ライフサイエンスコーパス: src

1 ent to empower it to allosterically activate Src.

2 eleted, fully retain the ability to activate Src.

3 lecting between the activation of ERK1/2 and Src.

4 horylated C-terminal tail failed to activate Src.

5 otein 1 (YAP1) and of its upstream regulator SRC.

6 of a PKCalpha expression vector or an active Src.

7 itutive phosphorylation of PANX1 Tyr(198) by SRC.

8 interaction between the alpha1 subunit and c-Src.

9 thereby promoted phosphorylation of Cav-1 by Src.

10 r by targeting cysteine 277 on the P-loop of SRC.

11 s thickness, and vitreous cavity depth, ACD (SRC = 0.64, SPCC(2) = 0.19) and IC (SRC = -0.26, SPCC(2)

12 abetes duration (beta = -0.0022 per 5 years; SRC = -0.0527; P = .0427).

13 .2733; P < .0001), male sex (beta = -0.0067; SRC = -0.0716; P = .0060), and longer diabetes duration

14 th, ACD (SRC = 0.64, SPCC(2) = 0.19) and IC (SRC = -0.26, SPCC(2) = 0.041) were the strongest determi

15 D were older age (beta = -0.0123 per decade; SRC = -0.2733; P < .0001), male sex (beta = -0.0067; SRC

16 gth, LV (SRC = -0.46, SPCC(2) = 0.1) and IC (SRC = -0.3, SPCC(2) = 0.047) were the strongest determin

17 58), which included LV and axial length, LV (SRC = -0.46, SPCC(2) = 0.1) and IC (SRC = -0.3, SPCC(2)

18 revealed that steroid receptor coactivators (Src)-1 and -2 serve a critical cooperative role in produ

19 umans, fifteen rare heterozygous variants in SRC-1 found in severely obese individuals impair leptin-

20 is of lungs from 18.5 days post-coitum (dpc) Src-1(-/-) /-2(-/-) (dKO) vs. WT fetuses.

21 e model of a loss of function human variant (SRC-1(L1376P)), leptin-induced depolarization of Pomc ne

22 nes most highly downregulated (~4.8 fold) in Src-1/-2 dKO fetal lungs encodes 11beta-hydroxysteroid d

23 global landscape of genes in MFL affected by Src-1/-2 double-deficiency, we conducted RNA-seq analysi

24 ta mRNA and protein were markedly reduced in Src-1/-2 double-deficient (Src-1/-2(d/d) ) fetal lungs,

25 rkedly reduced in Src-1/-2 double-deficient (Src-1/-2(d/d) ) fetal lungs, compared to WT.

26 lungs of WT fetuses, was markedly reduced in Src-1/-2(d/d) fetal lungs.

27 lung development and surfactant synthesis in Src-1/-2(d/d) fetuses are likely caused, in part, by dec

28 se 2 to the SIRT3 promoter, and depletion of SRC-2 enhanced SIRT3 expression and simultaneously reduc

29 spontaneous bone metastasis, suppression of SRC-2 reactivated SIRT3 expression and was sufficient to

30 c prostate cancer and suggests that blocking SRC-2 to enhance SIRT3 expression may be therapeutically

31 cantly elevated, and increased expression of SRC-2 with concomitant reduction of SIRT3 was found to b

32 coregulator steroid receptor coactivator-2 (SRC-2) enhances mitochondrial aconitase (ACO2) activity

33 Loss of steroid receptor coactivator-2 (SRC-2) results in a reversal to the fetal gene program a

34 Mechanistically, SRC-2-bound AR formed a repressive complex by recruiting

35 Additionally, preactivation of AMPK in SRC-2-CKO mice was accompanied by a dramatic improvement

36 ardiac function compared with saline-treated SRC-2-CKO mice.

37 nlike ERalpha, AR directly contacts a single SRC-3 and p300.

38 its complex structure with key coactivators, SRC-3 and p300.

39 in up-regulating the levels of the C-MYC and SRC-3 oncoproteins, FBXL16 promoted cancer cell growth a

40 catenin, and steroid receptor coactivator 3 (SRC-3).

