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 SFKs are key kinases phosphorylating immunoreceptor tyro

4 SFKs are often found attached to membranes, but little i

5 SFKs have been shown to phosphorylate EGFR on tyrosines

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

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

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

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

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

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

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

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

14 Biphosphorylated active SFK was observed more frequently in forkhead box protein

15 Interestingly, active SFK was found to be biphosphorylated (SFK_pY416(+)/pY527

16 M-) cells exhibited higher amounts of active SFKs and increased growth rate.

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

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

19 anoxic depolarization (AD) without affecting SFK activation.

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

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

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

23 resented a high sensitivity to dasatinib, an SFK inhibitor, pointing out YES1 status as a stratificat

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

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

26 mast-cell LynA is not rapidly degraded, and SFK-mediated signaling is amplified relative to macropha

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

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

29 we showed activation of EPH RTKs, c-KIT, and SFK members independent of mTORC1/2 activation.

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

31 e by combined treatment with osimertinib and SFK inhibitors.

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

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

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

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

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

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

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

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

40 Using a PANX1 Tyr(198)-specific antibody, SFK inhibitors, SRC knockdown, temperature-dependent SRC

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

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

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

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

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

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

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

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

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

50 ion in DCs by IL-6, dependent on concomitant SFK and ERK signaling.

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

52 The results demonstrate that PAG1 directs SFK intracellular localization to control activity and t

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

54 3 cells were more potently inhibited by dual SFK and IGF-1R/IR blockade compared to either pathway al

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

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

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

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

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

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

61 also reveal a previously unreported role for SFK activity in the regulation of chromatin structure at

62 d with ZAP-70, SYK lowered the threshold for SFK activity necessary to initiate antigen receptor sign

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

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

65 Furthermore, the HCK/SFK activity was linked to recruitment of the monocytic

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

67 s of F29 specificity for Fyn over homologous SFKs.

68 previous work and provided insight into how SFK Unique domains act to differentiate the family membe

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

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

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

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

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

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

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

76 tended to be SFK_pY527(+) (classic inactive SFK), and FOXA1(-) TNBC tended to be SFK_pY527(-) (SFK p

77 the MK lineage in mice results in increased SFK activity, but paradoxically hypoactive platelets res

78 y immunohistochemistry, indicating increased SFK activity in situ.

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

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

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

82 physiology, activity patterns of individual SFKs have remained elusive.

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

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

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

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

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

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

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

90 Inhibiting SFK signaling blocks both the expulsion of apoptotic cel

91 Interestingly, SFKs concomitantly activate inhibitory pathways that lim

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

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

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

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

96 lcium but is sensitive to SRC family kinase (SFK) inhibition, suggestive of channel regulation by tyr

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

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

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

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

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

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

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

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

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

106 thesis that regulation of SRC family kinase (SFK) signaling by the scaffold protein, PAG1, influences

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

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

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

110 flects a mechanosensitive Src family kinase (SFK) signaling pathway that is activated in neighbor cel

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

112 y directly activating the Src family kinase (SFK) Src42A,(3) which in turn phosphorylates the damage

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

114 comitant activation of an Src family kinase (SFK), hematopoietic cell kinase (HCK), specifically in D

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

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

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

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

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

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

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

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

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

124 2 mediated activation of Src family kinases (SFK) and STAT1, as the application of SFK inhibitor Dasa

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

126 es is that inhibition of Src family kinases (SFK) blocks TCR but not BCR signaling.

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

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

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

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

131 rough phosphorylation by Src family kinases (SFK).

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

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

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

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

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

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

138 Src family kinases (SFKs) are a group of nonreceptor tyrosine kinases that a

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

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

141 different members of the Src family kinases (SFKs) can promote RIP2 tyrosine phosphorylation and acti

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

143 how flaviviruses exploit Src family kinases (SFKs) for exit from infected cells.

