ライフサイエンスコーパス: SFK

1 SFK blockade alone had modest effects on proliferation,

2 SFK family member YES1 was amplified in osimertinib-resi

3 SFK inhibitors failed to potentiate platelet responses i

4 SFKs are inactivated by phosphorylation of their C-termi

5 SFKs did not appear to phosphorylate the PMCA directly b

6 SFKs have been shown to phosphorylate EGFR on tyrosines

7 These data indicate that Ca(2+)/SFKs/PI3K and PKC represent two alternative signaling pa

8 S increased binding of activated Tyr(P)(416)-SFK to GST-TRAF6, and preincubation of HMVEC-Ls with SFK

9 A SFK member, Fynb, was responsible for fin regeneration.

10 r agonist that activates platelets through a SFK-dependent signaling pathway.

11 and signaling and to interfere with aberrant SFK signaling networks in cancer cells.

12 del, we find that wounding rapidly activated SFK and calcium signaling in epithelia.

13 f in TRAF6 interacts directly with activated SFKs to couple LPS engagement of TLR4 to SFK activation

14 The hyaluronan receptor CD44 activates SFK-FAK signaling cascades and is expressed in sensory n

15 s induces a migratory response by activating SFKs and FAK, leading to foot process effacement and pro

16 ed increased glomerular expression of active SFKs and pFAK(Y397), both of which were inhibited by pod

17 ed increased glomerular expression of active SFKs and pFAK(Y397).

18 anoxic depolarization (AD) without affecting SFK activation.

19 nhibitors (dasatinib and BMS-754807, against SFK and IGF-1R/Insulin Receptor(IR), respectively).

20 ial component for the down-regulation of all SFKs.

21 odel in vivo upon treatment with AZD0530, an SFK inhibitor.

22 vation facilitates metastasis by inducing an SFK-dependent expansion of a prometastatic, CD24(+) tumo

23 ts requires the activation of the Erk1/2 and SFK pathways.

24 er cell lines decreased both cell growth and SFK activation.

25 Dual IGF-1R/IR and SFK inhibition may be a rational therapeutic approach in

26 g small-molecule inhibition of SYK, LCK, and SFK showed synergistic interactions and preclinical effi

27 e by combined treatment with osimertinib and SFK inhibitors.

28 oformansindependently activates both Rac and SFK pathways in NK cells, and unlike in tumor killing,Cr

29 recruitment of Src family kinases (SFK) and SFK-dependent phosphorylation of Panx1.

30 activation of SRC family kinases (SFKs) and SFK inhibition blocked cytokine secretion.

31 Csk and SFKs share a modular design with the kinase domain downs

32 the recently appreciated ability of ROS and SFKs to indirectly and chronically activate monomeric PD

33 e, we define an opposing function of another SFK, Lyn, which in contrast to other SFKs, strengthens e

34 n of SFK signaling with dasatinib or another SFK inhibitor, sarcatinib, suppressed RMS cell growth in

35 tify patients who could benefit from an anti-SFK-targeted therapy.

36 expressed monobodies revealed that they bind SFKs but no other SH2-containing proteins.

37 Inhibition of FAK in the lipid rafts blocked SFK response to fluid flow, while inhibition of SFK in t

38 gest that the concomitant inhibition of both SFK/FAK and EGFR may be a promising therapeutic strategy

39 ing E4orf4 action, in a manner controlled by SFK and Rab11a.

40 tive G(12/13) stimulation was potentiated by SFK inhibitors, which was abolished by intracellular cal

41 ons of SFLLRN or YFLLRNP were potentiated by SFK inhibitors.

42 as in the early phase of the response and by SFKs in the late phase.

43 asmic tyrosine Y658 can be phosphorylated by SFKs [7], which is maximally induced by low shear stress

44 is rarely mutated in human prostate cancer, SFK activity is increased in the majority of human prost

45 human lung tumors may explain how the CDCP1/SFK complex regulates motility and adhesion.

