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	AKT1	1 hits
2	AR	1 hits
3	AZI2	1 hits
4	CCL5	1 hits
5	CDC37	1 hits
6	ERAP1	1 hits
7	ERBB2	1 hits
8	GFAP	1 hits
9	HDAC2	1 hits
10	HSP90AA1	1 hits
11	IFNG	1 hits
12	IL23A	1 hits
13	IRF4	1 hits
14	KIT	1 hits
15	MAPK1	1 hits
16	MET	1 hits
17	MYC	1 hits
18	NFKB1	1 hits
19	NR1I3	1 hits
20	PARP1	1 hits
21	PDGFRB	1 hits
22	PIK3CA	1 hits
23	PRKCA	1 hits
24	PTEN	1 hits
25	PTK2	1 hits
26	RET	1 hits
27	RING1	1 hits
28	ST20	1 hits
29	STAT3	1 hits
30	TEC	1 hits
31	TFPI	1 hits
32	VEGFA	1 hits
33	WWOX	1 hits
34	YES1	1 hits

Related Sentences

#	PMID	Sentence
1	3021915	This cell line provides a GFAP-expressing brain tumor model that extends the use of autochthonous ASV-induced astrocytomas by allowing in vitro and in vivo studies.
2	14506272	We demonstrate here that US28 signals through the non-receptor protein-tyrosine kinases Src and focal adhesion kinase (FAK) and that this activity is necessary for US28-mediated SMC migration.
3	14506272	This association occurs earlier than the formation of the FAK.Src kinase complex, suggesting that US28 activates Src before FAK.
4	14506272	US28 binding to RANTES also promotes the formation of a Grb2.FAK complex, which is sensitive to treatment with the Src inhibitor PP2, further highlighting the critical role of Src in US28 activation of FAK.
5	14506272	These findings demonstrate that activation of FAK and Src plays a critical role in US28-mediated signaling and SMC migration.
6	14506272	We demonstrate here that US28 signals through the non-receptor protein-tyrosine kinases Src and focal adhesion kinase (FAK) and that this activity is necessary for US28-mediated SMC migration.
7	14506272	This association occurs earlier than the formation of the FAK.Src kinase complex, suggesting that US28 activates Src before FAK.
8	14506272	US28 binding to RANTES also promotes the formation of a Grb2.FAK complex, which is sensitive to treatment with the Src inhibitor PP2, further highlighting the critical role of Src in US28 activation of FAK.
9	14506272	These findings demonstrate that activation of FAK and Src plays a critical role in US28-mediated signaling and SMC migration.
10	14506272	We demonstrate here that US28 signals through the non-receptor protein-tyrosine kinases Src and focal adhesion kinase (FAK) and that this activity is necessary for US28-mediated SMC migration.
11	14506272	This association occurs earlier than the formation of the FAK.Src kinase complex, suggesting that US28 activates Src before FAK.
12	14506272	US28 binding to RANTES also promotes the formation of a Grb2.FAK complex, which is sensitive to treatment with the Src inhibitor PP2, further highlighting the critical role of Src in US28 activation of FAK.
13	14506272	These findings demonstrate that activation of FAK and Src plays a critical role in US28-mediated signaling and SMC migration.
14	14506272	We demonstrate here that US28 signals through the non-receptor protein-tyrosine kinases Src and focal adhesion kinase (FAK) and that this activity is necessary for US28-mediated SMC migration.
15	14506272	This association occurs earlier than the formation of the FAK.Src kinase complex, suggesting that US28 activates Src before FAK.
16	14506272	US28 binding to RANTES also promotes the formation of a Grb2.FAK complex, which is sensitive to treatment with the Src inhibitor PP2, further highlighting the critical role of Src in US28 activation of FAK.
17	14506272	These findings demonstrate that activation of FAK and Src plays a critical role in US28-mediated signaling and SMC migration.
18	16140770	RNA interference mediated knock-down of c-Yes, but not c-Src, and similarly reduced virus yield, specifically implicating c-Yes in WNV production.
