HIF1alpha signaling

101 enesis of DMD and identify NADPH oxidase and Src kinase as potential therapeutic targets.

102 Jak2 is required for the activation of both Src kinase as well as p38 MAPK.

103 These findings identify Src kinases as a critical regulator of chemokine secreti

104 and is a carrier for other adapter proteins, Src kinase-associated phosphoprotein 1 (SKAP1) and SKAP2

105 P=1.80x10(-8)), whereas SNPs associated with Src kinase-associated phosphoprotein 1 (SKAP1), matrix m

106 The Src kinase-associated phosphoprotein 2 (Skap2) is involv

107 identified a cytosolic adaptor protein named Src kinase-associated phosphoprotein 55 homologue (SKAP-

108 regulating integrin activation, we show that Src kinase-associated phosphoprotein of 55 kD (SKAP55) i

109 ves the interaction of ADAP with the adapter src kinase-associated phosphoprotein of 55 kDa (SKAP55).

110 es both ADAP and the ADAP-associated adapter Src kinase-associated phosphoprotein of 55 kDa (SKAP55).

111 kinase myristoylation, which is required for Src kinase association at the cellular membrane, blocks

112 P-1 localization and decreased activation of Src kinases at the synapse.

113 ese findings provide novel insights into how src- kinase-based regulation of a cbl adaptor regulates

114 ariant exhibits a 50% decrease in C-terminal Src kinase binding affinity and contributes to T cell hy

115 nt is dependent on the activation of Syk and Src kinases but is inhibited by CD19 costimulation, pres

116 K1 activation was abolished by inhibitors of Src kinases, but not Rac1 inhibitors, demonstrating that

117 P) ribosyltransferase that directly inhibits Src kinase by simultaneous amidation and ADP ribosylatio

118 ibition is mediated by a mechanism involving Src kinases, CD45, and SHIP-1 that is defective in MM ce

119 s degradation does not require the action of Src kinase, Cdc42 or Dyn2.

120 Hsp90 chaperones kinases, we reconstituted v-Src kinase chaperoning in vitro and show that its activa

121 To explain these findings, we designed Src kinase chimeras that gradually transform c-Src into

122 ond phosphorylation event include C-terminal Src kinase (Csk) and Bruton's tyrosine kinase (Btk).

123 h of two known inhibitors of Lck, C-terminal Src kinase (Csk) and protein tyrosine phosphatase N22 (P

124 controlled by the tyrosine kinase C-terminal Src kinase (CSK) and the tyrosine phosphatase CD45.

125 We identified C-terminal Src kinase (Csk) as a tyrosine kinase responsible for re

126 assessed the cooperative roles of C-terminal Src kinase (Csk) binding protein (Cbp) and Caveolin-1 (C

127 C-terminal Src kinase (Csk) binds to tyrosine phosphorylated JAM-A

128 C-terminal Src kinase (Csk) is a multidomain tyrosine kinase that i

129 tion of c-Src through deletion of C-terminal Src kinase (CSK) results in the development of invasive

130 while promoting the expression of C-terminal Src kinase (CSK), a negative regulator of Src family of

131 The C-terminal Src kinase (Csk), the primary negative regulator of Src-

132 nder the principal control of the C-terminal Src Kinase (Csk).

133 FKs and their negative regulator, C-terminal Src kinase (Csk).

134 -terminal tail by another kinase, C-terminal Src kinase (Csk).

135 The Drosophila C-terminal Src kinase (d-Csk) is a genetic modifier of warts (wts),

136 Time-dependent, Src kinase-dependent increases in serine and tyrosine ph

137 (EPEC and EHEC, respectively), which inhibit Src kinase-dependent phagocytosis by ADP-ribosylation.

138 on of the Rho GTPase pathway was followed by Src kinase-dependent phosphorylation of the Rap1-specifi

139 is an essential component of caveolae whose Src kinase-dependent phosphorylation on tyrosine 14 (Y14

140 brane-permeable CSD-competing peptides, that Src kinase-dependent pY14Cav1 regulation of focal adhesi

141 nals, depends on a directly downstream early Src kinase-dependent signal and emphasizes the importanc

142 ces IRAK1 and AKT phosphorylation, and it is Src kinase-dependent.

143 tyrosines in neural progenitors in vivo, and Src kinase directly phosphorylates CitK.

144 lizes the E2 conformation, thus exposing the Src kinase domain and its active site Tyr-418 for activa

145 the adjacent regulatory domains, whereas the Src kinase domains are autoinhibited by the assembly of

146 le blood and under flow conditions through a Src kinase driven pathway.

147 d, a mutant that cannot be phosphorylated by Src kinases exacerbated UVB-elicited apoptosis.