46 Combined SFK/FAK inhibition exhibited the most potent effects on

47 showed beta cells to express five different SFK proteins, only two of these, YES and Fyn kinases, we

48 45 and CD148 preferentially target different SFK members (Hck and Fgr versus Lyn, respectively) to po

49 They are excellent tools for dissecting SFK functions in normal development and signaling and to

50 3 cells were more potently inhibited by dual SFK and IGF-1R/IR blockade compared to either pathway al

51 d receptor 4 agonist peptide AYPGKF elicited SFK phosphorylation in P2Y(12) deficient platelets but s

52 GK1 was possibly due to enhancing endogenous SFK effect on WNK4 by decreasing the WNK4-PTP-1D associa

53 g axis is homologous to the well-established SFK-ITAM-Syk-signaling pathway used in vertebrate adapti

54 ivation in LSC and that LIC with exacerbated SFK activation was uniquely found within the JAM-C-expre

55 In cells expressing SFKs, IGF-1-stimulated phosphorylation of PTPalpha is me

56 ated a correlation between CDCP1 expression, SFK and protein kinase C (PKC) activity.

57 Negative feedback arises from SFK-mediated cis phosphorylation of the transmembrane ad

58 Positive feedback arises from SFK-mediated trans phosphorylation of BCR and receptor-b

59 icating that an unknown kinase distinct from SFKs can target PTPalpha.

60 Further, SFK mRNA expression was upregulated in primary HER2+ tum

61 These findings suggest that hippocampal SFKs contribute to the long-term stability of cocaine-re

62 ls and metastatic lesion formation; however, SFK inhibition did not kill dormant cells.

63 The immediate SFK and calcium signaling in epithelia was important for

64 ermine the specific role of Cav-1 and Cbp in SFK inhibition, we measured c-Src activity in the absenc

65 ts extracellular domain, promoted changes in SFK and FAK tyrosine phosphorylation, as well as in PKC(

66 thermore, expressing the SFKs Src and Fyn in SFK-deficient cells switches IGF-1-induced PTPalpha phos

67 g of these receptors triggers an increase in SFK activity and downstream tyrosine phosphorylation of

68 ition revealed that a very small increase in SFK activity was sufficient to potentiate T cell respons

69 o investigate the roles of these moieties in SFK membrane association, we used fluorescence recovery

70 Here we show that increased SFK and CDCP1 tyrosine phosphorylation is, surprisingly,

71 l-molecule inhibitor of Csk, which increased SFK activation and produced robust membrane-proximal sig

72 Surprisingly, receptor-independent SFK activation led to a downstream signaling blockade as

73 dentified increased expression of individual SFK members during prostate cancer progression, raising

74 The calcium ionophore A23187 induced SFK phosphorylation in both wild-type and G(q) deficient

75 flow selectively decreased cytokine-induced SFK/FAK activation.

76 AF6 decoy peptide decreased both LPS-induced SFK activation and barrier disruption.

77 -negative TIRAP/Mal each blocked LPS-induced SFK activation and increases in transendothelial [(14)C]

78 TRAF6 decoy peptide blocked both LPS-induced SFK ubiquitination and TRAF6 phosphorylation.

79 have previously shown that thrombin-induced SFK phosphorylation was inhibited by the calcium chelato

80 reaking pan-RAF inhibitors that also inhibit SFKs could provide first-line treatment for BRAF and NRA

81 ors (CCT196969, CCT241161) that also inhibit SFKs.

82 Interestingly, SFKs concomitantly activate inhibitory pathways that lim

83 rated that JAM-C controls Src family kinase (SFK) activation in LSC and that LIC with exacerbated SFK

84 acellular pathway through Src family kinase (SFK) activation.

85 ent in vivo evidence that Src family kinase (SFK) activity is critical for PCP regulation in the audi

86 tion site tyrosine in the SRC family kinase (SFK) FYN as well as Tyr142 in beta-catenin.

87 y to evaluate the role of Src family kinase (SFK) in regulating this dormant-to-proliferative switch.