41 aseline Ca(2+) to maximal levels and reduced Src activation and overall metabolic activity in macroph

42 on involves both arrestin and Galphas, while Src activation depends solely on arrestin.

43 SRC activation increased YAP/TAZ activity and the expres

44 RPTPalpha variant in HEK293T cells enhanced SRC activation, supporting the relevance of our proposed

45 nsmall cell lung cancer cell lines harboring SRC activation, thus providing evidence that this approa

46 MPs, which in turn modulates EC apoptosis by Src activation.

47 Whereas free betaarr1 had no effect on Src activity, betaarr1 in complex with M2 muscarinic or

48 other contexts, however, PTPROt can inhibit Src activity.

49 tion and proteasomal degradation of active c-SRC after its phosphorylation at Ser 104.

50 studies also suggest that hyperactivation of Src, alteration of autophagy and a mitochondrial deficit

51 ptin increases phosphorylation of Tyr-418 in Src, an indicator of kinase activation.

52 tion and migration through activation of FAK/Src and Akt1/mTOR signaling, respectively.

53 21 (GSK-3beta inhibitor) and Dasatinib (Abl, Src and c-Kit inhibitor) were found to confer miPSCs wit

54 , but argued about the interaction between c-Src and cav-1 under the condition.

55 adhesion protein and tumor suppressor, with SRC and ERK.

56 SRC and frailty index did not adequately predict complic

57 KO platelets, which was partially rescued in Src and Fyn in TKO platelets.

58 verses Type I priming, or the combination of Src and mitogen-activated protein kinase (MAPK) inhibito

59 eta, an isoform of PKC, is required for both Src and Pyk2 activation/phosphorylation in response to M

60 ion with subsequent activation of downstream SRC and STAT3.

61 ed pharmacological inhibitors of major PTKs: Src and the focal adhesion kinase (FAK) family kinases -

62 ated by the inhibition of phosphorylation of Src and vascular endothelial cadherin (VE-cadherin), whi

63 ransporter internalization/inactivation, and Src and VASP phosphorylation, but not apical plasma memb

64 tion increased the phosphorylation levels of Src and VE-cadherin and reduced the formation of the VEG

65 static genes and pathways, such as integrins-Src and VEGFA, and for the growth of HER2+ breast cancer

66 of TGR5 in ISCs, resulting in activation of SRC and YAP and activation of their target genes. Releas

67 nt Program (NSQIP) Surgical Risk Calculator (SRC) and a 5-factor NSQIP-derived frailty index.

68 s with standardized regression coefficients (SRCs) and semipartial correlation coefficients squares (

69 from an independent Safety Review Committee (SRC); and (3) their clinical experience.

70 ns amongst the Na/K-ATPase alpha1 subunit, c-Src, and caveolin-1 (cav-1) are essential for the Na/K-A

71 via a noncanonical pathway involving gp130, Src, and the Hippo pathway protein YAP.

72 Notably, Src- and SHP2-mediated regulation of KRAS activity exten

73 tail by >=2 readers, then adjudicated by the SRC as a group.

74 We and others have previously identified c-Src as a key mediator of thyroid cancer pro-tumorigenic

75 Using the tyrosine kinase Src as a model, we demonstrate efficient regulation of t

76 tail of the vasopressin 2 receptor activates Src as efficiently as GPCR-betaarr complexes.

77 nteractions between the alpha1 subunit and c-Src as well as between the alpha1 subunit and cav-1, but

78 proto-oncogene, nonreceptor tyrosine kinase (SRC) at Tyr(198) We demonstrate that PANX1-mediated ATP

79 stimulator of steroid receptor coactivators (SRCs) attenuates pathological remodeling post-MI.

80 cs activate Src by reducing the lag phase in Src autophosphorylation.

81 stabilization occurs mainly via the PKCalpha-Src axis.

82 stitutively inhibits I(Kv1.5) Disrupting the Src-binding motif of Kv1.5 through N-terminal truncation

83 losteric activation of proto-oncogene kinase Src by GPCR-betaarr complexes in vitro and establish the

84 rs reconstituted in lipid nanodiscs activate Src by reducing the lag phase in Src autophosphorylation

85 bitors, SRC knockdown, temperature-dependent SRC cells, and kinase assays, we found that PANX1-mediat

86 sia cortactin that plays a major role in the Src/cortactin/Arp2/3 signaling pathway controlling filop

87 ur findings suggest that therapies targeting SRC could help manage some YAP/TAZ-dependent cancers.

