Ignet

Gene Information

Gene symbol: STIM1

Gene name: stromal interaction molecule 1

HGNC ID: 11386

Synonyms: GOK, D11S4896E

Related Genes

#	Gene Symbol	Number of hits
1	ATP2A3	1 hits
2	CFTR	1 hits
3	EDN1	1 hits
4	F2	1 hits
5	GRIK2	1 hits
6	KCNE1	1 hits
7	KCNJ1	1 hits
8	KCNQ1	1 hits
9	MAPK1	1 hits
10	MBTPS1	1 hits
11	NFKB1	1 hits
12	NOS3	1 hits
13	ORAI1	1 hits
14	PRKAA2	1 hits
15	PRKAR2A	1 hits
16	RETN	1 hits
17	RPS27A	1 hits
18	S1PR3	1 hits
19	SCN5A	1 hits
20	TRPC3	1 hits
21	UBXD5	1 hits

Related Sentences

#	PMID	Sentence
1	17090780	It has been shown that store-operated Ca(2+) influx (SOC) plays critical roles in the activation of endothelial nitric oxide (NO) synthase (eNOS) and generation of NO in endothelial cells.
2	17090780	Recent studies indicate stromal interaction molecule 1 (STIM1) is the molecule responsible for SOC activation following Ca(2+) depletion in the ER.
3	17090780	In the current study, we used primary cultured rat mesangial cells to examine the effect of RA on SOC and STIM1.
4	17090780	Downregulation of STIM1 protein and BK-induced SOC by RA treatment or STIM1 dsRNA were associated with abolished NO production.
5	17090780	The 26S proteasome inhibitor lactacystin blocked the RA-mediated downregulation of BK-induced SOC, suggesting that ubiquitin-proteasome pathway may be involved in RA-mediated STIM1 protein downregulation in rat mesangial cells.
6	17090780	Our data suggest that glucose-induced eNOS expression and NO production in mesangial cells may contribute to hyperfiltration in diabetes and RA may exert beneficial effects by downregulation of STIM1 and SOC in mesangial cells.
7	17090780	It has been shown that store-operated Ca(2+) influx (SOC) plays critical roles in the activation of endothelial nitric oxide (NO) synthase (eNOS) and generation of NO in endothelial cells.
8	17090780	Recent studies indicate stromal interaction molecule 1 (STIM1) is the molecule responsible for SOC activation following Ca(2+) depletion in the ER.
9	17090780	In the current study, we used primary cultured rat mesangial cells to examine the effect of RA on SOC and STIM1.
10	17090780	Downregulation of STIM1 protein and BK-induced SOC by RA treatment or STIM1 dsRNA were associated with abolished NO production.
11	17090780	The 26S proteasome inhibitor lactacystin blocked the RA-mediated downregulation of BK-induced SOC, suggesting that ubiquitin-proteasome pathway may be involved in RA-mediated STIM1 protein downregulation in rat mesangial cells.
12	17090780	Our data suggest that glucose-induced eNOS expression and NO production in mesangial cells may contribute to hyperfiltration in diabetes and RA may exert beneficial effects by downregulation of STIM1 and SOC in mesangial cells.
13	17090780	It has been shown that store-operated Ca(2+) influx (SOC) plays critical roles in the activation of endothelial nitric oxide (NO) synthase (eNOS) and generation of NO in endothelial cells.
14	17090780	Recent studies indicate stromal interaction molecule 1 (STIM1) is the molecule responsible for SOC activation following Ca(2+) depletion in the ER.
15	17090780	In the current study, we used primary cultured rat mesangial cells to examine the effect of RA on SOC and STIM1.
16	17090780	Downregulation of STIM1 protein and BK-induced SOC by RA treatment or STIM1 dsRNA were associated with abolished NO production.
17	17090780	The 26S proteasome inhibitor lactacystin blocked the RA-mediated downregulation of BK-induced SOC, suggesting that ubiquitin-proteasome pathway may be involved in RA-mediated STIM1 protein downregulation in rat mesangial cells.
18	17090780	Our data suggest that glucose-induced eNOS expression and NO production in mesangial cells may contribute to hyperfiltration in diabetes and RA may exert beneficial effects by downregulation of STIM1 and SOC in mesangial cells.