88 y, inhibitors such as the SRC family kinase (SFK) inhibitor dasatinib reduced pPLCgamma2 and inhibite

89 at the pyrrolo-pyrimidine Src family kinase (SFK) inhibitor PP2 effectively promotes the endocrine sp

90 tely abolished by the pan-Src family kinase (SFK) inhibitor, PP2, or when Syk is inhibited.

91 he presence of PP2, a pan-src family kinase (SFK) inhibitor, suggesting that c-Cbl is phosphorylated

92 gonist was inhibited by a Src family kinase (SFK) inhibitor.

93 r enhanced sensitivity to SRC-family kinase (SFK) inhibitors in other malignancies.

94 CD8 associates with the Src-family kinase (SFK) Lck, which, in turn, initiates the rapid tyrosine p

95 Here we identify the Src family kinase (SFK) Lyn as a redox sensor that mediates initial neutrop

96 iously, we found that the Src family kinase (SFK) Lyn functions as a redox sensor in leukocytes that

97 ed by the redox-sensitive Src family kinase (SFK) Lyn within the responding blood cells [3].

98 ibitory SH2 domain of the SRC family kinase (SFK) LYN.

99 tributable to loss of the Src family kinase (SFK) Lyn.

100 Here we report that the Src-family kinase (SFK) regulator CD148 has a unique and critical role in t

101 s through redox-regulated Src family kinase (SFK) signaling in neutrophils.

102 ng activation mechanisms, Src family kinase (SFK) signaling is sufficient to transmit the CSF-1 linea

103 tor tyrosine kinase (RTK)/SRC-family kinase (SFK) signaling or mutant NRAS, which drive paradoxical r

104 aling was associated with SRC family kinase (SFK) signaling, specifically with YES kinase.

105 ed phosphorylation of the SRC family kinase (SFK) YES, increased expression of WNT target genes, and

106 EAR1 phosphorylation in a src family kinase (SFK)-dependent manner.

107 dition, contributed to by Src family kinase (SFK)-dependent pathways.

108 tes tumorigenesis through Src family kinase (SFK)-dependent phosphorylation of Dock180, a guanine nuc

109 ion and signaling via the Src family kinase (SFK)-Syk-PLCgamma2 pathway, and fibrinogen due to reduce

110 ding to the activation of Src Family Kinase (SFK)/hemopoietic cell kinase (Hck) and suppression of ap

111 the mechanism of Src family tyrosine kinase (SFK) inhibition by Csk.

112 d by the Src-family protein tyrosine kinase (SFK).

113 Here we report that Src family kinases (SFK) and focal adhesion kinase (FAK) sustain AKT and MAP

114 The Src family kinases (SFK) and insulin-like growth factor-1 (IGF-1) signaling

115 eceptors, recruitment of Src family kinases (SFK) and SFK-dependent phosphorylation of Panx1.

116 dhesion kinase (FAK) and Src family kinases (SFK) are known to play critical roles in mechanotransduc

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

118 Src family kinases (SFK) integrate signal transduction for multiple receptor

119 4) subverts signaling by Src family kinases (SFK) to perturb cellular morphology, membrane traffic, a

120 ry negative regulator of Src-family kinases (SFK), plays a crucial role in controlling basal and indu

121 on its interactions with Src family kinases (SFK).

122 rough phosphorylation by Src family kinases (SFK).

123 The Src family of protein kinases (SFK) plays key roles in regulating fundamental cellular

124 sis that the Src family of tyrosine kinases (SFK) in the dorsal hippocampus (DH) critically controls

125 oxygen species (ROS) and Src family kinases (SFKs) act downstream of PDGFRs to enhance PDGF-mediated

126 Src family kinases (SFKs) activation is required for integrin and chemokine

127 ng the binding sites for Src family kinases (SFKs) and phosphatidylinositol-3-kinase (PI3K) suggest a

128 eased phosphorylation of Src family kinases (SFKs) and putative Src substrates in several resistant c

129 led to the activation of SRC family kinases (SFKs) and SFK inhibition blocked cytokine secretion.

