ライフサイエンスコーパス: src

1 a 5 or 6 aa insertion into the SH3 domain of Src.

2 c of transformed cells without activation of Src.

3 t multimers with subsequent association with SRC.

4 uding epidermal growth factor receptor and c-Src.

5 elopment of a small molecule inhibitor of N1-Src.

6 protein cofilin, but not of RhoA, ROCK2 or c-Src.

7 pecificity and kinase activity compared to C-Src.

8 accompanied by activation of integrin beta1/Src.

9 l motility (-46 +/- 5%) with inhibition of p-SRC.

10 at tyrosine 10 by upstream kinases, HER2 and Src.

11 hat this unique PyMT behavior is mediated by Src.

12 uences in the SH3 domain to yield N1- and N2-Src.

13 oncogene activation, such as RAS, MYC, and c-SRC.

14 stream of RhoA signaling and is mediated via Src.

15 nd suggest that reduced levels of endogenous SRC-1 and apoA-IV expression are responsible for the imp

16 ed in cultured neuronal cells, we found that SRC-1 gene knockdown specifically in the NTS significant

17 oA-V promoter, implying the participation of SRC-1 in E2's stimulatory effect on apoA-IV gene express

18 tively demonstrate the critical roles of NTS SRC-1 in mediating E2's actions on food intake and apoA-

19 SRC-1 is colocalized with apoA-IV in the cells of the NT

20 n in the NTS was significantly attenuated in SRC-1 knockdown rats.

21 d SRC-1 with SI-2, a second-generation SRC-3/SRC-1 small-molecule inhibitor, targets the CSC/TIC popu

22 ment enhances the recruitment of ERalpha and SRC-1 to the estrogen response element at the apoA-V pro

23 We also show that inhibition of SRC-3 and SRC-1 with SI-2, a second-generation SRC-3/SRC-1 small-m

24 ors, such as steroid receptor coactivator-1 (SRC-1), to facilitate the transcription of targeted gene

25 ement in the CXCR4 promoter and recruits the SRC-1-p300 complex to promote H4K5 and H4K16 histone ace

26 e report that cardiomyocyte-specific loss of SRC-2 (SRC-2 CKO) results in a blunted hypertrophy accom

27 We found that SRC-2 CKO mice exhibit markedly decreased left ventricul

28 t that cardiomyocyte-specific loss of SRC-2 (SRC-2 CKO) results in a blunted hypertrophy accompanied

29 lated SRC-2 expression in vitro Furthermore, SRC-2 coactivated the transcription factors GATA-binding

30 These results suggest that SRC-2 coordinates cardiomyocyte secretion of VEGF downst

31 ulate angiogenesis, both of which stimulated SRC-2 expression in vitro Furthermore, SRC-2 coactivated

32 n, but the cardiomyocyte-specific effects of SRC-2 in these changes are unknown.

33 Pressure overload in mice lacking SRC-2 induces an abrogated hypertrophic response and dec

34 Of note, SRC-2 knockdown in cardiomyocytes decreased VEGF express

35 l key cardiac transcription factors and that SRC-2 loss results in extensive cardiac transcriptional

36 al regulator steroid receptor coactivator-2 (SRC-2) controls activation of several key cardiac transc

37 CARM1 recruitment lags behind the binding of SRC-3 and p300 to ER.

38 We also show that inhibition of SRC-3 and SRC-1 with SI-2, a second-generation SRC-3/SRC

39 Here we report that SRC-3 supports the TIC/CSC state and induces an epitheli

40 The steroid receptor coactivator 3 (SRC-3) is overexpressed in a wide range of cancers, driv

41 ER) recruits steroid receptor coactivator-3 (SRC-3) primary coactivator and secondary coactivators, p

42 organization of the pre-existing ERE/ERalpha/SRC-3/p300 complex.

43 C-3 and SRC-1 with SI-2, a second-generation SRC-3/SRC-1 small-molecule inhibitor, targets the CSC/TI

44 e inhibitor genistein, and the more specific Src/Abl kinase inhibitor dasatinib: both reduced ROS-ind

45 slational mechanisms, that is, activation of Src/Abl kinases and degradation of beta-catenin/E-cadher

46 Src inhibitor reduced Src activation and blocked the signaling transduction by

47 ociation with ICAM-1-mediates ICAM-1-induced Src activation and modulates VE-cadherin switching assoc

48 ited Src kinase and that leads to subsequent Src activation in fibroblasts plated on fibrotic matrix,

49 We demonstrate that PyMT-induced Src activation inhibits degradation of both wild-type an

50 e intracellular signaling pathway triggering Src activation of IRF4 remains unknown.