19	17562331	In this study, we demonstrated that the phosphoinositide-phospholipase C (PI-PLC) downstream signaling pathway is involved in M. bovis BCG-induced CXCL8 release, since A549 cells pretreated with U73122, a PI-PLC inhibitor, inhibited CXCL8 release, whereas U73343 the inactive analog had no effect.
20	17562331	In addition, our results demonstrated that M. bovis BCG-induced CXCL8 production by A549 cells was significantly blocked by using neomycin (another well-described inhibitor of PI-PLC with a different mechanism of action), Ro-32-0432 and Ro-31-8220 (two PKCalpha inhibitors), PP1 and PP2 (two potent and selective inhibitors of the Src-family tyrosine kinases), and Bay 11-7082 (an IkappaB phosphorylation inhibitor).
21	17562331	We also demonstrated that M. bovis BCG can rapidly induce translocation of PKCalpha from the cytosol to the membrane, and that treatment of cells with M. bovis BCG caused time-dependent increases in phosphorylation of c-Src at tyrosine 416.
22	17562331	Finally, our studies revealed that M. bovis BCG induced the association of c-Src and IKKalphabeta during the interaction of PKCalpha and IKKalphabeta.
23	17562331	Altogether, these results represent the first evidence to date suggesting that M. bovis BCG activates the PI-PLC/PKCalpha/c-Src/IKKalphabeta signaling pathway to induce CXCL8 release in human epithelial cells.
24	17562331	In this study, we demonstrated that the phosphoinositide-phospholipase C (PI-PLC) downstream signaling pathway is involved in M. bovis BCG-induced CXCL8 release, since A549 cells pretreated with U73122, a PI-PLC inhibitor, inhibited CXCL8 release, whereas U73343 the inactive analog had no effect.
25	17562331	In addition, our results demonstrated that M. bovis BCG-induced CXCL8 production by A549 cells was significantly blocked by using neomycin (another well-described inhibitor of PI-PLC with a different mechanism of action), Ro-32-0432 and Ro-31-8220 (two PKCalpha inhibitors), PP1 and PP2 (two potent and selective inhibitors of the Src-family tyrosine kinases), and Bay 11-7082 (an IkappaB phosphorylation inhibitor).
26	17562331	We also demonstrated that M. bovis BCG can rapidly induce translocation of PKCalpha from the cytosol to the membrane, and that treatment of cells with M. bovis BCG caused time-dependent increases in phosphorylation of c-Src at tyrosine 416.
27	17562331	Finally, our studies revealed that M. bovis BCG induced the association of c-Src and IKKalphabeta during the interaction of PKCalpha and IKKalphabeta.
28	17562331	Altogether, these results represent the first evidence to date suggesting that M. bovis BCG activates the PI-PLC/PKCalpha/c-Src/IKKalphabeta signaling pathway to induce CXCL8 release in human epithelial cells.
29	19072345	Targeted agents against important mitogenic pathways, including MEK/ERK, Src, PI3K/Akt, mTOR, Hedgehog and NF-kappaB, as well as agents targeting histone deacetylase, poly(ADP-ribose) polymerase, heat shock protein 90 and other agents such as beta-lapachone, hold considerable interest for further development.
30	19075917	Some of the patents and patent applications discuss newly discovered tumor suppressor genes, including WW Domain-Containing Oxidoreductase (WWOX), Cancer Associated Ring-1 (CAR-1), Human Cervical Cancer Suppressor 1 (HCCS-1), Src-suppressed C kinase substrate (SSeCKS), ADP-Ribosylation factor-like putative Tumor Suppressor gene 1 (ARTS1), and Deleted in Osteosarcoma (DOS).
31	19075917	Another patent application recently published describes a chimeric tumor suppressor gene generated by combining a portion of the rat PEG-3 protein with the human GADD34 protein, thus creating a protein with apoptotic activity.
32	20634889	Src kinases are required for a balanced production of IL-12/IL-23 in human dendritic cells activated by Toll-like receptor agonists.