130 NX1 is phosphorylated by Src family kinases (SFKs) and that this occurs on multiple tyrosine residues

131 The SRC family kinases (SFKs) and the receptor tyrosine kinase c-Kit are activat

132 Multiple SRC-family kinases (SFKs) are commonly activated in carcinoma and appear to

133 Src family kinases (SFKs) are involved in both NMDA-mediated activation of T

134 Src family kinases (SFKs) are pleiotropic activators that are responsible fo

135 wth factor receptors and SRC family kinases (SFKs) but does not affect the ability of PTEN to antagon

136 The Src family kinases (SFKs) c-Src and Yes mediate vascular leakage in response

137 EGF receptor (EGFR) and Src family kinases (SFKs) contribute to an aggressive phenotype.

138 in positively regulating Src family kinases (SFKs) in immunoreceptor signaling pathways in B cells an

139 de 3-kinases (PI3Ks) and Src-family kinases (SFKs) in these responses using human neutrophils treated

140 The Src family kinases (SFKs) Lck, Hck, and Fgr directly phosphorylate TBK1 at T

141 of c-Cbl, Vav1, and the Src-family kinases (SFKs) Lyn and Fgr.

142 Src family kinases (SFKs) play a central role in mediating the rapid respons

143 The Src family kinases (SFKs) play essential roles in collagen- and von Willebra

144 tion indicated that, the Src family kinases (SFKs) were found to phosphorylate CDCP1 at Tyr707 and Ty

145 The interactions of Src family kinases (SFKs) with the plasma membrane are crucial for their act

146 process was mediated by Src family kinases (SFKs), and nuclear EGFR had a role in resistance to cetu

147 migration, activation of Src-family kinases (SFKs), and phosphorylation of focal adhesion kinase at Y

148 exogenous NMDA activated Src family kinases (SFKs), as measured by increased phosphorylation of SFKs

149 d the involvement of the Src family kinases (SFKs), based upon the ability of SFK inhibitors to block

150 l inhibitory tyrosine of SRC family kinases (SFKs), implicating CD148 as a critical positive regulato

151 n occur in cells lacking Src family kinases (SFKs), indicating that an unknown kinase distinct from S

152 rosine kinases named the Src family kinases (SFKs), is overexpressed, associated with an aberrant mul

153 d-mediated activation of Src family kinases (SFKs), SFKs engage the receptor tyrosine kinase Axl via

154 nals in conjunction with Src family kinases (SFKs), spleen tyrosine kinase (Syk), and phospholipase g

155 duces forces to activate src family kinases (SFKs), which phosphorylate and transactivate VEGFRs [3-5

156 d with the inhibition of Src family kinases (SFKs), which was exacerbated by PTP1B overexpression and

157 or (TCR) is initiated by Src-family kinases (SFKs).

158 pression and activity of Src family kinases (SFKs).

159 , Syk acts downstream of Src family kinases (SFKs).

160 recognition of the eight Src family kinases (SFKs).

161 yrosines in the ITAMs by Src family kinases (SFKs).

162 hrough the activation of Src-family kinases (SFKs).

163 ctivate VEGFR2-recruited SRC family kinases (SFKs).

164 which in turn activates Src-family kinases (SFKs).

165 The Src family of tyrosine kinases (SFKs) regulate numerous aspects of cell growth and diffe

166 eceptors engage Src-family tyrosine kinases (SFKs) to initiate phagocytosis and macrophage activation

167 ich are Src family protein tyrosine kinases (SFKs).

168 ember of the Src family of tyrosine kinases (SFKs).

169 These findings link SFK and Shp2 signaling pathways to the regulation of RUN

170 We show that the Lyn SFK and the p85alpha subunit of class I(A) PI3K play opp

171 membrane-associated Csk adaptor to maintain SFK inhibition.

172 ecruitment to the plasma membrane to mediate SFK inhibition.

