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1 re detected between Na,K-ATPase and purified Src kinase.
2 atients show similar increased activation of SRC kinase.
3 90 does not influence the almost identical c-Src kinase.
4 t position 32 within the switch I region via Src kinase.
5 ne kinase but not of the highly homologous c-Src kinase.
6 ated by metabotropic NMDAR signaling through Src kinase.
7 ular cleavage of the beta3 chain, talin, and Src kinase.
8 ays, including MAPK, Smad, beta-catenin, and Src kinase.
9  explore the conformational landscape of a c-Src kinase.
10 hondria to the cytosol during HI through the Src kinase.
11 degrees C) or upon hyperphosphorylation with Src kinase.
12  were mainly mediated by activation of the c-Src kinase.
13 lex consisting of Na,K-ATPase, caveolin, and Src kinase.
14  G6G is a potent inhibitor of both Abl and c-Src kinases.
15 ide, activated neutrophils, or inhibition of Src kinases.
16 ggers phosphorylation of mammalian Robo3 via Src kinases.
17 tase Shp-2, and this process is dependent on Src kinases.
18 satinib inhibits tyrosine kinases, including Src kinases.
19 SH2, and catalytic domains seen in mammalian Src kinases.
20 phosphatidylinositol-3-OH kinase (PI3-K), or Src kinases.
21 clude a role as an anti-adhesive effector of Src kinases.
22 ar tyrosine kinase evolutionarily related to Src kinases.
23 eposition via neutrophil FcgammaRIIA and Abl/Src kinases.
24 alpha) is an important positive regulator of SRC kinase activation and a known promoter of cancer gro
25                       Furthermore, increased Src kinase activation promoted migration, invasion, and
26 ted, reactive oxygen species (ROS)-dependent Src kinase activation, was required for beta-catenin to
27 o a lack of CD45, a phosphatase required for Src kinase activation.
28 nt prevented the effect of leptin, whereas a Src kinase activator peptide mimicked it.
29 TG function (monodansylcadaverine; MDC) or c-Src kinase activity (PP2) disrupted the formation of thi
30 cts as a biomechanical sensor that regulates Src kinase activity and stress fiber formation.
31     We conclude that K6 negatively regulates Src kinase activity and the migratory potential of skin
32                      Our study suggests that Src kinase activity determines NEDD9 exchange at focal a
33 ts in increased cholesterol biosynthesis and Src kinase activity in breast cancer cells and suggest t
34 In this study, we demonstrate that increased Src kinase activity is associated with high-fat diet-acc
35 ocalization of SHIP, whereas neither PI3K or Src kinase activity is essential.
36                                Inhibition of Src kinase activity prevented the increase in phosphoryl
37                       AhR-complex-associated Src kinase activity promoted IDO1 phosphorylation and si
38 eductions in the protein kinase C, Pyk 2 and Src kinase activity that in tandem can decrease GluN2 ac
39                       Further, inhibition of Src kinase activity using caveolin-1 scaffolding domain
40   CD45 also enriched in AISs but to modulate Src kinase activity, because localization of CD45 at the
41 rate with actin remodeling pathways, notably SRC kinase activity, to establish and maintain long-last
42 the E2F1 transcription factor; this required Src kinase activity.
43 egrin and that this transactivation requires Src kinase activity.
44 rylation between SRC and AURKA that enhanced SRC kinase activity.
45  between Src kinase specific activity (total Src kinase activity/total Src content) and metastatic ag
46 gnaling, and clarifies how compartmentalized Src-kinase activity may drive cell fate.
47 nous CD44 rolled on E-selectin and activated Src kinases after binding anti-CD44 antibody.
48                    Moreover, the activity of Src kinases, along with oxidative stress, were significa
49 mpetitive antagonists or blocking downstream Src kinase) also increased sEPSC frequency similar to th
50 swelling, which triggers via integrins and c-Src kinase an activation of the epidermal growth factor
51 lated PAG serves as an anchor for C-terminal SRC kinase, an inhibitor of SRC-family kinases.