148 We demonstrate that members of the SRC kinase family (SKF) are key mediators of IFN-gamma p

149 The Src kinase family comprises nine homologous members whos

150 own to activate Stat3 such as Janus kinases, Src kinase family members or receptor tyrosine kinases.

151 Netrin-4-stimulated phosphorylation of Src kinase family, effectors of endothelial cell migrati

152 ymphocyte cell kinase (Lck), a member of the Src kinases family, mediates PC.

153 We recently demonstrated that Src kinase features an allosteric network that couples s

154 found that ectopically expressed Abl or the Src kinase Fgr phosphorylate Sos1, and the Src kinases H

155 Here, we show that Src kinase, followed by Fyn kinase and then Lyn kinase,

156 Here, we report that the c-Src kinase functions as a key adapter protein for the es

157 trast, there is consistent evidence that the Src kinase Fyn is activated by Abeta oligomers and leads

158 revealed the tyrosine phosphorylated form of src kinase Fyn was associated with Vav1 in platelets exp

159 nied by an activating phosphorylation of the Src kinases Fyn and Yes but not of c-Src.

160 LA2a-->15d-PGJ2-->PPARalpha/PPARbeta/delta-->Src kinase-->STAT1/STAT3 transcriptional mechanism.

161 cating a downregulation of expression of the Src kinase Hck.

162 e Src kinase Fgr phosphorylate Sos1, and the Src kinases Hck and Fgr are required for Abl and Sos1 ph

163 Here, we report increased levels of active Src kinase in LAM lungs and in TSC2(-/-) cells, caused b

164 actor (G-CSF) activates Lyn, the predominant Src kinase in myeloid cells, through Gab2-mediated recru

165 sion significantly correlated with activated Src kinase in patient samples and promoted tumor cell in

166 In the present study we test the role of Src kinase in regulating dynamic exchange of the focal a

167 functional and therapeutic relevance of the SRC kinase in synovial sarcoma.

168 poxia-ischemia (HI) results in activation of Src kinase in the newborn piglet brain.

169 ist for midline axon crossing independent of Src kinases in commissural neurons.

170 The overexpression of Src kinases in Hepa-1 cells led to decreased Nrf2, incre

171 gy between multiple inhibitors of Aurora and SRC kinases in ovarian and colorectal cancer cell lines,

172 so provide evidence for a regulatory role of src kinases in the activation of myeloid cells.

173 In this study, we investigated the role of Src kinases in the regulation of Nrf2 and downstream sig

174 Here we also show that the Src kinase inactivates the corepressive function of LCoR

175 stimulation, the interaction increases in a Src kinase-independent manner.

176 Cyclin D1 was induced by v-Src, and Src kinase induction of Trop2 ICD nuclear accumulation r

177 tion of either FAK or its signaling mediator Src kinase inhibited LMP2A-induced migration.

178 data indicate that F-actin stabilization and Src kinase inhibition represent potential therapeutic ta

179 ved in signaling by many of them, the use of Src kinase inhibition represents a promising way of limi

180 reover, we uncover an unexpected function of Src kinases: inhibition of midline axon crossing through

181 tion of a Smad2/3 inhibitor (SB431542) and a Src kinase inhibitor (PP2) blocked EMT with maintenance

182 at topical or systemic administration of the Src kinase inhibitor (TG100572) that inhibits downstream

183 ored after treating Bmpr2(+/-) PECs with the SRC kinase inhibitor 3-(4-chlorophenyl)-1-(1,1-dimethyle

184 y the OPRM1-Y336F mutant, by the presence of Src kinase inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-but

185 troarginine methyl ester (hydrochloride) and Src kinase inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-but

186 Blocking PKCzeta activation by a Src kinase inhibitor and a PKCzeta-pseudosubstrate preve

187 The Src kinase inhibitor dasatinib killed transformed BaF3 c

188 sing CBL mutants, whereas treatment with the SRC kinase inhibitor dasatinib resulted in equalization

189 ogen, which was blocked in the presence of a Src kinase inhibitor or in the absence of GPVI.

190 ): normoxic (Nx), HI and HI pre-treated with Src kinase inhibitor PP2 (PP2 + HI).

191 s was reduced by treatment of cells with the Src kinase inhibitor PP2 or by ectopic expression of a d

192 th the F-actin stabilizer phallacidin or the Src kinase inhibitor PP2 resulted in the significant red

193 vating kinase (MEK) inhibitor PD98059 or the Src kinase inhibitor PP2.

194 h the F-actin stabilizer phallacidin and the Src kinase inhibitor PP2.

195 The Janus kinase inhibitor AG490 and the Src kinase inhibitor Src-1, as well as rapamycin, have n

196 are the main regulators of this process, the SRC kinase inhibitor, saracatinib (AZD0530), completely

197 systemic therapy such as dasatinib, a potent SRC kinase inhibitor, with activity in bone.