173 ) deficient platelets but stimulated minimal SFK phosphorylation in platelets lacking G(q).

174 hosphorylation of Syk, Akt, and ERK, but not SFK (Src family kinase), was significantly reduced in Rh

175 ly kinases (SFKs), based upon the ability of SFK inhibitors to block glucose-stimulated Cdc42 and PAK

176 AP colocalize with and mediate activation of SFK.

177 ose gels to detect subcellular activities of SFK and FAK in three-dimensional (3D) settings.

178 der rigidity-dependent tension downstream of SFK activity.

179 Inhibition of SFK activity not only alters TLR-ligand localization and

180 Loss of Sphk2 and inhibition of SFK activity resulted in defective intravascular proplat

181 NK4-PTP-1D association because inhibition of SFK enabled SGK1 to reverse WNK4(Y1143F)-induced inhibit

182 response to fluid flow, while inhibition of SFK in the non-rafts blocked FAK activation by the cytok

183 We found that pharmacological inhibition of SFK signaling or Src knockdown results in the nuclear lo

184 Inhibition of SFK signaling with dasatinib or another SFK inhibitor, s

185 chanistically, we propose that inhibition of SFK/FAK signaling can promote endocrine specification by

186 Moreover, we show that inhibition of SFK/FAK signaling suppresses cell growth, increases the

187 The use of pharmacological inhibitors of SFK/Hck in combination with taxanes in a temporally cons

188 d new avenues of research into mechanisms of SFK regulation.

189 ng CD148 as a critical positive regulator of SFK signaling in ASM.

190 sine kinase that is activated as a result of SFK-mediated phosphorylation of BCR.

191 In line with the critical roles of SFK SH2 domains in kinase autoinhibition and T-cell rece

192 alterations in the phosphorylation state of SFK targets, including GluN2A and GluN2B N-methyl-D-aspa

193 ent of the TCR, induced potent activation of SFKs and proximal TCR signaling up to phospholipase C-ga

194 Wound-induced activation of SFKs in epithelia was dependent on injury-generated H(2)

195 Activation of SFKs requires depletion of tyrosine phosphatases from th

196 a pathway, possibly regulating activation of SFKs, which are crucial for initiation of CLEC-2 signali

197 tor (uPAR) functions as a major activator of SFKs, controlling phosphorylation of downstream targets,

198 ells, there was pronounced colocalization of SFKs and Csk at the site of TCR triggering, whereas in A

199 ected by PP2, suggesting the contribution of SFKs downstream of G(12/13), but not G(q)/G(i), as a neg

200 g that c-Cbl is phosphorylated downstream of SFKs.

201 correlated inversely with the expression of SFKs.

202 The pleiotropic functions of SFKs in cancer make them promising targets for intervent

203 of the distinct and overlapping functions of SFKs in platelets, and new avenues of research into mech

204 In addition, signaling independent of SFKs and initiated by Syk has been proposed.

205 Inhibition of SFKs also disrupted H(2)O(2)-mediated chemotaxis of prim

206 Pharmacological inhibition of SFKs ameliorated the protective effect of TCPTP deficien

207 In contrast, inhibition of SFKs by a selective inhibitor in human, or SFK deficienc

208 The evidence that inhibition of SFKs in human, or SFK deficiency in murine, neutrophils

209 Inhibition of SFKs using PP2 blocked BDNF-mediated phosphorylation of

210 er in their sensitivity to the inhibition of SFKs.

211 Small-molecule inhibitors of SFKs, which are conventional anti-tumor therapeutics, en

212 horylation and the functional integration of SFKs into innate antiviral immunity.

213 as measured by increased phosphorylation of SFKs at Y416.

214 e important for the functional regulation of SFKs in several tumor types.

215 how the kinase Csk, a negative regulator of SFKs, controls the basal state and the initiation of TCR

216 Dasatinib, highlighting the central role of SFKs in uPAR-promoted cell migration.

217 However, the roles of SFKs in G protein-coupled receptor-mediated platelet act

218 We conclude that WNK4 is a substrate of SFKs and that the association of c-Src and PTP-1D with W

219 egulates chemoattractant signaling acting on SFK activity.