88 describe our efforts to develop a selective SRC covalent inhibitor by targeting cysteine 277 on the

89 prevented EphB1 binding to Cav-1 as well as Src-dependent Cav-1 phosphorylation, indicating the impo

90 enchymal transition and cell invasion in a c-SRC-dependent manner.

91 c cancer cell migration via microtubule- and Src-dependent pathways.

92 lasma membrane and promotes activation of an SRC-dependent signaling cascade that controls YAP nuclea

93 n in a cGAS/STING-independent, but TBK1- and SRC-dependent, manner.

94 The SRC did not identify risk of complications in the entire

95 sses NB pathogenesis by an integrin-mediated Src-disruption pathway.

96 7F-FXR, ameliorated atherosclerosis, whereas Src down-regulation exacerbated it.

97 activating protein GIT ArfGAP 1 (GIT1) as an SRC effector that regulates both YAP and TAZ.

98 served that Ph-like ALL cells have activated SRC, ERK, and PI3K signaling consistent with activated B

99 se findings indicate cooperation between the SRC, ERK1/2, and AKT kinases to reduce DLC1 Rho-GAP and

100 angiogenesis by transcriptionally regulating SRC expression.

101 owed that Ach upregulated TGFbetaRII through Src-extracellular signal-regulated kinase 1/2 pathway to

102 PK in high glucose condition interferes with Src-extracellular signal-regulated kinase 1/2 signaling,

103 signaling pathways including CREB, mTOR, and Src-FAK.

104 ed MFL epithelial cells was prevented by the SRC family inhibitor, SI-2.

105 Treatment of intact ECs with Src family inhibitors induced cytoplasmic localization o

106 of intracellular calcium but is sensitive to SRC family kinase (SFK) inhibition, suggestive of channe

107 We tested the hypothesis that regulation of SRC family kinase (SFK) signaling by the scaffold protei

108 This reflects a mechanosensitive Src family kinase (SFK) signaling pathway that is activa

109 nding macrophages by directly activating the Src family kinase (SFK) Src42A,(3) which in turn phospho

110 identified the concomitant activation of an Src family kinase (SFK), hematopoietic cell kinase (HCK)

111 Previous studies with various Src family kinase biosensors showed that the nuclear kin

112 The Src family kinase Fgr was identified as a downstream eff

113 lly disordered SH4 and Unique domains of the Src family kinase Hck.

114 nical trials using single agent dasatinib, a SRC family kinase inhibitor, have failed in sarcomas.

115 rotein HER-2 increased the activation of the Src family kinase LCK and cytokine-induced STAT-5 signal

116 Src family kinase Lck plays critical roles during T cell

117 respond to antigen because it activates the Src family kinase Lck, which phosphorylates the T cell a

118 C-2 receptor clustering, followed by Syk and Src family kinase phosphorylation, determined by the clu

119 2)R-cGMP downstream signaling molecules Src (Src family kinase), ERK (extracellular signal-related ki

120 yrosine phosphorylation is controlled by the Src family kinase.

121 ustion through TICAM2 mediated activation of Src family kinases (SFK) and STAT1, as the application o

122 n of these differences is that inhibition of Src family kinases (SFK) blocks TCR but not BCR signalin

123 Src family kinases (SFKs) are a group of nonreceptor tyr

124 Here we investigate how flaviviruses exploit Src family kinases (SFKs) for exit from infected cells.

125 The Src family kinases (SFKs) Src, Lyn, and Fyn are essentia

126 embrane protein that acts as a substrate for SRC family kinases (SFKs), is overexpressed in a subset

127 TrkA was transactivated by Src family kinases and extracellular signal-regulated ki

128 cence pathway and suggest that inhibition of SRC family kinases as personalized treatment in patients

129 ovide pharmacological evidence for a role of Src family kinases in CVP development.

130 ving cells, providing evidence for a role of Src family kinases in regulating growth factor induced A

131 entified activated ephrin (EPH) receptor and Src family kinases upon NF2 loss.