52                We showed that proto-oncogene Src kinase and Akt are direct targets of miR-23b.
53 bility to directly inhibit the activation of Src kinase and by its binding to the scaffold protein Ci
54                    FN-induced EMT depends on Src kinase and extracellular signal-regulated kinase/mit
55    This newly identified interaction between Src kinase and HNF4alpha has important implications for
56 ne alpha1D369Nbeta1FXYD1) and purified human Src kinase and human caveolin 1 or interactions between
57              Na,K-ATPase is proposed to bind Src kinase and inhibit its activity, whereas ouabain, th
58 ntracellular HMGB1, through associating with Src kinase and inhibiting interactions between Src and F
59 esent study supports that the interaction of Src Kinase and integrins plays a critical role in the de
60 w that this trait results from activation of Src kinase and key Src substrates that promote cell migr
61 ription factor-1 cascade, which requires Fyn-Src kinase and lipid rafts in human taste bud cells (TBC
62                                              Src kinase and MLCK inhibitors blocked this synergistic
63 chanism involving calcium, oxidative stress, Src kinase and MLCK.
64            Mechanisms were investigated with src kinase and other inhibitors.
65 8 to beta1 integrins is elucidated requiring Src kinase and potential implication of the C2beta isofo
66 showed that protein-tyrosine kinases such as Src kinase and PTPs such as PTPalpha and PTPepsilon modu
67  the coupling of FcgammaRI to FcgammaRIIB by Src kinase and resulting activation of SH2 domain-contai
68 ate that integrin alpha v (alphaV) recruited Src kinase and that leads to subsequent Src activation i
69 hat activate the focal-adhesion kinase and c-Src kinase and their downstream MAP-ERK kinase/extracell
70  adhesion kinase and ERKs 1/2, and decreased Src kinases and aquaporins 3 and 4.
71  protein tyrosine phosphatase that regulates Src kinases and collagen-induced platelet activation.
72 ng an additional and unexpected link between Src kinases and MAPK signaling.
73 gical studies additionally support roles for Src kinases and MAPK/ERK downstream of beta-arrestin2 in
74 ess-activated GSK3beta acted upstream to the Src kinases and phosphorylated the Src kinases, leading
75  have previously been shown to interact with Src kinases and PLCgamma.
76 ractions with endothelial selectins activate Src kinases and spleen tyrosine kinase (Syk), leading to
77  plasma membrane and receptor association to Src-kinases and phosphatidylinositol-3-kinase signalling
78 ough PKC and interaction with beta-arrestin, Src kinase, and hence the mitogen-activated-protein-kina
79 axis consisting of the integrin alphavbeta3, Src kinase, and the transcription factor Slug suppresses
80 taining phosphatase-1 (Shp-1) and C-terminal Src kinase, and we use modeling of early TCR signaling t
81  complex, posttranslational modifications of Src kinases, and morphological changes consistent with t
82 ession, activating focal adhesion kinase and Src kinases, and promoting cell migration and invasion.
83  DJ-1 directly bound to Lyn but not to other Src kinases, and this interaction was specific for human
84 ents to healthy control levels, suggesting a Src kinase- and actin-dependent mechanism.
85 /mechanistic target of rapamycin complex 2-, Src kinase-, and mRNA binding-dependent manner.
86                                  Exactly how SRC kinases are activated and hippo signaling is lost in
87  show that, in the Drosophila embryonic CNS, Src kinases are dispensable for midline attraction of co
88                                      Because Src kinases are involved in bridging the membrane to the
89                                    Mammalian Src kinases are normally regulated in a reciprocal fashi
90 mmon early signaling mediators, we show that Src kinases are required for lytic granule convergence,
91 t on integrin-mediated adhesion, and because SRC kinases are the main regulators of this process, the
92                        These findings reveal Src kinase as a critical oncogenic driver underlying JMM
93 hogenicity of LAM cells and they rationalize Src kinase as a novel therapeutic target for treatment o
94 enin specifically complexed to HIF1alpha and Src kinase as critically involved in HIF1alpha signaling
95 enesis of DMD and identify NADPH oxidase and Src kinase as potential therapeutic targets.