220 SFK-PDGFRalpha complex that was dependent on SFK-mediated phosphorylation of PDGFRalpha and activated

221 howing that miR-205 inhibits proto-oncogenic SFKs, indicating a therapeutic potential of miR-205 in t

222 f SFKs by a selective inhibitor in human, or SFK deficiency in murine, neutrophils resulted in the in

223 vidence that inhibition of SFKs in human, or SFK deficiency in murine, neutrophils results in suppres

224 another SFK, Lyn, which in contrast to other SFKs, strengthens endothelial junctions and thereby rest

225 tivation was consistently abolished by a pan-SFK inhibitor but not by Syk or PI3K inhibitors.

226 emostatic consequences of targeting platelet SFKs.

227 he auditory sensory epithelium and that PTK7-SFK signaling regulates tyrosine phosphorylation of junc

228 on of NMDARs during anoxia/ischemia recruits SFKs to open Panx1, leading to sustained neuronal depola

229 d late regeneration and suggests that redox, SFK, and calcium signaling are immediate "wound signals"

230 Redox-SFK signaling in epithelium is also necessary for wound

231 We found that redox-SFK signaling through p22phox and Yes-related kinase is

232 Thus, redox-SFK signaling in adjacent tissues is essential for coord

233 nding to the same proline-rich motif reduced SFK binding to WT GST-TRAF6 compared with the Pro --> Al

234 amma2 pathway, and fibrinogen due to reduced SFK activity.

235 preincubation of platelets with a selective SFK inhibitor, PP2.

236 ndependent cell growth and activates several SFK members.

237 ted activation of Src family kinases (SFKs), SFKs engage the receptor tyrosine kinase Axl via its jux

238 t development of inhibitors against specific SFK members could provide unique targeted therapeutic st

239 ouse trachea and human bronchi with specific SFK inhibitors.

240 e possibility that small molecules targeting SFKs could modulate pDC responses in human diseases.

241 These data indicate that SFK activity is necessary for BDNF-mediated suppression

242 Together, these results indicate that SFK phosphorylation in response to thrombin receptor sti

243 We observed that SFK and FAK in the lipid rafts and nonrafts are differen

244 dies performed in human islets revealed that SFK phosphorylation was induced only by glucose and with

245 Our results show that SFK SH2 domains can be targeted with unprecedented poten

246 These findings suggest that SFK and FAK exert distinctive molecular hierarchy depend

247 n an Abl-independent manner, suggesting that SFK activity dominantly regulates IGF-1/IGF-1 receptor s

248 We conclude that SFKs, especially Fyn, activated downstream of G(12/13) n

249 rowing body of evidence has established that SFKs also contribute to Gq- and Gi-coupled receptor sign

250 PGKF-induced PKC activation, indicating that SFKs downstream of G(12/13) regulate platelet responses

251 in G(q)-deficient platelets, indicating that SFKs negatively regulate platelet responses through modu

252 d genetic inhibitor treatments revealed that SFKs are required for signal initiation and Syk activati

253 of the response to fMLF or TNF suggests that SFKs are indispensable for Vav phosphorylation.

254 The SFK inhibitor dasatinib enhanced the antitumor effect of

255 The SFK inhibitor PP2 or a selective Syk inhibitor (BAY 61-3

256 The SFK inhibitor PP2 prevented Src activation and Panx1 ope

257 a signaling cascade fully interrupted by the SFK inhibitor PP1 and the PI3K inhibitor LY294002.

258 tically reduced the apoptosis induced by the SFK inhibitors PP2 and dasatinib.

259 ctively perturb the interactions of even the SFK SH2 family against the rest of the SH2 domains.