132 This response required the NMDA-R, LRP1, Src family kinases, and Trk receptors.

133 Finally, inhibition of Src family kinases, known to be involved in HB-EGF proce

134 In addition to abrogating myristoylation of Src family kinases, PCLX-001 also promotes their degrada

135 rosine residues that, when phosphorylated by Src family kinases, potentiate NMDAR activity.

136 could be attributed to reduced activation of Src family kinases.

137 his study, we investigated the activation of Src family of cytoplasmic tyrosine kinases (SFKs) and tw

138 Interactions of LCK proto-oncogene, SRC family tyrosine kinase (LCK), and the IL-2-inducible

139 naling pathway, including LCK proto-oncogene SRC family tyrosine kinase (LCK), LYN proto-oncogene SRC

140 ly tyrosine kinase (LCK), LYN proto-oncogene SRC family tyrosine kinase (LYN), zeta chain of T-cell r

141 The SRC family tyrosine kinase YES1 is upregulated in rhabdo

142 Signaling is proximally mediated by Src family tyrosine kinases, the most abundant being Lyn

143 SRC1, another highly conserved member of the SRC family, interacts with RORgammat to regulate Th17 di

144 SRC (proto-oncogene tyrosine-protein kinase Src) family kinases (SFKs), can be found in a significan

145 The corolla amplified active phosphorylated Src-family kinases (pSFK), LAT and PLC-gamma over T cell

146 ation, and Integrin beta1 phosphorylation by Src-family kinases.

147 ique and often contradictory roles played by Src-family-kinases (SFKs) in regulating cell physiology,

148 verexpression of tyrosine kinases, including SRC, FES, YES1, and BLK, induced MEK-independent ERK act

149 ibroblasts transformed by the proto-oncogene Src form individual invadopodia that can spontaneously s

150 covalent inhibitor 15a, which discriminates SRC from other covalent targets of SM1-71 including TAK1

151 any immune pathways and comprises two tandem Src homology (SH) 2 domains, an SH2-kinase linker, and a

152 previously unknown interactions of BCAP with Src homology 2 (SH2) and SH3 domain-containing adaptor p

153 The Src homology 2 (SH2) domain has a highly conserved archi

154 mic-resolution models, we develop fusions of Src homology 2 (SH2) domain or a phosphorylatable SH2-bi

155 short linear peptides, such as those of the Src homology 2 (SH2) domain with phosphotyrosine-contain

156 -chain-associated protein kinase 70 (Zap70), Src homology 2 (SH2) domain-containing leukocyte protein

157 Kinetics of binding were assessed in Src homology 2 domain (SH2) or phosphotyrosine-binding (

158 in that the YLK motif is contained within an SRC homology 2 domain and is directly phosphorylated by

159 Activation of the Src homology 2 domain-containing collagen-related (Shc)

160 Src homology 2 domain-containing phosphatase (SHP2) is a

161 Src homology 2 domain-containing phosphatase 2 (SHP2) is

162 Src Homology 2-containing Inositol Phosphatase-1 (SHIP-1

163 quence (PRS) in CD3e that binds to the first Src homology 3 (SH3) domain of Nck (Nck-SH3.1).

164 mily of cellular proteins and also binds the Src homology 3 (SH3) domain-containing proteins CD2AP an

165 Src homology 3 (SH3) domains bind proline-rich linear mo

166 namics for the binding of a fluorine-labeled Src homology 3 (SH3) protein domain to four proline-rich

167 amodule, denoted PSG, which consists of PDZ, Src homology 3 (SH3), and guanylate kinase-like domains.

168 ved C-terminal polyproline sequence with the Src homology 3 domain of SNX9.

169 inal ubiquitin-association domain, a central Src homology 3 domain, and a C-terminal histidine phosph

170 Arf GAP with Src homology 3 domain, ankyrin repeat, and pleckstrin ho

171 s of desmoplakin: two spectrin repeats and a Src homology 3 domain.