96                      These findings identify Src kinases as a critical regulator of chemokine secreti
97 onal experimentation leaving CSK (C-terminal Src kinase) as the strongest candidate for ibrutinib-ind
98 and is a carrier for other adapter proteins, Src kinase-associated phosphoprotein 1 (SKAP1) and SKAP2
99 P=1.80x10(-8)), whereas SNPs associated with Src kinase-associated phosphoprotein 1 (SKAP1), matrix m
100 eotide polymorphism rs7804356 located in the Src kinase-associated phosphoprotein 2 (SKAP2) gene is a
101                                          The Src kinase-associated phosphoprotein 2 (Skap2) is involv
102 identified a cytosolic adaptor protein named Src kinase-associated phosphoprotein 55 homologue (SKAP-
103 regulating integrin activation, we show that Src kinase-associated phosphoprotein of 55 kD (SKAP55) i
104 ves the interaction of ADAP with the adapter src kinase-associated phosphoprotein of 55 kDa (SKAP55).
105 es both ADAP and the ADAP-associated adapter Src kinase-associated phosphoprotein of 55 kDa (SKAP55).
106 kinase myristoylation, which is required for Src kinase association at the cellular membrane, blocks
107 P-1 localization and decreased activation of Src kinases at the synapse.
108 ese findings provide novel insights into how src- kinase-based regulation of a cbl adaptor regulates
109 ariant exhibits a 50% decrease in C-terminal Src kinase binding affinity and contributes to T cell hy
110 nt is dependent on the activation of Syk and Src kinases but is inhibited by CD19 costimulation, pres
111 K1 activation was abolished by inhibitors of Src kinases, but not Rac1 inhibitors, demonstrating that
112 P) ribosyltransferase that directly inhibits Src kinase by simultaneous amidation and ADP ribosylatio
113 ibition is mediated by a mechanism involving Src kinases, CD45, and SHIP-1 that is defective in MM ce
114 s degradation does not require the action of Src kinase, Cdc42 or Dyn2.
115 Hsp90 chaperones kinases, we reconstituted v-Src kinase chaperoning in vitro and show that its activa
116       To explain these findings, we designed Src kinase chimeras that gradually transform c-Src into
117                       We also identified the SRC kinase contributing to ETV2-mediated activation of t
118 ond phosphorylation event include C-terminal Src kinase (Csk) and Bruton's tyrosine kinase (Btk).
119 h of two known inhibitors of Lck, C-terminal Src kinase (Csk) and protein tyrosine phosphatase N22 (P
120 controlled by the tyrosine kinase C-terminal Src kinase (CSK) and the tyrosine phosphatase CD45.
121 se A (PKA) complex that activates C-terminal Src kinase (CSK) and thereby down-regulates kinases invo
122                     We identified C-terminal Src kinase (Csk) as a tyrosine kinase responsible for re
123                                   C-terminal Src kinase (Csk) binds to tyrosine phosphorylated JAM-A
124                                   C-terminal Src kinase (Csk) is a multidomain tyrosine kinase that i
125 pressing either LAIR-1 mutants or C-terminal Src kinase (CSK) mutants, and 3) T cells from mice that
126 tion of c-Src through deletion of C-terminal Src kinase (CSK) results in the development of invasive
127 while promoting the expression of C-terminal Src kinase (CSK), a negative regulator of Src family of
128                                   C-terminal Src kinase (CSK), a negative regulator of TCR signaling,
129 raction of PTPN22 with the carboxyl-terminal Src kinase (CSK), an interaction that is impaired by the
130                               The C-terminal Src kinase (Csk), the primary negative regulator of Src-
131    Platelet SFKs are inhibited by C-terminal Src kinase (Csk), which phosphorylates a conserved tyros
132 nder the principal control of the C-terminal Src Kinase (Csk).