19	17090780	It has been shown that store-operated Ca(2+) influx (SOC) plays critical roles in the activation of endothelial nitric oxide (NO) synthase (eNOS) and generation of NO in endothelial cells.
20	17090780	Recent studies indicate stromal interaction molecule 1 (STIM1) is the molecule responsible for SOC activation following Ca(2+) depletion in the ER.
21	17090780	In the current study, we used primary cultured rat mesangial cells to examine the effect of RA on SOC and STIM1.
22	17090780	Downregulation of STIM1 protein and BK-induced SOC by RA treatment or STIM1 dsRNA were associated with abolished NO production.
23	17090780	The 26S proteasome inhibitor lactacystin blocked the RA-mediated downregulation of BK-induced SOC, suggesting that ubiquitin-proteasome pathway may be involved in RA-mediated STIM1 protein downregulation in rat mesangial cells.
24	17090780	Our data suggest that glucose-induced eNOS expression and NO production in mesangial cells may contribute to hyperfiltration in diabetes and RA may exert beneficial effects by downregulation of STIM1 and SOC in mesangial cells.
25	17090780	It has been shown that store-operated Ca(2+) influx (SOC) plays critical roles in the activation of endothelial nitric oxide (NO) synthase (eNOS) and generation of NO in endothelial cells.
26	17090780	Recent studies indicate stromal interaction molecule 1 (STIM1) is the molecule responsible for SOC activation following Ca(2+) depletion in the ER.
27	17090780	In the current study, we used primary cultured rat mesangial cells to examine the effect of RA on SOC and STIM1.
28	17090780	Downregulation of STIM1 protein and BK-induced SOC by RA treatment or STIM1 dsRNA were associated with abolished NO production.
29	17090780	The 26S proteasome inhibitor lactacystin blocked the RA-mediated downregulation of BK-induced SOC, suggesting that ubiquitin-proteasome pathway may be involved in RA-mediated STIM1 protein downregulation in rat mesangial cells.
30	17090780	Our data suggest that glucose-induced eNOS expression and NO production in mesangial cells may contribute to hyperfiltration in diabetes and RA may exert beneficial effects by downregulation of STIM1 and SOC in mesangial cells.
31	18439569	STIM1 regulates acidic Ca2+ store refilling by interaction with SERCA3 in human platelets.
32	18439569	Electrotransjection of cells with anti-STIM1 (Y(231)-K(243)) antibody, directed towards a cytoplasmic sequence of STIM1, significantly reduced acidic store refilling, which was tested by remobilizing Ca(2+) from the acidic stores using 2,5-di-(t-butyl)-1,4-hydroquinone (TBHQ) after a brief refilling period that followed thrombin stimulation.
33	18439569	Platelet treatment with thrombin or thapsigargin in combination with ionomycin, to induce extensive Ca(2+) store depletion, resulted in a transient increase in the interaction between STIM1 and SERCA3, reaching a maximum 30 s after stimulation.
34	18439569	The coupling between STIM1 and SERCA3 was abolished by electrotransjection with anti-STIM1 antibody.
35	18439569	The interaction between STIM1 and SERCA3 induced by thrombin or by treatment with thapsigargin plus ionomycin is reduced in platelets from type 2 diabetic patients, as well as Ca(2+) reuptake into the acidic Ca(2+) stores.
36	18439569	These findings provide evidence for a role of STIM1 in acidic store refilling in platelets probably acting as a Ca(2+) sensor and regulating the activity of SERCA3.
37	18439569	STIM1 regulates acidic Ca2+ store refilling by interaction with SERCA3 in human platelets.