172 The disruption of the noncanonical Src homology 3 recognition motif by P366L reduces syndap

173 proline-rich region between their N-terminal Src homology and Bcr homology domains disrupts homodimer

174 Small Src homology domain 2 (SH2) and 3 (SH3) adapter proteins

175 signal-regulated kinase 1 and 2 (ERK1/2) and Src homology phosphatase 2 (SHP2) ensures selective inte

176 The Src homology phosphatase 2 (SHP2) is a cytoplasmic enzym

177 Here, we show that the Src homology phosphotyrosyl phosphatase 2 (Shp2) encoded

178 overexpressed on cancer cells, activates the Src homology region 2 (SH2) domain -phosphatases SHP-1 a

179 r through multiple weak interactions between Src homology three and proline-rich domains of synaptic

180 . revealed a new TGF-beta-dependent role for Src homology/collagen adaptor protein (SHCA) in the init

181 ubstrate 2 (Frs2) and Rous sarcoma oncogene (Src) Homology Phosphatase 2 (Shp2) to activate Mitogen-A

182 of HSF1 protein expression and show that the Src-homology 3 (SH3) domain of ABL2 directly interacts w

183 Mechanistically, this response involves src-homology phosphatase activation leading to Akt-media

184 western blotting revealed the activation of Src in ECs was significantly increased by 5% CS-induced

185 ated a central role for beta3 integrin and c-Src in msuPAR2 signaling and in human FSGS kidney biopsi

186 ted co-existence of the alpha1 subunit and c-Src in same protein complex, as well as a direct interac

187 To increase the efficacy of targeting Src in the clinic, we sought to define mechanisms of res

188 SRC, in turn, increases PLAT expression through NF-kB ac

189 We also show that SRC increases the activity of YAP and TAZ by repressing

190 In conclusion, Src inhibition causes phosphorylation of S269 independen

191 In contrast, SRC inhibition or knockdown repressed both YAP/TAZ activ

192 Silencing of c-SRC or treatment with the c-SRC inhibitor dasatinib together with FBXL7 depletion pr

193 However, development of a selective SRC inhibitor has been challenging, and FDA-approved SRC

194 wed obvious increase after pretreatment with Src inhibitor in target ECs.

195 ht to define mechanisms of resistance to the Src inhibitor, dasatinib, to identify key pathways to ta

196 bitor has been challenging, and FDA-approved SRC inhibitors, dasatinib and bosutinib, are multitarget

197 is residual phosphorylation was abolished by Src inhibitors, revealing an unexpected mechanism in whi

198 SRC is a major regulator of many signaling pathways and

199 ere, we demonstrate that the tyrosine kinase Src is activated under DNA damage stress and phosphoryla

200 se A (PKA) complex that activates C-terminal Src kinase (CSK) and thereby down-regulates kinases invo

201 pressing either LAIR-1 mutants or C-terminal Src kinase (CSK) mutants, and 3) T cells from mice that

202 C-terminal Src kinase (CSK), a negative regulator of TCR signaling,

203 raction of PTPN22 with the carboxyl-terminal Src kinase (CSK), an interaction that is impaired by the

204 Platelet SFKs are inhibited by C-terminal Src kinase (Csk), which phosphorylates a conserved tyros

205 alpha) is an important positive regulator of SRC kinase activation and a known promoter of cancer gro

206 nt prevented the effect of leptin, whereas a Src kinase activator peptide mimicked it.

207 rate with actin remodeling pathways, notably SRC kinase activity, to establish and maintain long-last

208 We also identified the SRC kinase contributing to ETV2-mediated activation of t

209 ting analysis demonstrated that depletion of Src kinase family members (c-Src, Yes, and Fyn) or cav-1

210 induces phosphorylation of kinases from the Src kinase family, a hallmark of integrin signaling acti

211 microtubule end-binding protein 3 (EB3) and SRC kinase in the neuronal and behavioral responses to v

212 Moreover, pretreatment of M with a specific Src kinase inhibitor, PP2 completely prevents NE-induced

213 We identified Lyn as the specific Src kinase isoform that is activated by MCP-1 and acts u

214 In this study, we found that VP reduces Src kinase phosphorylation: by suppressing Src using the

215 ts of the disordered N terminal (SH4UD) of c-Src kinase without reweighting or constraining the simul

216 mpetitive antagonists or blocking downstream Src kinase) also increased sEPSC frequency similar to th

217 onal experimentation leaving CSK (C-terminal Src kinase) as the strongest candidate for ibrutinib-ind

218 lly modulating kinase global conformation to Src kinase, providing insight into known regulatory mech

219 eotide polymorphism rs7804356 located in the Src kinase-associated phosphoprotein 2 (SKAP2) gene is a

220 port that leptin augments NMDAR function via Src kinase-mediated phosphorylation of the GluN2A subuni

221 ated by metabotropic NMDAR signaling through Src kinase.