133 FKs and their negative regulator, C-terminal Src kinase (Csk).
134 -terminal tail by another kinase, C-terminal Src kinase (Csk).
135                    The Drosophila C-terminal Src kinase (d-Csk) is a genetic modifier of warts (wts),
136                          Phosphorylation was Src kinase dependent, and we identified Yes-1 and PTPN13
137 (EPEC and EHEC, respectively), which inhibit Src kinase-dependent phagocytosis by ADP-ribosylation.
138 on of the Rho GTPase pathway was followed by Src kinase-dependent phosphorylation of the Rap1-specifi
139  is an essential component of caveolae whose Src kinase-dependent phosphorylation on tyrosine 14 (Y14
140 brane-permeable CSD-competing peptides, that Src kinase-dependent pY14Cav1 regulation of focal adhesi
141 nals, depends on a directly downstream early Src kinase-dependent signal and emphasizes the importanc
142 ces IRAK1 and AKT phosphorylation, and it is Src kinase-dependent.
143 tyrosines in neural progenitors in vivo, and Src kinase directly phosphorylates CitK.
144 lizes the E2 conformation, thus exposing the Src kinase domain and its active site Tyr-418 for activa
145 the adjacent regulatory domains, whereas the Src kinase domains are autoinhibited by the assembly of
146 le blood and under flow conditions through a Src kinase driven pathway.
147           We demonstrate that members of the SRC kinase family (SKF) are key mediators of IFN-gamma p
148                                          The Src kinase family comprises nine homologous members whos
149 ting analysis demonstrated that depletion of Src kinase family members (c-Src, Yes, and Fyn) or cav-1
150 own to activate Stat3 such as Janus kinases, Src kinase family members or receptor tyrosine kinases.
151  induces phosphorylation of kinases from the Src kinase family, a hallmark of integrin signaling acti
152       Netrin-4-stimulated phosphorylation of Src kinase family, effectors of endothelial cell migrati
153 ymphocyte cell kinase (Lck), a member of the Src kinases family, mediates PC.
154                We recently demonstrated that Src kinase features an allosteric network that couples s
155  found that ectopically expressed Abl or the Src kinase Fgr phosphorylate Sos1, and the Src kinases H
156                   Here, we report that the c-Src kinase functions as a key adapter protein for the es
157 trast, there is consistent evidence that the Src kinase Fyn is activated by Abeta oligomers and leads
158                                          The Src kinase Fyn plays critical roles in memory formation
159 nied by an activating phosphorylation of the Src kinases Fyn and Yes but not of c-Src.
160 LA2a-->15d-PGJ2-->PPARalpha/PPARbeta/delta-->Src kinase-->STAT1/STAT3 transcriptional mechanism.
161 cating a downregulation of expression of the Src kinase Hck.
162 e Src kinase Fgr phosphorylate Sos1, and the Src kinases Hck and Fgr are required for Abl and Sos1 ph
163   Here, we report increased levels of active Src kinase in LAM lungs and in TSC2(-/-) cells, caused b
164 actor (G-CSF) activates Lyn, the predominant Src kinase in myeloid cells, through Gab2-mediated recru
165 sion significantly correlated with activated Src kinase in patient samples and promoted tumor cell in
166     In the present study we test the role of Src kinase in regulating dynamic exchange of the focal a
167  functional and therapeutic relevance of the SRC kinase in synovial sarcoma.
168  microtubule end-binding protein 3 (EB3) and SRC kinase in the neuronal and behavioral responses to v
169 poxia-ischemia (HI) results in activation of Src kinase in the newborn piglet brain.
170 ist for midline axon crossing independent of Src kinases in commissural neurons.
171 gy between multiple inhibitors of Aurora and SRC kinases in ovarian and colorectal cancer cell lines,
172 so provide evidence for a regulatory role of src kinases in the activation of myeloid cells.
173   In this study, we investigated the role of Src kinases in the regulation of Nrf2 and downstream sig
174                   Here we also show that the Src kinase inactivates the corepressive function of LCoR
175  stimulation, the interaction increases in a Src kinase-independent manner.
