Ignet

Gene Information

Gene symbol: CRTC1

Gene name: CREB regulated transcription coactivator 1

HGNC ID: 16062

Synonyms: KIAA0616, FLJ14027, TORC1

Related Genes

#	Gene Symbol	Number of hits
1	CD4	1 hits
2	RHEB	1 hits
3	T	1 hits
4	TBX21	1 hits
5	TH1L	1 hits

Related Sentences

#	PMID	Sentence
1	28424242	mTORC1 Promotes T-bet Phosphorylation To Regulate Th1 Differentiation.
2	28424242	mTORC1 Promotes T-bet Phosphorylation To Regulate Th1 Differentiation.
3	28424242	mTORC1 Promotes T-bet Phosphorylation To Regulate Th1 Differentiation.
4	28424242	mTORC1 Promotes T-bet Phosphorylation To Regulate Th1 Differentiation.
5	28424242	mTORC1 Promotes T-bet Phosphorylation To Regulate Th1 Differentiation.
6	28424242	mTORC1 Promotes T-bet Phosphorylation To Regulate Th1 Differentiation.
7	28424242	CD4⁺ T cells lacking the mTORC1 activator Rheb fail to secrete IFN-γ under Th1 polarizing conditions.
8	28424242	CD4⁺ T cells lacking the mTORC1 activator Rheb fail to secrete IFN-γ under Th1 polarizing conditions.
9	28424242	CD4⁺ T cells lacking the mTORC1 activator Rheb fail to secrete IFN-γ under Th1 polarizing conditions.
10	28424242	CD4⁺ T cells lacking the mTORC1 activator Rheb fail to secrete IFN-γ under Th1 polarizing conditions.
11	28424242	CD4⁺ T cells lacking the mTORC1 activator Rheb fail to secrete IFN-γ under Th1 polarizing conditions.
12	28424242	CD4⁺ T cells lacking the mTORC1 activator Rheb fail to secrete IFN-γ under Th1 polarizing conditions.
13	28424242	We hypothesized that this phenotype is due to defects in regulation of the canonical Th1 transcription factor T-bet at the level of protein phosphorylation downstream of mTORC1.
14	28424242	We hypothesized that this phenotype is due to defects in regulation of the canonical Th1 transcription factor T-bet at the level of protein phosphorylation downstream of mTORC1.
15	28424242	We hypothesized that this phenotype is due to defects in regulation of the canonical Th1 transcription factor T-bet at the level of protein phosphorylation downstream of mTORC1.
16	28424242	We hypothesized that this phenotype is due to defects in regulation of the canonical Th1 transcription factor T-bet at the level of protein phosphorylation downstream of mTORC1.
17	28424242	We hypothesized that this phenotype is due to defects in regulation of the canonical Th1 transcription factor T-bet at the level of protein phosphorylation downstream of mTORC1.
18	28424242	We hypothesized that this phenotype is due to defects in regulation of the canonical Th1 transcription factor T-bet at the level of protein phosphorylation downstream of mTORC1.
19	28424242	By analyzing activated murine wild-type and Rheb-deficient CD4⁺ T cells, as well as murine CD4⁺ T cells activated in the presence of rapamycin, a pharmacologic inhibitor of mTORC1, we were able to identify six T-bet phosphorylation sites.
20	28424242	By analyzing activated murine wild-type and Rheb-deficient CD4⁺ T cells, as well as murine CD4⁺ T cells activated in the presence of rapamycin, a pharmacologic inhibitor of mTORC1, we were able to identify six T-bet phosphorylation sites.
21	28424242	By analyzing activated murine wild-type and Rheb-deficient CD4⁺ T cells, as well as murine CD4⁺ T cells activated in the presence of rapamycin, a pharmacologic inhibitor of mTORC1, we were able to identify six T-bet phosphorylation sites.
22	28424242	By analyzing activated murine wild-type and Rheb-deficient CD4⁺ T cells, as well as murine CD4⁺ T cells activated in the presence of rapamycin, a pharmacologic inhibitor of mTORC1, we were able to identify six T-bet phosphorylation sites.
23	28424242	By analyzing activated murine wild-type and Rheb-deficient CD4⁺ T cells, as well as murine CD4⁺ T cells activated in the presence of rapamycin, a pharmacologic inhibitor of mTORC1, we were able to identify six T-bet phosphorylation sites.
24	28424242	By analyzing activated murine wild-type and Rheb-deficient CD4⁺ T cells, as well as murine CD4⁺ T cells activated in the presence of rapamycin, a pharmacologic inhibitor of mTORC1, we were able to identify six T-bet phosphorylation sites.
25	28424242	Five of these are novel, and four sites are consistently dephosphorylated in both Rheb-deficient CD4⁺ T cells and T cells treated with rapamycin, suggesting mTORC1 signaling controls their phosphorylation.
26	28424242	Five of these are novel, and four sites are consistently dephosphorylated in both Rheb-deficient CD4⁺ T cells and T cells treated with rapamycin, suggesting mTORC1 signaling controls their phosphorylation.
27	28424242	Five of these are novel, and four sites are consistently dephosphorylated in both Rheb-deficient CD4⁺ T cells and T cells treated with rapamycin, suggesting mTORC1 signaling controls their phosphorylation.
28	28424242	Five of these are novel, and four sites are consistently dephosphorylated in both Rheb-deficient CD4⁺ T cells and T cells treated with rapamycin, suggesting mTORC1 signaling controls their phosphorylation.
29	28424242	Five of these are novel, and four sites are consistently dephosphorylated in both Rheb-deficient CD4⁺ T cells and T cells treated with rapamycin, suggesting mTORC1 signaling controls their phosphorylation.
30	28424242	Five of these are novel, and four sites are consistently dephosphorylated in both Rheb-deficient CD4⁺ T cells and T cells treated with rapamycin, suggesting mTORC1 signaling controls their phosphorylation.
31	28424242	The reduced activity of the triple mutant T-bet is associated with its failure to recruit chromatin remodeling complexes to the Ifng gene promoter.
32	28424242	The reduced activity of the triple mutant T-bet is associated with its failure to recruit chromatin remodeling complexes to the Ifng gene promoter.
33	28424242	The reduced activity of the triple mutant T-bet is associated with its failure to recruit chromatin remodeling complexes to the Ifng gene promoter.
34	28424242	The reduced activity of the triple mutant T-bet is associated with its failure to recruit chromatin remodeling complexes to the Ifng gene promoter.
35	28424242	The reduced activity of the triple mutant T-bet is associated with its failure to recruit chromatin remodeling complexes to the Ifng gene promoter.
36	28424242	The reduced activity of the triple mutant T-bet is associated with its failure to recruit chromatin remodeling complexes to the Ifng gene promoter.
37	28424242	These results establish a novel mechanism by which mTORC1 regulates Th1 differentiation, through control of T-bet phosphorylation.
38	28424242	These results establish a novel mechanism by which mTORC1 regulates Th1 differentiation, through control of T-bet phosphorylation.
39	28424242	These results establish a novel mechanism by which mTORC1 regulates Th1 differentiation, through control of T-bet phosphorylation.
40	28424242	These results establish a novel mechanism by which mTORC1 regulates Th1 differentiation, through control of T-bet phosphorylation.
41	28424242	These results establish a novel mechanism by which mTORC1 regulates Th1 differentiation, through control of T-bet phosphorylation.
42	28424242	These results establish a novel mechanism by which mTORC1 regulates Th1 differentiation, through control of T-bet phosphorylation.