51 ed amino acid, Gly449, that is necessary for Src activation.

52 ation found that depletion of p120 increases Src activity and that loss of p120 binding results in in

53 Src activity and tyrosine phosphorylation of VE-cadherin

54 Moreover, c-Src activity is sufficient to drive M fate, even in nonm

55 The current view is that SRC acts primarily downstream of cell-surface receptors

56 hich consequently triggers the activation of SRC and attenuates the expression of beta-catenin, respe

57 satinib or crizotinib (inhibitors of IGF-1R, Src and c-Met/ALK, respectively) led to synergistic effe

58 tool for distinguishing the functions of N1-Src and C-Src in neurons and is a starting point for the

59 For example, in choanoflagellates, Src and Csk are both active, but the negative regulatory

60 Although Src and Csk orthologs are present across holozoan organi

61 based growth assays to characterize holozoan Src and Csk orthologs.

62 urvival and cell migration through decreased SRC and ERK activation.

63 h an increased phosphorylation level of both Src and extracellular signal regulated kinase proteins a

64 ding to integrin-mediated phosphorylation of Src and extracellular signal-regulated kinase (ERK).

65 rk linked to tight spatial control of active Src and FAK levels, and so crucially regulates their can

66 l receptor signaling, monobodies binding the Src and Hck SH2 domains selectively activated respective

67 particular, treatment with a combination of Src and HER-family member inhibitors resulted in synergi

68 Src and IGF-1R phosphorylated the prometastatic molecule

69 N1) that targets the unique SH3 domain of N1-Src and inhibits N1-Src in cells.

70 we show that PTP4A1 directly interacts with SRC and inhibits SRC basal activation independently of i

71 ation abolished the tumorigenic potential of Src and its synergy with androgen receptor in mediating

72 ects of Csk on Gliotactin are independent of Src and likely occur through an adherens junction associ

73 nd to FAK, abnormally high levels of phospho-Src and phospho-FAK accumulate at focal adhesions, posit

74 s the cellular nonreceptor tyrosine kinase c-Src and recruits the Hippo pathway effectors, Yap (yes-a

75 ifically, alpha6beta4-mediated activation of Src and STAT3 suppresses expression of ACSL4, an enzyme

76 GCs to stabilize HIF through activation of c-src and subsequent destabilization of pVHL.

77 of actin-mediated phagocytosis that leads to Src and Syk kinase activation, Ca(2+) mobilization, and

78 ignaling, such as caveolin, phospholipase C, Src, and the IP3 receptor.

79 e show that LMP1 physically interacts with c-Src, and the phosphatidylinositol 3 kinase (PI3K) subuni

80 odels (standardized regression coefficients [SRCs] and semipartial correlation coefficients squared [

81 Srcs are also enriched in the brain, where they play key

82 However, the exact functions of the N-Srcs are unknown and it is likely that N-Src signalling

83 h inhibition of MDA-MB453 cells, implicating Src as a mediator of resistance to HER2-targeting agents

84 Src association was normal as assayed by in vitro kinase

85 reatment, ERalpha-36 rapidly associates with Src at the level of the plasma membrane, initiating down

86 Instead, we found that Src attenuates the SCF(beta-TrCP) E3-ligase activity in

87 a1 regulates the targeting of active phospho-Src away from focal adhesions into autophagic structures

88 4A1 directly interacts with SRC and inhibits SRC basal activation independently of its phosphatase ac

89 gnalling events have been misattributed to C-Src because they cannot be distinguished by conventional

90 Inhibition of integrin beta1/Src blocked collagen-induced resistance to TPB and inhib

91 deltaKD is not a substrate for Src, but Src phosphorylates deltaKD-T507A at Tyr(334) (i

92 results suggest that negative regulation of Src by Csk is more ancient than previously thought and t

93 riant of C-Src, N1-Src, which differs from C-Src by just 5 or 6 aa.