176          Cyclin D1 was induced by v-Src, and Src kinase induction of Trop2 ICD nuclear accumulation r
177 tion of either FAK or its signaling mediator Src kinase inhibited LMP2A-induced migration.
178 data indicate that F-actin stabilization and Src kinase inhibition represent potential therapeutic ta
179 reover, we uncover an unexpected function of Src kinases: inhibition of midline axon crossing through
180 at topical or systemic administration of the Src kinase inhibitor (TG100572) that inhibits downstream
181 ored after treating Bmpr2(+/-) PECs with the SRC kinase inhibitor 3-(4-chlorophenyl)-1-(1,1-dimethyle
182 y the OPRM1-Y336F mutant, by the presence of Src kinase inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-but
183 troarginine methyl ester (hydrochloride) and Src kinase inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-but
184             Blocking PKCzeta activation by a Src kinase inhibitor and a PKCzeta-pseudosubstrate preve
185 sing CBL mutants, whereas treatment with the SRC kinase inhibitor dasatinib resulted in equalization
186 ogen, which was blocked in the presence of a Src kinase inhibitor or in the absence of GPVI.
187 ): normoxic (Nx), HI and HI pre-treated with Src kinase inhibitor PP2 (PP2 + HI).
188                             Furthermore, the Src kinase inhibitor PP2 rescued cytokine-induced epithe
189 th the F-actin stabilizer phallacidin or the Src kinase inhibitor PP2 resulted in the significant red
190 vating kinase (MEK) inhibitor PD98059 or the Src kinase inhibitor PP2.
191 h the F-actin stabilizer phallacidin and the Src kinase inhibitor PP2.
192     The Janus kinase inhibitor AG490 and the Src kinase inhibitor Src-1, as well as rapamycin, have n
193  Moreover, pretreatment of M with a specific Src kinase inhibitor, PP2 completely prevents NE-induced
194 are the main regulators of this process, the SRC kinase inhibitor, saracatinib (AZD0530), completely
195 systemic therapy such as dasatinib, a potent SRC kinase inhibitor, with activity in bone.
196 n occur when TCR signaling is blocked with a Src kinase inhibitor.
197                                              Src kinase inhibitors effectively blocked internalizatio
198      Treatment of these resistant cells with Src kinase inhibitors partially blocked PI3K-Akt signali
199                            Consistently, the Src kinase inhibitors PP2 and dasatinib reduced chemokin
200                                     Notably, Src kinase inhibitors reduced migration and invasion pro
201 tion-state-sensitive classifier for selected Src kinase inhibitors when data from a single charge sta
202                                              Src kinase inhibitors, microtubule inhibitors, and PGE(2
203                                   IFN-gamma, Src kinase inhibitors, or TLR2 antibodies prevented the
204  buckyballs as a novel class of non-receptor Src kinases inhibitors.
205                                              Src-kinase inhibitors hold great potential as targeted t
206                                              Src-kinase inhibitors, and not conventional tyrosine kin
207 mulatory capacity of a group of novel drugs, src-kinase inhibitors, thereby opening new opportunities
208    However, the contribution of integrin and Src kinase interaction to lung fibrosis has not been mec
209 ic residues central to the Ptpn22-C-terminal Src kinase interaction.
210 raction led to the recruitment of C-terminal src kinase into lipid rafts, causing a preferential supp
211                                              SRC kinase is also constitutively activated in Bmpr2(+/-
212 llectively, these data provide evidence that Src kinase is an important mediator of signaling events
213  vivo We further show that myristoylation of Src kinase is essential to facilitate Src-induced and hi