38	18439569	Electrotransjection of cells with anti-STIM1 (Y(231)-K(243)) antibody, directed towards a cytoplasmic sequence of STIM1, significantly reduced acidic store refilling, which was tested by remobilizing Ca(2+) from the acidic stores using 2,5-di-(t-butyl)-1,4-hydroquinone (TBHQ) after a brief refilling period that followed thrombin stimulation.
39	18439569	Platelet treatment with thrombin or thapsigargin in combination with ionomycin, to induce extensive Ca(2+) store depletion, resulted in a transient increase in the interaction between STIM1 and SERCA3, reaching a maximum 30 s after stimulation.
40	18439569	The coupling between STIM1 and SERCA3 was abolished by electrotransjection with anti-STIM1 antibody.
41	18439569	The interaction between STIM1 and SERCA3 induced by thrombin or by treatment with thapsigargin plus ionomycin is reduced in platelets from type 2 diabetic patients, as well as Ca(2+) reuptake into the acidic Ca(2+) stores.
42	18439569	These findings provide evidence for a role of STIM1 in acidic store refilling in platelets probably acting as a Ca(2+) sensor and regulating the activity of SERCA3.
43	18439569	STIM1 regulates acidic Ca2+ store refilling by interaction with SERCA3 in human platelets.
44	18439569	Electrotransjection of cells with anti-STIM1 (Y(231)-K(243)) antibody, directed towards a cytoplasmic sequence of STIM1, significantly reduced acidic store refilling, which was tested by remobilizing Ca(2+) from the acidic stores using 2,5-di-(t-butyl)-1,4-hydroquinone (TBHQ) after a brief refilling period that followed thrombin stimulation.
45	18439569	Platelet treatment with thrombin or thapsigargin in combination with ionomycin, to induce extensive Ca(2+) store depletion, resulted in a transient increase in the interaction between STIM1 and SERCA3, reaching a maximum 30 s after stimulation.
46	18439569	The coupling between STIM1 and SERCA3 was abolished by electrotransjection with anti-STIM1 antibody.
47	18439569	The interaction between STIM1 and SERCA3 induced by thrombin or by treatment with thapsigargin plus ionomycin is reduced in platelets from type 2 diabetic patients, as well as Ca(2+) reuptake into the acidic Ca(2+) stores.
48	18439569	These findings provide evidence for a role of STIM1 in acidic store refilling in platelets probably acting as a Ca(2+) sensor and regulating the activity of SERCA3.
49	18439569	STIM1 regulates acidic Ca2+ store refilling by interaction with SERCA3 in human platelets.
50	18439569	Electrotransjection of cells with anti-STIM1 (Y(231)-K(243)) antibody, directed towards a cytoplasmic sequence of STIM1, significantly reduced acidic store refilling, which was tested by remobilizing Ca(2+) from the acidic stores using 2,5-di-(t-butyl)-1,4-hydroquinone (TBHQ) after a brief refilling period that followed thrombin stimulation.
51	18439569	Platelet treatment with thrombin or thapsigargin in combination with ionomycin, to induce extensive Ca(2+) store depletion, resulted in a transient increase in the interaction between STIM1 and SERCA3, reaching a maximum 30 s after stimulation.
52	18439569	The coupling between STIM1 and SERCA3 was abolished by electrotransjection with anti-STIM1 antibody.
53	18439569	The interaction between STIM1 and SERCA3 induced by thrombin or by treatment with thapsigargin plus ionomycin is reduced in platelets from type 2 diabetic patients, as well as Ca(2+) reuptake into the acidic Ca(2+) stores.
54	18439569	These findings provide evidence for a role of STIM1 in acidic store refilling in platelets probably acting as a Ca(2+) sensor and regulating the activity of SERCA3.
55	18439569	STIM1 regulates acidic Ca2+ store refilling by interaction with SERCA3 in human platelets.