260 of bilateral intra-DH microinfusions of the SFK inhibitor, PP2 (62.5 ng per 0.5 mul per hemisphere),

261 We hypothesized that infusion of the SFK inhibitor, PP2, into the PrL cortex prior to a BDNF

262 ls to induce BCR signaling downstream of the SFK Lyn.

263 ade associated with rapid degradation of the SFK LynA.

264 ein expression indicated upregulation of the SFK members Yes (v-Yes-1 yamaguchi sarcoma viral oncogen

265 proteins, termed monobodies, for six of the SFK SH2 domains with nanomolar affinity.

266 These results suggest that targeting the SFK-p-Dock180(Y722)-Rac1 signaling pathway may offer a n

267 veloped interfering peptide that targets the SFK consensus-like sequence of Panx1 (Y308) attenuated t

268 eviously in WT HL60 cells, we found that the SFK inhibitor PP2 significantly increases G1/G0 cell cyc

269 ed DDR2 mutations were more sensitive to the SFK inhibitor dasatinib than those with WT DDR2.

270 signaling molecules that couple TLR4 to the SFK-driven barrier disruption are unknown.

271 r 6), leading to integrin activation via the SFK (Src family kinase)-Syk (spleen tyrosine kinase)-PLC

272 Treatment with the SFK and c-KIT inhibitor dasatinib selectively inhibits h

273 The SFKs, Src, Fyn, and Lyn, induce phosphorylation of Dock1

274 Our studies identify CD148 and the SFKs it regulates in ASM as potential targets for the tr

275 Furthermore, expressing the SFKs Src and Fyn in SFK-deficient cells switches IGF-1-i

276 nstruct or shRNA directed to message for the SFKs Lck or Fyn, but not Src.

277 nced CD8(+) T cells in colocalization of the SFKs and their negative regulator, C-terminal Src kinase

278 We show here that the SFKs LYN, HCK, or FGR are overexpressed and activated in

279 ion of Dock180(Y722) and inhibition of these SFKs by pharmacological inhibitors or shRNA depletion ma

280 ectively regulated by CD148 and loss of this SFK resulted in opposite signaling phenotypes in B1 and

281 est that activation of alpha7 by ZP leads to SFK-dependent EGFR activation, Ca(2+) influx, and the ac

282 orylation and NE assembly are susceptible to SFK inhibition.

283 ted SFKs to couple LPS engagement of TLR4 to SFK activation and loss of barrier integrity in HMVEC-Ls

284 he mechanisms involved and highlight a tonic SFK-mediated signalling that precedes pathogen encounter

285 During the TRAF6-SFK association, TRAF6 catalyzed Lys(63)-linked ubiquiti

286 To better understand SFK-mediated nuclear translocation of EGFR, we investiga

287 or no PDGFs, promoted formation of a unique SFK-PDGFRalpha complex that was dependent on SFK-mediate

288 This phosphorylation is dependent upon SFK activity; thus Y783 phosphorylation and NE assembly

289 the trafficking of Drp1 to mitochondria upon SFK activation and unravel a novel functional interplay

290 dasatinib, whereas Akt2 phosphorylation was SFK independent and only inhibited by BMS-754807.

291 ked ubiquitination of c-Src and Fyn, whereas SFK activation increased tyrosine phosphorylation of TRA

292 Whereas SFKs are membrane-associated, Csk is a cytoplasmic prote

293 ivation and the molecular mechanisms whereby SFKs are activated by G protein-coupled receptor stimula

294 progression, raising the question of whether SFKs display functional equivalence.

295 translocation of EGFR, we investigated which SFK member(s) controlled this process as well as the EGF

296 ols thrombopoiesis, which is associated with SFK expression and activity in MKs.

297 When used in combination with SFK inhibitors, the action of MP07-66 is synergistically

298 Rac cytotoxicity pathway in conjunction with SFK, to killC. neoformans.

299 ST-TRAF6, and preincubation of HMVEC-Ls with SFK-selective tyrosine kinase inhibitors, PP2 and SU6656

300 n genetic ablation as well as treatment with SFK inhibitors ablate pDC (but not conventional DC) resp