214                                              Src kinase is known to regulate fibroblast migration.
215            We identified Lyn as the specific Src kinase isoform that is activated by MCP-1 and acts u
216 correlated with diminished expression of the Src kinase Lck, protein kinase C-theta, and NF-kappaB, k
217 am to the Src kinases and phosphorylated the Src kinases, leading to their nuclear localization and N
218                     Persistent activation of Src kinase leads to activation of the autophagy represso
219                                Activation of Src kinase leads to rapid induction of protrusion with p
220                    Unregulated activation of Src kinases leads to aberrant signalling, uncontrolled g
221 metic glutamic acid or transfection with the Src kinases Lyn or c-Src inhibited hydrogen peroxide-ind
222 nstitutively bound the adaptor protein Grb2, src-kinase Lyn and signal transducer phospholipase gamma
223                        Our data suggest that Src kinase may represent a potential target that could i
224                      Inhibiting TNF-alpha or src kinases may be a therapeutic option to normalize bar
225 ated progression of prostate tumors and that Src kinases mediate this pathological process.
226                                              Src kinase-mediated interactions between prostate cancer
227 stoyl CoA and myristoylated Src and promoted Src kinase-mediated oncogenic signaling in human cells.
228 port that leptin augments NMDAR function via Src kinase-mediated phosphorylation of the GluN2A subuni
229 o-like kinase 1 (Plk1) kinase by enhancing c-Src kinase-mediated tyrosine phosphorylation of Plk1.
230       Together, our results establish that c-Src kinase mediates stresses generated by E2 in long-ter
231           Our results suggest that targeting Src kinase myristoylation, which is required for Src kin
232 interaction is confirmed, the lack of direct Src kinase/Na,K-ATPase binding requires reassessment of
233 tress, through a signaling pathway requiring Src kinases, NADPH oxidase, superoxide radical anion, an
234 ect interactions between the Na,K-ATPase and Src kinase (non-receptor tyrosine kinase).
235 mical enzyme assays to determine the role of Src kinase on mitochondrial membrane apoptotic protein t
236 that TI-VAMP is phosphorylated in vitro by c-Src kinase on tyrosine 45 of the Longin domain.
237 y effect of the anticancer drug dasatinib on Src kinase oncogenic potential in vivo We further show t
238 ng antibody and inhibitors of peroxynitrite, src kinase, or MMP blocked the migration.
239                        CD4 then recruits the Src kinase p56(Lck) (Lck) to the TCR-CD3 complex to phos
240 to be associated with aberrant regulation of Src-kinase p56(Lck).
241 ntigen receptor (TCR) and the active form of Src kinase p56lck (Lck) using single and dual-color phot
242 n elucidated through characterization of the Src kinase pathway.
243 n beta1 play a role in the activation of the Src kinase pathway.
244 AT pathway and enhanced by inhibitors of the Src kinase pathway.
245 gesting possible cross-talk between Smad and Src kinase pathways.
246 eveals an unappreciated relationship between Src kinases, paxillin, and survival of breast cancer pat
247                    In turn, H2O2 activates a Src kinase/phospholipase C-gamma1 (PLC-gamma1) signaling
248                Here we show that activated c-Src kinase phosphorylates Y281 and Y302 of Mdm2, resulti
249  Na,K-ATPase was found to be a substrate for Src kinase phosphorylation at Tyr-144.
250 ese effects were associated with a transient Src kinase phosphorylation at Tyr416 and with a strong t
251 ) and VE-cadherin expression and increase in Src kinase phosphorylation downstream of VEGFR2 were acc
252 ic effects were prevented by deletion of a c-Src kinase phosphorylation DYD motif, identified in sili
253      In this study, we found that VP reduces Src kinase phosphorylation: by suppressing Src using the
254        The studies together demonstrate that Src kinases play a critical role in nuclear export and d
255                      Moreover, inhibition of Src kinases prevented the activation of RhoA and ROCK, i
256 lly modulating kinase global conformation to Src kinase, providing insight into known regulatory mech
257                         However, blockade of Src kinase reduced phosphorylation of p38 but not JNK, e
258                        Inhibition of Nox2 or Src kinase reduces oxidative stress and partially rescue
259     With these features in mind, we examined Src kinase regulation at the structural, enzymatic, and
260 ction of T cells reduced the expression of a Src-kinase regulatory phosphatase (PTPRE), while ZKV inf
261 st CD36 or with a pharmacologic inhibitor of SRC kinases restored the antiaggregative phenotype in th
262  culture can be triggered by activation of v-Src kinase, resulting in increased cell motility, invasi
263                      These findings identify Src kinase(s) as a mediator of TGFbeta1-induced pY654-be
264 direct fluorescence imaging or imaging of an Src kinase sensor in mammalian cells.