222 degrees C) or upon hyperphosphorylation with Src kinase.

223 gnaling, and clarifies how compartmentalized Src-kinase activity may drive cell fate.

224 buckyballs as a novel class of non-receptor Src kinases inhibitors.

225 st CD36 or with a pharmacologic inhibitor of SRC kinases restored the antiaggregative phenotype in th

226 CD226, initiated phosphorylation of Y319 by Src kinases, thereby enabling ubiquitination of CD226 by

227 Tyr(198)-specific antibody, SFK inhibitors, SRC knockdown, temperature-dependent SRC cells, and kina

228 -catenin and enhances its phosphorylation by Src, leading to beta-catenin activation and disseminatin

229 The Src family kinases (SFKs) Src, Lyn, and Fyn are essential for platelet activation

230 orylation of hepatic FXR by FGF15/19-induced Src maintains cholesterol homeostasis and protects again

231 f CDCP1 and the subsequent activation of the SRC/MAPK pathway.

232 terminal conformation of Kv1.5 that relieves Src-mediated tonic channel inhibition and results in an

233 We specifically detected SRC-mediated Tyr(198) phosphorylation at the plasma memb

234 on of Src or overexpression of a kinase-dead Src mutant prevented the effect of leptin, whereas a Src

235 de 3, R0 resection, BRAF V600E mutation, and SRC mutation as independent prognostic factors for OS (P

236 d SRC mutations were mutually exclusive, and SRC mutation was significantly associated with left-side

237 BRAF V600E and SRC mutations were mutually exclusive, and SRC mutation

238 0 resection, yet none harbored BRAF V600E or SRC mutations.

239 LightR-Src off-kinetics can be tuned by modulating the LightR p

240 nd demonstrate that KRAS phosphorylation via Src on Tyr32 and Tyr64 alters the conformation of switch

241 Hyperactive c-Src, on the other hand, reciprocally inhibits the ubiqui

242 y reduced by chemical inhibitors of MET or c-Src or by siRNA-mediated knockdown of MET.

243 ms, such as the non-receptor tyrosine kinase Src or N-methyl-D-aspartate receptors.

244 Pharmacological inhibition of Src or overexpression of a kinase-dead Src mutant preven

245 Silencing of c-SRC or treatment with the c-SRC inhibitor dasatinib toge

246 We showed that MCP-1 induces Src phosphorylation in a similar time frame and that the

247 mice manifested podocyte injury, including c-Src phosphorylation, proteinuria, and focal segmental gl

248 vation of ROS by hydrogen peroxide increased Src phosphorylation, while ROS reduction by N-acetyl cys

249 elial nitric oxide synthase (eNOS)-dependent Src, PI3K, and MAPK signaling.

250 rin activation, and disrupted downstream FAK/Src/PI3K(p55)/Akt signaling.

251 Inhibitors of YAP1 and SRC prevented organoid growth induced by TGR5 activation

252 The kinase Src promotes osteoclast activity and is activated in ost

253 lar reactive oxygen species (ROS) levels and Src protein phosphorylation in CD34(+) cells.

254 ling induces the phosphorylation of Creb and Src proteins in parallel to Gli induction, identifying a

255 y 2 domain and is directly phosphorylated by SRC proto-oncogene, nonreceptor tyrosine kinase (SRC) at

256 tioning of late endosomes allows delivery of SRC proto-oncogene, nonreceptor tyrosine kinase (SRC) to

257 lecular alterations of YES1, a member of the SRC (proto-oncogene tyrosine-protein kinase Src) family

258 ether, our results suggest that the PKCalpha-Src-PTEN pathway regulated by PHF8/c-Jun is a potential

259 The SRC received details and images (color fundus photograph

260 Furthermore, pharmacological inhibition of c-Src restores APC(Cdh1) tumor suppressor function to repr

261 Similarly, inhibiting FAK/Src results in chemosensitization.

262 The SRC reviewed data from cases of investigator-reported IO

263 We show that Src's cellular interactions are highly influenced by the

264 tatus of the cell also has a large effect on Src's interactome.

