Ignet

Gene Information

Gene symbol: SRC

Gene name: v-src sarcoma (Schmidt-Ruppin A-2) viral oncogene homolog (avian)

HGNC ID: 11283

Synonyms: ASV, c-src

Related Genes

#	Gene Symbol	Number of hits
1	ADRBK1	1 hits
2	AGT	1 hits
3	AKT1	1 hits
4	ANG	1 hits
5	BCL2	1 hits
6	BTC	1 hits
7	CCND1	1 hits
8	CYSLTR2	1 hits
9	EDN1	1 hits
10	EGFR	1 hits
11	G6PD	1 hits
12	GCG	1 hits
13	GLP1R	1 hits
14	IGF1R	1 hits
15	INS	1 hits
16	IRS1	1 hits
17	MAPK1	1 hits
18	MAPK8	1 hits
19	MCM8	1 hits
20	MYOG	1 hits
21	NTRK3	1 hits
22	PRKAA1	1 hits
23	PRKCA	1 hits
24	PRKD1	1 hits
25	PTK2B	1 hits
26	PTPN1	1 hits
27	PTPRA	1 hits
28	SHC1	1 hits

Related Sentences

#	PMID	Sentence
1	1332046	Bacterial fusion proteins containing the src homology 2 domains (SH2 domains) of the 85-kDa subunit (p85) of the PtdIns 3'-kinase bound quantitatively to tyrosine phosphorylated, but not unphosphorylated, IRS-1, and this association was blocked by phosphotyrosine-containing synthetic peptides.
2	7504175	Tyrosine-phosphorylated IRS-1 binds specifically to various cellular proteins containing Src homology 2 (SH2) domains (SH2 proteins).
3	8048169	IRS-1 undergoes multisite tyrosine phosphorylation and mediates downstream signals by 'docking' various proteins that contain Src homology 2 domains.
4	11230339	Ang II-directed migration was also blocked by the Src kinase inhibitor PP2 (10 micromol/L), by the extracellular-regulated protein kinase (ERK 1/2) inhibitor PD98059 (30 micromol/L), and by the p38-MAPK inhibitor SB203580 (10 micromol/L), indicating that Src, ERK 1/2, and p38 are all involved in Ang II-induced migration of HPBM and human THP-1 monocytes.
5	11230339	This study demonstrates a novel proatherogenic action of Ang II on human monocytes by stimulating their migration, through an AT1-R-dependent process, involving signaling through Src, ERK 1/2, and p38.
6	12351660	Consistent with previous reports, PTPalpha positively regulated the activity of the protein-tyrosine kinase Src.
7	12351660	Treatment of L6 cells with PP2 or SU6656, specific inhibitors of Src family kinases, and transient transfection of dominant-inhibitory Src inhibited the formation of myotubes and expression of myogenin.
8	15044356	The proliferative effects of GLP-1 appear to involve multiple intracellular pathways, including stimulation of Akt, activation of protein kinase Czeta, and transactivation of the epidermal growth factor receptor through the c-src kinase.
9	15265871	Using pharmacological and genetic inhibitors, we found that inhibition of either c-Src or PI3K abolished AMPK that was enhanced by metformin.
10	15866871	We also show that PTP1B forms a complex with Src and p130(Cas), and that the proline-rich motif PPRPPK (residues 309-314) in PTP1B is essential for the complex formation.
11	16767106	Taken together, these results indicate that Ang II can regulate the development of mesangial matrix expansion in the early phase of diabetic nephropathy through Src and Smad1.
12	17652764	Phosphorylation of the adaptor protein Shc (Src homology 2 domain containing) transforming protein 1) was increased in RECs grown in high glucose.
13	17991742	We show that endogenous TrkC associated with c-Src in human and mouse cancer cells which express TrkC.
14	17991742	Suppression of c-Src by RNA interference in highly metastatic 4T1 mammary cancer cells, which express endogenous TrkC, resulted in markedly decreased expression of cyclin D1 and suppression of activation of Ras-Erk1/2 and PI3K-Akt.
15	17991742	Therefore these data indicate that TrkC induces the PI3K-Akt cascade through the activation of c-Src.
16	19230846	Inhibition of PI3 kinase and Src kinases decreased (p < 0.05) G6PD activity in the fa/fa but not in the lean rat liver, suggesting that G6PD activity is regulated by PI3/Src kinase signaling pathways.
17	19455054	BHE elevated antiapoptotic proteins Bcl-2 and heme oxygenase-1 and stimulated the phosphorylation of survival protein Akt simultaneously decreasing the apoptotic proteins Bax and Src.
18	20029537	In addition, both ET-1 and Ang II evoked tyrosine phosphorylation of c-Src, a nonreceptor PTK, whereas pharmacological inhibition of c-Src PTK activity by PP2, a specific inhibitor of Src-family tyrosine kinase, significantly reduced PKB phosphorylation as well as tyrosine phosphorylation of IGF-1R induced by the 2 vasoactive peptides.
19	20029537	In conclusion, these data suggest that IGF-1R PTK and c-Src PTK play a critical role in mediating PKB phosphorylation as well as hypertrophic and proliferative responses induced by ET-1 and Ang II in A10 VSMC.
20	15692059	Inhibition of src kinase by PP1 (10 microM) inhibited the increase in p42/p44 MAPK activation in response to BK.
21	21962514	Conversely, unsaturated FA with known beneficial effects on glucose metabolism prevent c-Src membrane partitioning and activation, which are dependent on its myristoylation, and block JNK activation.
22	21966580	These include phosphorylation/arrestin-dependent activation of protein kinase D1, Src family kinase-dependent activation of the sodium channel NALCN and the involvement of regulator of G protein signaling (RGS)-4.
23	11278940	Downstream of binding to the receptor, Src phosphorylates and activates G-protein-linked receptor kinase 2 (GRK2), a response obligate for agonist-induced desensitization.
24	12502502	We hypothesized that the GLP-1R could activate PI 3-kinase and promote beta-cell proliferation through transactivation of the epidermal growth factor (EGF) receptor (EGFR), an event possibly linked to GPCRs via activation of c-Src and the production of putative endogenous EGF-like ligands.
25	12502502	Both the c-Src inhibitor PP1 and the EGFR-specific inhibitor AG1478 blocked GLP-1-induced [(3)H]thymidine incorporation in INS(832/13) cells as well as in isolated rat islets, while only AG1478 inhibited the proliferative action of betacellulin (BTC), an EGFR agonist.
26	15086914	Protein kinase C (PKC) inhibition by GF109203X and PKC down-regulation with long-time phorbol myristate acetate (PMA) treatment both inhibited BMK1 and Src kinase activation.
27	20232313	Importantly, selective inhibition of c-Src, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) prior to exposure to C-IV prevented mesenchymal transition and effectively preserved insulin expression.