198 n occur when TCR signaling is blocked with a Src kinase inhibitor.

199 Src kinase inhibitors are being tested in clinical trial

200 Src kinase inhibitors effectively blocked internalizatio

201 induced by FGFR1 fusion genes, implying that Src kinase inhibitors may offer a useful option to treat

202 Treatment of these resistant cells with Src kinase inhibitors partially blocked PI3K-Akt signali

203 Consistently, the Src kinase inhibitors PP2 and dasatinib reduced chemokin

204 Notably, Src kinase inhibitors reduced migration and invasion pro

205 Src kinase inhibitors, microtubule inhibitors, and PGE(2

206 IFN-gamma, Src kinase inhibitors, or TLR2 antibodies prevented the

207 Src-kinase inhibitors hold great potential as targeted t

208 Src-kinase inhibitors, and not conventional tyrosine kin

209 mulatory capacity of a group of novel drugs, src-kinase inhibitors, thereby opening new opportunities

210 However, the contribution of integrin and Src kinase interaction to lung fibrosis has not been mec

211 ic residues central to the Ptpn22-C-terminal Src kinase interaction.

212 raction led to the recruitment of C-terminal src kinase into lipid rafts, causing a preferential supp

213 SRC kinase is also constitutively activated in Bmpr2(+/-

214 llectively, these data provide evidence that Src kinase is an important mediator of signaling events

215 vivo We further show that myristoylation of Src kinase is essential to facilitate Src-induced and hi

216 Src kinase is known to regulate fibroblast migration.

217 Our results indicated that Src kinase is pathogenically activated in lymphomagenesi

218 correlated with diminished expression of the Src kinase Lck, protein kinase C-theta, and NF-kappaB, k

219 am to the Src kinases and phosphorylated the Src kinases, leading to their nuclear localization and N

220 Persistent activation of Src kinase leads to activation of the autophagy represso

221 Activation of Src kinase leads to rapid induction of protrusion with p

222 Unregulated activation of Src kinases leads to aberrant signalling, uncontrolled g

223 metic glutamic acid or transfection with the Src kinases Lyn or c-Src inhibited hydrogen peroxide-ind

224 nstitutively bound the adaptor protein Grb2, src-kinase Lyn and signal transducer phospholipase gamma

225 Our data suggest that Src kinase may represent a potential target that could i

226 Inhibiting TNF-alpha or src kinases may be a therapeutic option to normalize bar

227 ated progression of prostate tumors and that Src kinases mediate this pathological process.

228 Src kinase-mediated interactions between prostate cancer

229 stoyl CoA and myristoylated Src and promoted Src kinase-mediated oncogenic signaling in human cells.

230 o-like kinase 1 (Plk1) kinase by enhancing c-Src kinase-mediated tyrosine phosphorylation of Plk1.

231 Together, our results establish that c-Src kinase mediates stresses generated by E2 in long-ter

232 Our results suggest that targeting Src kinase myristoylation, which is required for Src kin

233 interaction is confirmed, the lack of direct Src kinase/Na,K-ATPase binding requires reassessment of

234 tress, through a signaling pathway requiring Src kinases, NADPH oxidase, superoxide radical anion, an

235 ect interactions between the Na,K-ATPase and Src kinase (non-receptor tyrosine kinase).

236 mical enzyme assays to determine the role of Src kinase on mitochondrial membrane apoptotic protein t

237 that TI-VAMP is phosphorylated in vitro by c-Src kinase on tyrosine 45 of the Longin domain.

238 y effect of the anticancer drug dasatinib on Src kinase oncogenic potential in vivo We further show t

239 ng antibody and inhibitors of peroxynitrite, src kinase, or MMP blocked the migration.

240 CD4 then recruits the Src kinase p56(Lck) (Lck) to the TCR-CD3 complex to phos

241 to be associated with aberrant regulation of Src-kinase p56(Lck).

242 ntigen receptor (TCR) and the active form of Src kinase p56lck (Lck) using single and dual-color phot

243 n beta1 play a role in the activation of the Src kinase pathway.

244 n elucidated through characterization of the Src kinase pathway.

245 AT pathway and enhanced by inhibitors of the Src kinase pathway.

246 gesting possible cross-talk between Smad and Src kinase pathways.