265 part of a proximity ligation assay to study Src's localization and interactions in situ.

266 previously undiscovered interaction between Src's SH4 and catalytic domains.

267 fted with human hematopoietic stem cells (hu-SRC-SCID) are susceptible to lethal S. Typhi infection.

268 Detailed analysis of c-Src SH2 domain binding to a panel of phosphorylation-def

269 /K-ATPase and promotes its ion transport and Src signaling activity in a ligand-independent manner.

270 Using this system, we identified Src signaling as an important driver of invasion and met

271 mpound 15a exhibited sustained inhibition of SRC signaling both in vitro and in vivo.

272 STAT6, PI3K-Akt-NF-kappaB, and Src signaling mediated the cellular and molecular events

273 g the nuclear import of GAPDH by suppressing Src signaling or through a GAPDH Tyr41 mutation impairs

274 CB HPSCs, at least in part, via ROS-mediated Src signaling pathway.

275 ors of cell cycle progression, YAP, AXL, and SRC signaling, and chemotherapeutic agents.

276 1510 under conditions with enhanced MET or c-Src signaling, including in human lung cancer cell lines

277 in murine ALL was associated with changes in Src signaling, including the upregulation of phosphoryla

278 1 expression, resulting in inhibition of FAK/Src signaling, induction of apoptosis and re-sensitizati

279 ROCK-mediated myosin II phosphorylation, and SRC signaling, which led to histotype-dependent loss of

280 a or IL-1beta stimulation compared to FAK or Src specific inhibitors (PF-228 or Dasatinib), which inh

281 f AT(2)R-cGMP downstream signaling molecules Src (Src family kinase), ERK (extracellular signal-relat

282 SRC stimulation with MCB-613 (and derivatives) is a pote

283 An independent Safety Review Committee (SRC), supported by Novartis Pharma AG, analyzed investig

284 stimulating mitochondrial ATP production, c-Src suppresses energy stress, permitting sustained activ

285 ors that promote the activation of ERK1/2 or Src, the kinases that lead to cell growth and proliferat

286 pathway wherein leptin modulates NMDARs via Src to regulate beta-cell excitability and suggests NMDA

287 proto-oncogene, nonreceptor tyrosine kinase (SRC) to the plasma membrane and promotes activation of a

288 complex formation is dependent on Erk1/2 and Src, two kinases known to interact with and be activated

289 rylation, without activating Pyk2-Tyr-402 or Src-Tyr-419.

290 ch contains the binding motif for endogenous Src tyrosine kinase that constitutively inhibits I(Kv1.5

291 al testing of the engineered proteins, using Src tyrosine kinase, GEF Vav2, and Rho GTPase Rac1 as ex

292 Cortactin is a Src tyrosine phosphorylation substrate that regulates mu

293 s Src kinase phosphorylation: by suppressing Src using the inhibitor dasatinib and siRNA, we could in

294 n), which increases VEGF receptor 2 (VEGFR2)-Src-VE-cadherin complex formation, resulting in increase

295 erin and reduced the formation of the VEGFR2-Src-VE-cadherin complex, which led to reduced cell surfa

296 Discrimination of the SRC was lowest for reoperation (C-index, 0.533) and high

297 ee-dimensional culture conditions, activated Src, was reversible, and was stabilized by bortezomib, a

298 omplexes containing the alpha1 subunit and c-Src, which might have different signaling functions.

299 sis, CD151 on EMPs was predicted to activate Src, which was further confirmed by both FRET and wester

300 of cav-1 did not affect the interaction of c-Src with the alpha1 subunit.

301 Our results identify the Src/YAP axis as a key player in promoting the proliferat

302 at depletion of Src kinase family members (c-Src, Yes, and Fyn) or cav-1 clearly reduced the interact