94 n is mediated by the combined action of JAK, SRC, c-ABL, and JNK kinases.

95 We show that Src causes a 5-AzaC-sensitive decrease in both mRNA and

96 of n1-src, while preserving c-src Loss of n1-src causes a striking absence of primary neurogenesis, i

97 The MfR protein subunits Met and SRC, cloned from Daphnia pulex, were fused to the fluoro

98 in vivo Collectively, these results identify SRC coactivators as regulators of stem-like capacity in

99 e as shown by its ability to engage an MTSS1-Src-cortactin inhibitory axis.

100 miR-193b was found to regulate FAK-SRC-CRKL signaling through CRKL and FAK.

101 ed by Trio downstream of PDGF in a PI3K- and Src-dependent manner.

102 ns using the small molecule JP-153 inhibited Src-dependent phosphorylation of paxillin (Y118) and dow

103 ished covert attention, the covert-attention SRC effect disappeared and the overt-attention SRC effec

104 eye tracker to monitor fixation, we found an SRC effect relative to the site of covert attention indu

105 C effect disappeared and the overt-attention SRC effect retained full strength, excluding non-attenti

106 but not elimination, of the overt-attention SRC effect.

107 ated by the stimulus-response-compatibility (SRC) effect: When subjects press, e.g., a left key to re

108 ial cells and that syntenin is mandatory for SRC exosomal function.

109 y to the n1-src microexon, indicates that n1-src expression is highly enriched in the open neural pla

110 hibian Xenopus tropicalis, and found that n1-src expression is regulated in embryogenesis, with highe

111 Given the n1-src expression pattern, we investigated a possible role

112 trated that VEGF-dependent activation of the Src/FAK/paxillin signalsome is required for human retina

113 g the tyrosine phosphorylation of C-Raf with Src family inhibitors blocks growth, basal dimerization,

114 Finally, we demonstrated that JAM-C controls Src family kinase (SFK) activation in LSC and that LIC w

115 the autophosphorylation site tyrosine in the SRC family kinase (SFK) FYN as well as Tyr142 in beta-ca

116 alternative signaling activation mechanisms, Src family kinase (SFK) signaling is sufficient to trans

117 We identified Src family kinase activation mediated by mu-receptors as

118 cription and secretion through inhibition of Src family kinase activation, particularly Lck, downstre

119 signals through an evolutionarily conserved Src family kinase cascade to drive cytoskeletal rearrang

120 regulated kinase (ERK1/2) was blocked by the Src family kinase inhibitor PP2, indicating that the act

121 , and cerebrospinal fluid penetration of the Src family kinase inhibitor saracatinib in patients with

122 ng to regulate T cell lineage commitment and SRC family kinase LCK and STAT5 signaling to regulate al

123 The Src Family kinase Lck sets a critical threshold for T ce

124 er kinetics of Erk1/2 activation through the src family kinase(s)-Syk signaling pathway.

125 leading to integrin activation via the SFK (Src family kinase)-Syk (spleen tyrosine kinase)-PLCgamma

126 Here we report that Src family kinases (SFK) and focal adhesion kinase (FAK)

127 Focal adhesion kinase (FAK) and Src family kinases (SFK) are known to play critical role

128 Here we show the role of Src family kinases (SFK) in mouse and human pDCs.

129 ER2 are activated through phosphorylation by Src family kinases (SFK).

130 engagement of LFA-1 led to the activation of SRC family kinases (SFKs) and SFK inhibition blocked cyt

131 Src family kinases (SFKs) are involved in both NMDA-medi

132 The Src family kinases (SFKs) Lck, Hck, and Fgr directly pho

133 PECAM-1 transduces forces to activate src family kinases (SFKs), which phosphorylate and trans

134 ition and substrate recognition of the eight Src family kinases (SFKs).

135 urn is required to activate VEGFR2-recruited SRC family kinases (SFKs).

136 CD38, via Src family kinases and adapters, interacts with a MAPK s

137 ultimerization of DCC, activation of FAK and Src family kinases, and increases in exocytic vesicle fu

138 Furthermore, TNFalpha, via SRC family kinases, increases pro-proliferative NOTCH2 s

139 gnificant homology with other members of the Src family kinases, which may lead to unintended off-tar

140 Phosphorylation of paxillin by Src family kinases, which regulates adhesion turnover, i

141 g Abl localization and Abl/Arg activation by Src family kinases.