265     Mouse embryonic fibroblasts deficient in Src kinases showed nuclear accumulation of Nrf2, inducti
266                      Moreover, activation of Src kinase signaling and FOXO1 inhibition decreased the
267              Inhibition of Janus kinase 2 or SRC kinase signaling downstream of mutated CSF3R is feas
268                Using ChIP-seq, we identified Src kinase signaling inhibitor 1 (Srcin1; also referred
269 is G-protein-dependent and involves cAMP and Src kinase signaling pathways.
270  regulated at the protein level by oncogenic Src kinase signals through SIAH2, thus contributing to b
271 , we do observe a direct correlation between Src kinase specific activity (total Src kinase activity/
272                   Caveolin-1 (Cav1), a major Src kinase substrate phosphorylated on tyrosine-14 (Y14)
273 uitment of actin capping protein (CP) to the Src kinase substrate, cortactin, at the cell periphery,
274         The large GTPase Dynamin 2 (Dyn2), a Src-kinase substrate, regulates membrane-cytoskeletal dy
275 an modify the activation state of downstream Src kinases, such as Lyn, in lymphocytes.
276 ions that blocked CD36 ligation or inhibited Src kinases, suggesting a tyrosine kinase-dependent mech
277 e Src-family kinase Lyn and linked TLR9 to a Src-kinase Syk-transcription factor STAT3 cascade essent
278 ulation, raising a note of caution regarding src kinase-targeted intervention in plaque inflammation.
279 etwork of dynamically coupled amino acids in Src kinase that connects regulatory sites to the ATP- an
280 ntal support for long-range communication in Src kinase that leads to the relative stabilization of a
281 rface adhesion receptors, as well as FAK and Src kinases that are essential regulators of the migrati
282 ough Csk is known as a negative regulator of Src kinases, the effects of Csk on Gliotactin are indepe
283                         Similar to mammalian Src kinases, the enzymatic activities of CoSrc1 and CoSr
284  CD226, initiated phosphorylation of Y319 by Src kinases, thereby enabling ubiquitination of CD226 by
285                      Upon phosphorylation by Src kinases, this motif enabled binding of DNAM-1 to ada
286     We demonstrate that H2O2 acts through an Src kinase to activate a negative regulator of PI3K sign
287             Mechanistically, Clec12A engages Src kinase to positively regulate the TBK1-IRF3 signalin
288 -mediated signaling by recruiting C-terminal Src kinase to the membrane and/or receptor complex follo
289 ouse DCT cells via ROS-induced activation of Src kinase, up-regulation of the K(+) channel Kir4.1, an
290                                By activating Src kinase using uniRapR in single cells and whole organ
291 drogen/deuterium exchange of Hsp90-dependent Src kinase variants further reveal increased transitions
292 yrosine kinases-Abl via pY251 and C-terminal Src kinase via pY239.
293                           We also found that Src kinase was activated in the MMTV-expressing cells an
294 med normal mammary epithelial cells and that Src kinases were important mediators in this transformat
295        Coupling of SLAMF7 to SHIP-1 required Src kinases, which phosphorylated SLAMF7.
296 strates) bind with negative cooperativity to Src kinase while products (ADP and phosphopeptide) bind
297 ve conformation of the catalytic domain of c-Src kinase while the tyrosine 416 in the activation loop
298 ctin-1 undergoes tyrosine phosphorylation by Src kinases with subsequent Syk activation.
299 ed by the receptor recruiting and activating Src kinase within the receptor complex, leading to phosp
300 ts of the disordered N terminal (SH4UD) of c-Src kinase without reweighting or constraining the simul

 
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