56	18439569	Electrotransjection of cells with anti-STIM1 (Y(231)-K(243)) antibody, directed towards a cytoplasmic sequence of STIM1, significantly reduced acidic store refilling, which was tested by remobilizing Ca(2+) from the acidic stores using 2,5-di-(t-butyl)-1,4-hydroquinone (TBHQ) after a brief refilling period that followed thrombin stimulation.
57	18439569	Platelet treatment with thrombin or thapsigargin in combination with ionomycin, to induce extensive Ca(2+) store depletion, resulted in a transient increase in the interaction between STIM1 and SERCA3, reaching a maximum 30 s after stimulation.
58	18439569	The coupling between STIM1 and SERCA3 was abolished by electrotransjection with anti-STIM1 antibody.
59	18439569	The interaction between STIM1 and SERCA3 induced by thrombin or by treatment with thapsigargin plus ionomycin is reduced in platelets from type 2 diabetic patients, as well as Ca(2+) reuptake into the acidic Ca(2+) stores.
60	18439569	These findings provide evidence for a role of STIM1 in acidic store refilling in platelets probably acting as a Ca(2+) sensor and regulating the activity of SERCA3.
61	18439569	STIM1 regulates acidic Ca2+ store refilling by interaction with SERCA3 in human platelets.
62	18439569	Electrotransjection of cells with anti-STIM1 (Y(231)-K(243)) antibody, directed towards a cytoplasmic sequence of STIM1, significantly reduced acidic store refilling, which was tested by remobilizing Ca(2+) from the acidic stores using 2,5-di-(t-butyl)-1,4-hydroquinone (TBHQ) after a brief refilling period that followed thrombin stimulation.
63	18439569	Platelet treatment with thrombin or thapsigargin in combination with ionomycin, to induce extensive Ca(2+) store depletion, resulted in a transient increase in the interaction between STIM1 and SERCA3, reaching a maximum 30 s after stimulation.
64	18439569	The coupling between STIM1 and SERCA3 was abolished by electrotransjection with anti-STIM1 antibody.
65	18439569	The interaction between STIM1 and SERCA3 induced by thrombin or by treatment with thapsigargin plus ionomycin is reduced in platelets from type 2 diabetic patients, as well as Ca(2+) reuptake into the acidic Ca(2+) stores.
66	18439569	These findings provide evidence for a role of STIM1 in acidic store refilling in platelets probably acting as a Ca(2+) sensor and regulating the activity of SERCA3.
67	19447651	Enhanced expression of STIM1/Orai1 and TRPC3 in platelets from patients with type 2 diabetes mellitus.
68	19447651	Expression of TRPC1, 3 and 6, STIM1 and Orai1 was analyzed by Western blotting in DM2 patients and controls.
69	19447651	We have found that expression of TRPC3, Orai1 and STIM1 is enhanced in DM2 subjects as compared to controls.
70	19447651	Enhanced expression of STIM1/Orai1 and TRPC3 in platelets from patients with type 2 diabetes mellitus.
71	19447651	Expression of TRPC1, 3 and 6, STIM1 and Orai1 was analyzed by Western blotting in DM2 patients and controls.
72	19447651	We have found that expression of TRPC3, Orai1 and STIM1 is enhanced in DM2 subjects as compared to controls.
73	19447651	Enhanced expression of STIM1/Orai1 and TRPC3 in platelets from patients with type 2 diabetes mellitus.
74	19447651	Expression of TRPC1, 3 and 6, STIM1 and Orai1 was analyzed by Western blotting in DM2 patients and controls.
75	19447651	We have found that expression of TRPC3, Orai1 and STIM1 is enhanced in DM2 subjects as compared to controls.
76	21270296	SOCE was observed in VSMCs lacking either S1P(2) or S1P(3) receptors, suggesting that S1P acts via multiple signaling pathways.
77	21270296	Finally, S1P-induced SOCE was larger in proliferative than in contractile VSMCs, correlating with increases in STIM1, Orai1, S1P(1), and S1P(3) receptor mRNA.