247 eveals an unappreciated relationship between Src kinases, paxillin, and survival of breast cancer pat

248 In turn, H2O2 activates a Src kinase/phospholipase C-gamma1 (PLC-gamma1) signaling

249 Src kinase phosphorylates the GluN2B CTD, but it is unkn

250 Here we show that activated c-Src kinase phosphorylates Y281 and Y302 of Mdm2, resulti

251 Na,K-ATPase was found to be a substrate for Src kinase phosphorylation at Tyr-144.

252 ese effects were associated with a transient Src kinase phosphorylation at Tyr416 and with a strong t

253 ) and VE-cadherin expression and increase in Src kinase phosphorylation downstream of VEGFR2 were acc

254 ic effects were prevented by deletion of a c-Src kinase phosphorylation DYD motif, identified in sili

255 The studies together demonstrate that Src kinases play a critical role in nuclear export and d

256 Moreover, inhibition of Src kinases prevented the activation of RhoA and ROCK, i

257 nd abnormal BBB permeability in part because Src kinase proto-oncogene members stimulate proliferatio

258 However, blockade of Src kinase reduced phosphorylation of p38 but not JNK, e

259 Inhibition of Nox2 or Src kinase reduces oxidative stress and partially rescue

260 With these features in mind, we examined Src kinase regulation at the structural, enzymatic, and

261 ction of T cells reduced the expression of a Src-kinase regulatory phosphatase (PTPRE), while ZKV inf

262 culture can be triggered by activation of v-Src kinase, resulting in increased cell motility, invasi

263 These findings identify Src kinase(s) as a mediator of TGFbeta1-induced pY654-be

264 direct fluorescence imaging or imaging of an Src kinase sensor in mammalian cells.

265 Mouse embryonic fibroblasts deficient in Src kinases showed nuclear accumulation of Nrf2, inducti

266 Moreover, activation of Src kinase signaling and FOXO1 inhibition decreased the

267 Inhibition of Janus kinase 2 or SRC kinase signaling downstream of mutated CSF3R is feas

268 Using ChIP-seq, we identified Src kinase signaling inhibitor 1 (Srcin1; also referred

269 is G-protein-dependent and involves cAMP and Src kinase signaling pathways.

270 regulated at the protein level by oncogenic Src kinase signals through SIAH2, thus contributing to b

271 , we do observe a direct correlation between Src kinase specific activity (total Src kinase activity/

272 Caveolin-1 (Cav1), a major Src kinase substrate phosphorylated on tyrosine-14 (Y14)

273 uitment of actin capping protein (CP) to the Src kinase substrate, cortactin, at the cell periphery,

274 The large GTPase Dynamin 2 (Dyn2), a Src-kinase substrate, regulates membrane-cytoskeletal dy

275 an modify the activation state of downstream Src kinases, such as Lyn, in lymphocytes.

276 ions that blocked CD36 ligation or inhibited Src kinases, suggesting a tyrosine kinase-dependent mech

277 e Src-family kinase Lyn and linked TLR9 to a Src-kinase Syk-transcription factor STAT3 cascade essent

278 ulation, raising a note of caution regarding src kinase-targeted intervention in plaque inflammation.

279 etwork of dynamically coupled amino acids in Src kinase that connects regulatory sites to the ATP- an

280 ntal support for long-range communication in Src kinase that leads to the relative stabilization of a

281 rface adhesion receptors, as well as FAK and Src kinases that are essential regulators of the migrati

282 ough Csk is known as a negative regulator of Src kinases, the effects of Csk on Gliotactin are indepe

283 Similar to mammalian Src kinases, the enzymatic activities of CoSrc1 and CoSr

284 Upon phosphorylation by Src kinases, this motif enabled binding of DNAM-1 to ada

285 We demonstrate that H2O2 acts through an Src kinase to activate a negative regulator of PI3K sign

286 -mediated signaling by recruiting C-terminal Src kinase to the membrane and/or receptor complex follo

287 within a box that also contained a protein (Src kinase) to which that ligand was known to bind.

288 ouse DCT cells via ROS-induced activation of Src kinase, up-regulation of the K(+) channel Kir4.1, an

289 By activating Src kinase using uniRapR in single cells and whole organ

290 drogen/deuterium exchange of Hsp90-dependent Src kinase variants further reveal increased transitions

291 yrosine kinases-Abl via pY251 and C-terminal Src kinase via pY239.

292 We also found that Src kinase was activated in the MMTV-expressing cells an

293 med normal mammary epithelial cells and that Src kinases were important mediators in this transformat

294 Coupling of SLAMF7 to SHIP-1 required Src kinases, which phosphorylated SLAMF7.

295 g conformations, first identified in CDK and Src kinases, which turned out to be central to understan

296 strates) bind with negative cooperativity to Src kinase while products (ADP and phosphopeptide) bind

297 ve conformation of the catalytic domain of c-Src kinase while the tyrosine 416 in the activation loop

298 ecently described transmembrane substrate of Src kinases whose expression and phosphorylation has bee

299 ctin-1 undergoes tyrosine phosphorylation by Src kinases with subsequent Syk activation.

300 ed by the receptor recruiting and activating Src kinase within the receptor complex, leading to phosp