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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
26 ted, reactive oxygen species (ROS)-dependent Src kinase activation, was required for beta-catenin to
29 TG function (monodansylcadaverine; MDC) or c-Src kinase activity (PP2) disrupted the formation of thi
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
38 eductions in the protein kinase C, Pyk 2 and Src kinase activity that in tandem can decrease GluN2 ac
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
45 between Src kinase specific activity (total Src kinase activity/total Src content) and metastatic ag
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
53 bility to directly inhibit the activation of Src kinase and by its binding to the scaffold protein Ci
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
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
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
71 protein tyrosine phosphatase that regulates Src kinases and collagen-induced platelet activation.
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
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
87 show that, in the Drosophila embryonic CNS, Src kinases are dispensable for midline attraction of co
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
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
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
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
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
115 Hsp90 chaperones kinases, we reconstituted v-Src kinase chaperoning in vitro and show that its activa
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
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
129 raction of PTPN22 with the carboxyl-terminal Src kinase (CSK), an interaction that is impaired by the
131 Platelet SFKs are inhibited by C-terminal Src kinase (Csk), which phosphorylates a conserved tyros
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
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
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
155 found that ectopically expressed Abl or the Src kinase Fgr phosphorylate Sos1, and the Src kinases H
157 trast, there is consistent evidence that the Src kinase Fyn is activated by Abeta oligomers and leads
160 LA2a-->15d-PGJ2-->PPARalpha/PPARbeta/delta-->Src kinase-->STAT1/STAT3 transcriptional mechanism.
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
168 microtubule end-binding protein 3 (EB3) and SRC kinase in the neuronal and behavioral responses to v
171 gy between multiple inhibitors of Aurora and SRC kinases in ovarian and colorectal cancer cell lines,
173 In this study, we investigated the role of Src kinases in the regulation of Nrf2 and downstream sig
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
185 sing CBL mutants, whereas treatment with the SRC kinase inhibitor dasatinib resulted in equalization
189 th the F-actin stabilizer phallacidin or the Src kinase inhibitor PP2 resulted in the significant red
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
198 Treatment of these resistant cells with Src kinase inhibitors partially blocked PI3K-Akt signali
201 tion-state-sensitive classifier for selected Src kinase inhibitors when data from a single charge sta
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
210 raction led to the recruitment of C-terminal src kinase into lipid rafts, causing a preferential supp
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
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
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
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.
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
235 mical enzyme assays to determine the role of Src kinase on mitochondrial membrane apoptotic protein t
237 y effect of the anticancer drug dasatinib on Src kinase oncogenic potential in vivo We further show t
241 ntigen receptor (TCR) and the active form of Src kinase p56lck (Lck) using single and dual-color phot
246 eveals an unappreciated relationship between Src kinases, paxillin, and survival of breast cancer pat
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
256 lly modulating kinase global conformation to Src kinase, providing insight into known regulatory mech
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
265 Mouse embryonic fibroblasts deficient in Src kinases showed nuclear accumulation of Nrf2, inducti
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/
273 uitment of actin capping protein (CP) to the Src kinase substrate, cortactin, at the cell periphery,
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
284 CD226, initiated phosphorylation of Y319 by Src kinases, thereby enabling ubiquitination of CD226 by
286 We demonstrate that H2O2 acts through an Src kinase to activate a negative regulator of PI3K sign
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
291 drogen/deuterium exchange of Hsp90-dependent Src kinase variants further reveal increased transitions
294 med normal mammary epithelial cells and that Src kinases were important mediators in this transformat
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
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