78	21678413	Resistin and endothelin-1 (ET-1) are upregulated in people with type II diabetes mellitus, central obesity, and hypertension.
79	21678413	Resistin-enhanced ET-1-increased Ca(2+) reactions were reversed by blockers of store-operated Ca(2+) entry (SOCE) and extracellular-signal-regulated kinase (ERK).
80	21678413	Furthermore, resistin-enhanced ET-1 Ca(2+) reactions and the resistin-dependent activation of SOCE were abolished under STIM1-siRNA treatment, indicating that STIM1 plays an important role in resistin-enhanced ET-1 Ca(2+) reactions in VSMCs.
81	21678413	Resistin appears to exert effects on ET-1-induced Ca(2+) increases by enhancing the activity of ERK-dependent SOCE (STIM1-partcipated), and may accelerate and prolong ET-1-increased blood pressure via the same pathway.
82	21678413	Resistin and endothelin-1 (ET-1) are upregulated in people with type II diabetes mellitus, central obesity, and hypertension.
83	21678413	Resistin-enhanced ET-1-increased Ca(2+) reactions were reversed by blockers of store-operated Ca(2+) entry (SOCE) and extracellular-signal-regulated kinase (ERK).
84	21678413	Furthermore, resistin-enhanced ET-1 Ca(2+) reactions and the resistin-dependent activation of SOCE were abolished under STIM1-siRNA treatment, indicating that STIM1 plays an important role in resistin-enhanced ET-1 Ca(2+) reactions in VSMCs.
85	21678413	Resistin appears to exert effects on ET-1-induced Ca(2+) increases by enhancing the activity of ERK-dependent SOCE (STIM1-partcipated), and may accelerate and prolong ET-1-increased blood pressure via the same pathway.
86	23527285	In the present study, we identified that the major endoplasmic reticulum stress (ERS) marker, Grp78 and ERS-induced apoptotic factor, CHOP, were time-dependently increased by exposure of β-TC3 cells to FFA.
87	23527285	The expression of ATF6 and the phosphorylation levels of PERK and IRE1, which trigger ERS signaling, markedly increased after FFA treatments.
88	23527285	We also found that FFA-induced ERS was mediated by the store-operated Ca(2+) entry through promoting the association of STIM1 and Orai1.
89	23527285	Moreover, calpain-2 was required for FFA-induced expression of CHOP and activation of caspase-12 and caspase-3, thus promoting cell apoptosis in β-TC3 cells.
90	23846758	Orai1 and STIM1 transcription is stimulated by NF-κB (nuclear factor kappa B).
91	23846758	Serum- and glucocorticoid-inducible kinase 1 (SGK1) up-regulates NF-κB-activity in megakaryocytes and thus Orai1-expression and SOCE in platelets.
92	23846758	Additional potential regulators of Orai1/STIM1 and thus SOCE in platelets include AMP activated kinase (AMPK), protein kinase A (PKA), reactive oxygen species, lipid rafts, pH and mitochondrial Ca2+ buffering.
93	23846758	Orai1 and STIM1 transcription is stimulated by NF-κB (nuclear factor kappa B).
94	23846758	Serum- and glucocorticoid-inducible kinase 1 (SGK1) up-regulates NF-κB-activity in megakaryocytes and thus Orai1-expression and SOCE in platelets.
95	23846758	Additional potential regulators of Orai1/STIM1 and thus SOCE in platelets include AMP activated kinase (AMPK), protein kinase A (PKA), reactive oxygen species, lipid rafts, pH and mitochondrial Ca2+ buffering.
96	23933686	SGK1 is activated by insulin and growth factors via phosphatidylinositol-3-kinase, 3-phosphoinositide dependent-kinase PDK1, and mTOR.
97	23933686	NCC, NKCC, NHE1, NHE3, SGLT1, several amino acid transporters) and many ion channels (e.g.
98	23933686	ENaC, SCN5A, TRPV4-6, Orai1/STIM1, ROMK, KCNE1/KCNQ1, GluR6, CFTR).
99	23933686	SGK1 further up-regulates a number of enzymes (e.g. glycogen-synthase-kinase-3, ubiquitin-ligase Nedd4-2), and transcription factors (e.g. forkhead-transcription-factor FOXO3a, β-catenin, nuclear-factor-kappa-B NFκB).