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

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

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

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

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

149 The Src family kinases (SFKs) Src, Lyn, and Fyn are essential for platelet activ

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

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

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

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

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

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

156 tyrosine-protein kinase Src) family kinases (SFKs), can be found in a significant subset of patients

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

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

159 acts as a substrate for SRC family kinases (SFKs), is overexpressed in a subset of CRPC.

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

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

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

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

164 The activity of Src-family kinases (SFKs), which phosphorylate immunoreceptor tyrosine-based

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

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

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

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

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

170 d with the inhibition of Src-family kinases (SFKs).

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

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

173 adictory roles played by Src-family-kinases (SFKs) in regulating cell physiology, activity patterns o

174 Src family of cytoplasmic tyrosine kinases (SFKs) and two SFK substrates-CUB-domain containing prote

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

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

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

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

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

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

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

182 nases (SFK) and STAT1, as the application of SFK inhibitor Dasatinib blocks neutrophil exhaustion tri

183 length scale associated with the concept of SFK subcellular localization.

184 cifically visualizing active conformation of SFK-Fyn in live cells.

185 der rigidity-dependent tension downstream of SFK activity.

186 Expression of SFK phosphorylated at Y416 (SFK_pY416(+)) in tumor cells

187 hosphorylate ITAM sequences independently of SFK, allowing it to compensate for the loss of SFK activ

188 able to initiate signaling independently of SFK.

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

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

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

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

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

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

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

196 K, allowing it to compensate for the loss of SFK activity, whereas its T cell paralog ZAP-70 is not c

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

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

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

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

201 Thus, immunoreceptor sensing of SFK activity is a complex process regulated at multiple

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

203 n such pathways may depend on the actions of SFKs.

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

205 Activation of SFKs requires depletion of tyrosine phosphatases from th

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

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

208 rophil ROS response required the activity of SFKs, Syk, Btk, PLCgamma2, and PKC.

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

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

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

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

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

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

215 er in their sensitivity to the inhibition of SFKs.

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

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

218 as measured by increased phosphorylation of SFKs at Y416.

219 e that reduced inhibitory phosphorylation of SFKs leads to thrombocytopenia, with Csk being the domin

220 the K. pneumoniae-induced phosphorylation of SFKs, Syk, and Pyk2 implicating SKAP2 as proximal to the

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

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

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

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

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

226 hosphorylation of the inhibitory tyrosine of SFKs was almost completely abolished in DKO platelets, w

227 egulates chemoattractant signaling acting on SFK activity.

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

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

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

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

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

233 Platelet SFKs are inhibited by C-terminal Src kinase (Csk), which

234 emostatic consequences of targeting platelet SFKs.

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

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

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

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

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

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

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

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

243 ndependent cell growth and activates several SFK members.

244 and FOXA1(-) TNBC tended to be SFK_pY527(-) (SFK poised for activation).

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

246 ouse trachea and human bronchi with specific SFK inhibitors.

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

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

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

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

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

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

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

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

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

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

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

258 The SFK inhibitor dasatinib enhanced the antitumor effect of

259 The SFK inhibitor PP2 prevented Src activation and Panx1 ope

260 zebrafish,(6-9) where H(2)O(2) activates the SFK Lyn to drive neutrophil chemotaxis.

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

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

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

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

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

266 ade associated with rapid degradation of the SFK LynA.

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

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

269 s the development of therapies targeting the SFK/CDCP1/PKCdelta pathway for TNBC treatment.

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

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

272 We reported previously that the SFK LynA is uniquely susceptible to rapid ubiquitin-medi

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

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

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

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

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

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

279 gical inhibition or genetic depletion of the SFKs, Lyn in particular, block virus secretion.

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

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

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 cytoplasmic tyrosine kinases (SFKs) and two SFK substrates-CUB-domain containing protein 1 (CDCP1) a

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

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

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

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

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

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

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

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

295 , revealing an unexpected mechanism in which SFKs autoinhibit their activity by phosphorylating their

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