142 late neurogenesis.SIGNIFICANCE STATEMENT The Src family of nonreceptor tyrosine kinases acts in signa

143 was blocked in cultured microglia by PP2, a Src family protein tyrosine kinase inhibitor.

144 We identified an Src family tyrosine kinase, hematopoietic cell kinase (H

145 Protein phosphatase 2A (PP2A), YAP, Src family tyrosine kinases, Shc, phosphatidylinositol 3

146 These results support a model in which Src-family kinase binding induces conformational changes

147 Our previous work showed that the src-family kinase Lck is a targetable mediator of BCR si

148 Upon Fc receptor activation, Src-family kinase signaling leads to segregation of Fcga

149 factor-beta (TGF-beta), RhoA/Rho-kinase and Src-family kinases (SrcFK) have independently been impli

150 either the SH3 or tandem SH3-SH2 domains of Src-family kinases reveal distinct dimer conformations o

151 Activation of Src-family tyrosine kinases on the Golgi is essential fo

152 to ERalpha by steroid receptor coregulators (SRCs) for enhancer maturation and maintenance.

153 strong selectivity for either the SrcA (Yes, Src, Fyn, Fgr) or SrcB subgroup (Lck, Lyn, Blk, Hck).

154 Overactivation of Src has been linked to the pathogenesis of autosomal dom

155 orly understood and its high similarity to C-Src has made it difficult to delineate its function.

156 and others have previously shown that the N-Srcs have altered substrate specificity and kinase activ

157 hotyrosine-dependent binding modules such as Src homology 2 (SH2) and phosphotyrosine-binding (PTB) d

158 mediates lysine-63 ubiquitination within the Src homology 2 (SH2) domain of STAT3, which is an essent

159 y point mutations of Lyn catalytic domain or Src homology 2 (SH2) or SH3 domains or of the cysteine r

160 The adaptor protein Src homology 2 domain-containing leukocyte phosphoprotei

161 In addition, DJ-1 reduced Src homology 2 domain-containing phosphatase 2 phosphata

162 The 66-kDa Src homology 2 domain-containing protein (p66Shc) is a m

163 e sulfenic acid state, we visualize oxidized Src homology 2 domain-containing protein-tyrosine phosph

164 s and shared binding partners, including the Src homology 2 domain-containing protein-tyrosine phosph

165 It's signals are mediated by SHIP (Src homology 2-containing inositol 5' phosphatase), in p

166 FUS (fused in sarcoma) to a multivalent poly-Src homology 3 (SH3) domain protein that phase-separates

167 ecular interaction between GK and the nearby Src homology 3 (SH3) domain, leading to a closed conform

168 that has been shown to interact with several Src homology 3 (SH3) domain-containing proteins.

169 CB is expressed with or without a src homology 3 (SH3) domain.

170 Proteins of the Src homology and collagen (Shc) family are typically inv

171 We observed that ICAM-1 interacts with Src homology domain 2-containing phosphatase-2 (SHP-2),

172 proline rich, the hypothesis that it targets Src homology domain 3 (SH3) domains was tested, but muta

173 The Src homology domain containing phosphatase 2 (SHP2) and

174 ic protein tyrosine phosphatase (VE-PTP) and Src homology phosphatase 2 (SHP2), both of which are imp

175 of several tumor suppressor genes, including Src homology region 2 domain-containing phosphatase-1 (S

176 /protein kinase A-mediated activation of the Src homology region 2 domain-containing phosphatase-1 (S

177 ctor encoding a dominant negative isoform of Src homology region 2 domain-containing tyrosine phospha

178 (CagA) and CagA-signaling molecules (phospho-Src homology-2 domain-containing phosphatase [p-SHP2] an

179 The binding of Src-homology 2 (SH2) domains to phosphotyrosine (pY) sit

180 in regulators acting downstream of activated Src identified the replication-dependent histone chapero

181 Mechanistically, SRC impacts on syndecan endocytosis and on syntenin-synd

182 These data reveal an essential role for n1-src in amphibian neural development and suggest that alt

183 ays broad substrate specificity and inhibits Src in an activity-independent manner.