33	22661045	In addition to the Bcr-Abl1 oncoprotein, TKIs also inhibit off-target kinases (e.g. c-kit, Src, Tec), some of them having physiological functions in immune responses.
34	22772426	Molecular pathways involved in the progression of mHRPC include the androgen receptor, angiogenesis, endothelin receptor, tyrosine kinases (SRC, MET, vascular endothelial growth factor receptor, RET), and the receptor activator of nuclear factor-kB-ligand.
35	22930672	Control of adaptive immune responses by Staphylococcus aureus through IL-10, PD-L1, and TLR2.
36	22930672	Herein we report that Staphylococcus aureus induces IL-10, Th17-inducing cytokines IL-6 and IL-23, chemokines, and regulates dendritic cell markers.
37	22930672	S. aureus inhibits T-cell IL-2 responses through modulation of HLA-DR, CD86 and PD-L1.
38	22930672	IFN-gamma, Src kinase inhibitors, or TLR2 antibodies prevented the down-modulation of HLA-DR by S. aureus.
39	22930672	IL-10 and PD-L1 antagonists may boost immunity to vaccines for S. aureus and other microbes.
40	24100507	Among the seven STAT family proteins, STAT3 is constitutively activated in many diverse cancers.
41	24100507	STAT3 downstream proteins involved in cell proliferation and survival, such as c-Myc and Mcl-1, are downregulated by MLS-2384 in prostate cancer cells, whereas survivin is downregulated in A2058 cells.
42	24100507	Our findings support further development of MLS-2384 as a potential small-molecule therapeutic agent that targets JAK, Src, and STAT3 signaling in multiple human cancer cells.
43	24391506	Murine gammaherpesvirus M2 protein induction of IRF4 via the NFAT pathway leads to IL-10 expression in B cells.
44	24391506	Here, employing an inducible B cell expression system, we have determined that M2 activates the NFAT pathway in a Src kinase-dependent manner--leading to induction of the plasma cell-associated transcription factor, Interferon Regulatory Factor-4 (IRF4).
45	24391506	Furthermore, we show that expression of IRF4 alone in a B cell line up-regulates IL-10 expression in culture supernatants, revealing a novel role for IRF4 in B cell induced IL-10.
46	24391506	Consistent with the latter observation, we show that IRF4 can regulate the IL-10 promoter in B cells.
47	24391506	In primary murine B cells, addition of cyclosporine (CsA) resulted in a significant decrease in M2-induced IL-10 levels as well as IRF4 expression, emphasizing the importance of the NFAT pathway in M2- -mediated induction of IL-10.
48	24489651	Elevated TFPI1 in DOX resistant cells was active, as thrombin protein levels were coincidentally low.
49	24489651	We observed elevated HIF1α protein in DOX resistant cells, and in cells with forced expression of TFPI1, suggesting TFPI1 induces HIF1α.
50	24489651	TFPI1 also induced c-MYC, c-SRC, and HDAC2 protein, as well as DOX resistance in parental cells.
51	24489651	Growth of cells in 1% O2 induced elevated HIF1α, BCRP and MDR-1 protein, and these cells were resistant to DOX.
52	24489651	Our in vitro results were consistent with in vivo patient datasets, as tumors harboring increased BCRP and MDR-1 expression also had increased TFPI1 expression.
53	24734217	Dasatinib (DAS) is a potent inhibitor of the BCR-ABL, SRC, c-KIT, PDGFR, and ephrin tyrosine kinases that has demonstrated only modest clinical efficacy in melanoma patients.
54	24734217	The superior efficacy of the combinatorial treatment regimen included a reduction in hypoxic-signaling associated with reduced levels of immunosuppressive CD11b⁺Gr1⁺ myeloid-derived suppressor cells (MDSC) and CD4⁺Foxp3⁺ regulatory T (Treg) populations in the melanoma microenvironment.
55	25025958	Effective targeting of the human epidermal growth factor receptor 2 (HER2) has changed the natural history of HER2 overexpressing (HER2+) metastatic breast cancer.
56	25025958	Ongoing studies are evaluating novel therapeutic approaches to overcome primary and secondary drug resistance in tumours, including inhibition of PI3K/TOR, HSP90, IGF-IR and angiogenesis.
57	25025958	Despite efforts to identify predictors of preferential benefit from HER2-targeted therapies (e.g., truncated HER2, PTEN loss and SRC activation), HER2 protein overexpression and/or gene amplification remains the most important predictive factor of response to HER2-targeted therapies.
58	25691576	5-Azacytidine-induced protein 2 (AZI2) is a TNF receptor (TNFR)-associated factor family member-associated NF-κB activator-binding kinase 1-binding protein that regulates the production of IFNs.
59	25691576	We revealed that the higher longevity of AZI2-deficient osteoclasts is due to an augmented activation of proto-oncogene tyrosine-protein kinase Src (c-Src), which is a critical player in osteoclast survival.
60	25691576	We found that AZI2 inhibits c-Src activity by regulating the activation of heat shock protein 90 (Hsp90), a chaperone involved in c-Src dephosphorylation.
61	25691576	Furthermore, we demonstrated that AZI2 indirectly inhibits c-Src by interacting with the Hsp90 co-chaperone Cdc37.
62	25691576	Strikingly, administration of a c-Src inhibitor markedly prevented bone loss in AZI2 knock-out mice.
63	25691576	5-Azacytidine-induced protein 2 (AZI2) is a TNF receptor (TNFR)-associated factor family member-associated NF-κB activator-binding kinase 1-binding protein that regulates the production of IFNs.
64	25691576	We revealed that the higher longevity of AZI2-deficient osteoclasts is due to an augmented activation of proto-oncogene tyrosine-protein kinase Src (c-Src), which is a critical player in osteoclast survival.
65	25691576	We found that AZI2 inhibits c-Src activity by regulating the activation of heat shock protein 90 (Hsp90), a chaperone involved in c-Src dephosphorylation.
66	25691576	Furthermore, we demonstrated that AZI2 indirectly inhibits c-Src by interacting with the Hsp90 co-chaperone Cdc37.
67	25691576	Strikingly, administration of a c-Src inhibitor markedly prevented bone loss in AZI2 knock-out mice.
68	25691576	5-Azacytidine-induced protein 2 (AZI2) is a TNF receptor (TNFR)-associated factor family member-associated NF-κB activator-binding kinase 1-binding protein that regulates the production of IFNs.
69	25691576	We revealed that the higher longevity of AZI2-deficient osteoclasts is due to an augmented activation of proto-oncogene tyrosine-protein kinase Src (c-Src), which is a critical player in osteoclast survival.
70	25691576	We found that AZI2 inhibits c-Src activity by regulating the activation of heat shock protein 90 (Hsp90), a chaperone involved in c-Src dephosphorylation.
71	25691576	Furthermore, we demonstrated that AZI2 indirectly inhibits c-Src by interacting with the Hsp90 co-chaperone Cdc37.
72	25691576	Strikingly, administration of a c-Src inhibitor markedly prevented bone loss in AZI2 knock-out mice.
73	25691576	5-Azacytidine-induced protein 2 (AZI2) is a TNF receptor (TNFR)-associated factor family member-associated NF-κB activator-binding kinase 1-binding protein that regulates the production of IFNs.
74	25691576	We revealed that the higher longevity of AZI2-deficient osteoclasts is due to an augmented activation of proto-oncogene tyrosine-protein kinase Src (c-Src), which is a critical player in osteoclast survival.
75	25691576	We found that AZI2 inhibits c-Src activity by regulating the activation of heat shock protein 90 (Hsp90), a chaperone involved in c-Src dephosphorylation.
76	25691576	Furthermore, we demonstrated that AZI2 indirectly inhibits c-Src by interacting with the Hsp90 co-chaperone Cdc37.
77	25691576	Strikingly, administration of a c-Src inhibitor markedly prevented bone loss in AZI2 knock-out mice.