184 Ambra1 binds to both FAK and Src in cancer cells.

185 Our study uncovers a function of SRC in cell-cell communication, supported by syntenin ex

186 unique SH3 domain of N1-Src and inhibits N1-Src in cells.

187 tern, we investigated a possible role for n1-src in neurogenesis.

188 distinguishing the functions of N1-Src and C-Src in neurons and is a starting point for the developme

189 t and suggest that alternative splicing of C-Src in the developing vertebrate nervous system evolved

190 Here we investigated the role of n1-src in the early development of the amphibian Xenopus tr

191 e involvement of MOPs, DOPs, beta-arr2 and c-Src in the inhibition by morphine of GABAergic inhibitor

192 ence of primary neurogenesis, implicating n1-src in the specification of neurons early in neural deve

193 Overall, we identified a new Src-independent role for Csk in the control of Gliotacti

194 ion of Src kinase is essential to facilitate Src-induced and high-fat diet-accelerated tumor progress

195 mpairs AJ activity, which appears to reflect Src-induced phosphorylation, internalization and degrada

196 The high-fat diet not only accelerated Src-induced prostate tumorigenesis in mice but also comp

197 In old arteries, Src inhibition (saracatinib) increased: (i) 140 kDa VE-c

198 Src inhibition increased VE-cadherin at adherens junctio

199 roliferation inhibition in vitro, anti-human Src inhibition, hERG activity, in vivo pharmacokinetic d

200 lated with similar cytotoxic activity of the SRC inhibitor KX2-391 and inhibition of SRC phosphorylat

201 ulator of HIF, and that treatment with the c-src inhibitor PP2 rescued this effect, suggesting a role

202 Src inhibitor reduced Src activation and blocked the sig

203 Inhibition of Pxn phosphorylation by the Src inhibitor saracatinib or its knockdown via shRNA dra

204 Importantly, Src inhibitor significantly reduces fibroblast migration

205 The application of the c-Src inhibitor, PP2, to WT neurons also reduced inhibitio

206 demonstrate that combined use of MEK1/2 and Src inhibitors effectively suppresses development of int

207 s study suggests that cocktail of MEK1/2 and Src inhibitors represents an effective therapeutic strat

208 they cannot be distinguished by conventional Src inhibitors that target the kinase domain.

209 In humans, the tyrosine kinase Src is inhibited via phosphorylation of its C-terminal t

210 N1-Src is poorly understood and its high similarity to C-Sr

211 Furthermore, we show that Src is upstream of PI3K for activation of both IRF4 and

212 of major cancer pathways such as Ras/ERK1/2, Src, JAK/STAT, JNK, NF-kappaB, and PTEN/PI3K/AKT.

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

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

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

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

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

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

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

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

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

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

223 Src kinase is known to regulate fibroblast migration.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

243 eposition via neutrophil FcgammaRIIA and Abl/Src kinases.

244 the primary nervous system is reduced in n1-src-knockdown embryos, accompanied by a severely impaire

245 B13 exposure blocked Src myristoylation and Src localization to the cytoplasmic membrane, attenuatin

246 in the absence of n1-src, while preserving c-src Loss of n1-src causes a striking absence of primary

247 of IPSCs by morphine involves a beta-arr2/c-Src mediated mechanism.

248 ne chaperone CAF1 as an important factor for Src-mediated increased cell motility and invasion.

249 netic remodeling through DNA methylation for Src-mediated induction of cancer phenotypes.

250 ion to the cytoplasmic membrane, attenuating Src-mediated oncogenic signaling.

251 kinase (FAK) autoactivation at the point of Src-mediated phosphorylation of FAK Y861/Y925.

252 ct, suggesting a role for GCs in promoting c-src-mediated proteosomal degradation of pVHL.

253 R75 binding, which further facilitated the c-Src-mediated transactivation of epidermal growth factor

254 ently shown that IRF4 is activated through c-Src-mediated tyrosine phosphorylation in virus-transform

255 ates IRF4 transcriptional activity, and that Src mediates LMP1 activation of IRF4.

256 We show that Src mediates VE-cadherin disassembly in response to meta

257 pathway previously shown to be disrupted in Src(-/-) mice.

258 ic acid oligo probes complementary to the n1-src microexon, indicates that n1-src expression is highl

259 Using antisense knockdown of the n1-src microexon, we have studied neuronal development in t

260 that was mimicked by shRNA targeting the N1-Src microexon.

261 B13 exposure blocked Src myristoylation and Src localization to the cytoplasm

262 volved a neuron-specific splice variant of C-Src, N1-Src, which differs from C-Src by just 5 or 6 aa.

263 sms, including animals and protists, the Csk-Src negative regulatory mechanism appears to have evolve

264 aspora owczarzaki is active and that the Csk-Src negative regulatory mechanism is present in Csk and

265 t via canonical signaling mechanisms such as Src (non-receptor tyrosine kinase), PI3K, ERK, or MAPK p

266 not prevent the initial activation of either Src or FAK.

267 ersonalized therapeutic approaches targeting Src or MEK in ERalpha-36-positive patients.

268 The tyrosine kinase, c-Src, participates in mu opioid receptor (MOP) mediated i

269 ibition (CASP-9, CASP-7, DFF-45, NPM, YWHAZ, Src, PAX2, MAPK8), cell cycle promotion and cancer progr

270 deltaKD is not a substrate for Src, but Src phosphorylates deltaKD-T507A at Tyr(334) (in the new

271 the SRC inhibitor KX2-391 and inhibition of SRC phosphorylation.

272 atrix anchorage as well as signaling through Src, PI3K, and Rac1, and increasingly stiff collagen pro

273 e regulatory mechanism is present in Csk and Src proteins from C. owczarzaki and the choanoflagellate

274 imulated ITG-dependent focal adhesion kinase/Src proto-oncogene non-receptor tyrosine kinase signalin

275 nic signaling molecules (iNOS, STAT3/pSTAT3, Src/pSrc).

276 co-expressing constitutively active MEK1 and Src rather than either alone.

277 splay reduced barrier function and excessive Src-related tyrosine phosphorylation of the adherens jun

278 ggest that upregulation of collagen/integrin/Src signaling contributes to resistance to combinatorial

279 or pharmacological disruption of alphavbeta3/Src signaling drives PUMA expression, specifically deple

280 In turn, focal adhesion formation and FAK/SRC signaling is activated in mesenchymal tumor cells by

281 he extracellular matrix (ECM), increased FAK/Src signaling, and ultimately YAP/TAZ activation.

282 e N-Srcs are unknown and it is likely that N-Src signalling events have been misattributed to C-Src b

283 Alternative splicing involving an N1-Src-specific microexon leads to a 5 or 6 aa insertion in

284 by Synchrotron Radiation Circular Dichroism (SRCD) spectroscopy.

285 The presence of the neuronal-specific N1-Src splice variant of the C-Src tyrosine kinase is conse

286 loss-of-function studies, we establish that SRC stimulates the secretion of exosomes having promigra

287 Cas family scaffolding protein p130Cas is a Src substrate localized in focal adhesions (FAs) and fun

288 diator of alum adjuvanticity in vivo and the Src-Syk pathway as a potential leverage point in the rat

289 Src tyrosine kinase activity and tyrosine phosphorylatio

290 r protein that is required for activation of SRC tyrosine kinase and simultaneously coordinates the a

291 onal-specific N1-Src splice variant of the C-Src tyrosine kinase is conserved through vertebrate evol

292 lian brain the ubiquitous tyrosine kinase, C-Src, undergoes splicing to insert short sequences in the

293 ll motility and invasiveness phenotypes when Src was activated.

294 neuron-specific splice variant of C-Src, N1-Src, which differs from C-Src by just 5 or 6 aa.

295 nctional interplay among p300, Mediator, and SRCs, which has implications for hormone-dependent gene

296 t in the Xenopus embryo in the absence of n1-src, while preserving c-src Loss of n1-src causes a stri

297 Accordingly, inhibition of Abl/Src with bosutinib reduced FcgammaRIIA-mediated glomerul

298 or-ligand interactions mediate activation of Src within endothelial cells that is necessary for phosp

299 ctor (Met) and steroid receptor coactivator (SRC), would be expressed coincident with the timing of s

300 regeneration assay, host SCID mice carrying Src(Y529F)-transduced regeneration tissues were fed a lo