Ignet

Gene Information

Gene symbol: T

Gene name: T, brachyury homolog (mouse)

HGNC ID: 11515

Related Genes

#	Gene Symbol	Number of hits
1	CD4	1 hits
2	CD8A	1 hits
3	GZMB	1 hits
4	IFNG	1 hits
5	IL17C	1 hits
6	INS	1 hits
7	STAT1	1 hits
8	TBX21	1 hits
9	TCF7L2	1 hits
10	TGFB1	1 hits

Related Sentences

#	PMID	Sentence
1	15096540	T-bet controls autoaggressive CD8 lymphocyte responses in type 1 diabetes.
2	15096540	The T-box transcription factor T-bet is known to control lineage commitment and interferon-gamma production by T helper 1 (Th1) CD4 lymphocytes.
3	15096540	We report here that T-bet is essential for development of CD8 lymphocyte-dependent autoimmune diabetes (type 1 diabetes [T1D]) in the rat insulin promoter-lymphocytic choriomeningitis virus (LCMV) transgenic model for virally induced T1D.
4	15096540	In the absence of T-bet, autoaggressive (anti-LCMV) CD8 lymphocytes were reduced in number and produced less IFN-gamma, but increased IL-2 compared with controls.
5	15096540	Further analysis showed that T-bet intrinsically controls the generation, but not apoptosis, maintenance, or secondary expansion of antiviral effector/memory CD8 lymphocytes.
6	16888219	In the pancreas of VIP-treated animals, regulatory T cell markers predominate, as indicated by the upregulation of FoxP3 and transforming growth factor-beta (TGF-beta), and the downregulation of the transcription factor, T-bet.
7	21965303	The transcription factor T-cell factor 7-like 2 (TCF7L2) confers type 2 diabetes risk mainly through impaired insulin secretion, perturbed incretin effect and reduced beta-cell survival.
8	21965303	TCF7L2 binds to 3646 gene promoters in INS-1 cells in high or low glucose, including Tp53, Pten, Uggt1, Adamts9 and Fto.
9	21965303	SiRNA-mediated reduction in TCF7L2 activity resulted in increased apoptosis and increased expression of Tp53, which resulted in elevated p53 protein activity and an increased expression of the p53 target gene Tp53inp1 (encoding p53-induced-nuclear-protein 1).
10	21965303	These results identify the p53-p53INP1 pathway as a molecular mechanism through which TCF7L2 may affect beta-cell survival and established a molecular link between Tcf7l2 and two type 2 diabetes-associated genes, Tp53inp1 and Adamts9.
11	23479229	IL-21 promotes CD8+ CTL activity via the transcription factor T-bet.
12	23479229	IL-21 is an IL-2 family cytokine and a growth factor for multiple lymphocyte effector lineages, including cytotoxic CD8(+) T cells.
13	23479229	This is most likely the result of impaired CD8(+) CTL function in the absence of IL-21 signaling.
14	23479229	Currently, the mechanisms by which IL-21 promotes CTL differentiation in CD8(+) T cells remain unclear, particularly the identity of the relevant transcription factor(s).
15	23479229	We demonstrate that IL-21 induces the expression of the transcription factor T-bet in CD8(+) T cells, predominantly via STAT1, and that T-bet is required for the induction of cytolytic molecules, including perforin and granzyme B in response to IL-21.
16	23479229	Finally, we show that IL-21-induced CTL function is T-bet dependent, as T-bet deficiency results in defective IL-21-dependent cytotoxicity in CD8(+) T cells in vitro and in vivo.
17	23479229	Thus, IL-21 drives CD8(+) CTL differentiation via the actions of the transcription factor T-bet.
18	23479229	IL-21 promotes CD8+ CTL activity via the transcription factor T-bet.
19	23479229	IL-21 is an IL-2 family cytokine and a growth factor for multiple lymphocyte effector lineages, including cytotoxic CD8(+) T cells.
20	23479229	This is most likely the result of impaired CD8(+) CTL function in the absence of IL-21 signaling.
21	23479229	Currently, the mechanisms by which IL-21 promotes CTL differentiation in CD8(+) T cells remain unclear, particularly the identity of the relevant transcription factor(s).
22	23479229	We demonstrate that IL-21 induces the expression of the transcription factor T-bet in CD8(+) T cells, predominantly via STAT1, and that T-bet is required for the induction of cytolytic molecules, including perforin and granzyme B in response to IL-21.
23	23479229	Finally, we show that IL-21-induced CTL function is T-bet dependent, as T-bet deficiency results in defective IL-21-dependent cytotoxicity in CD8(+) T cells in vitro and in vivo.
24	23479229	Thus, IL-21 drives CD8(+) CTL differentiation via the actions of the transcription factor T-bet.
25	23479229	IL-21 promotes CD8+ CTL activity via the transcription factor T-bet.
26	23479229	IL-21 is an IL-2 family cytokine and a growth factor for multiple lymphocyte effector lineages, including cytotoxic CD8(+) T cells.
27	23479229	This is most likely the result of impaired CD8(+) CTL function in the absence of IL-21 signaling.
28	23479229	Currently, the mechanisms by which IL-21 promotes CTL differentiation in CD8(+) T cells remain unclear, particularly the identity of the relevant transcription factor(s).
29	23479229	We demonstrate that IL-21 induces the expression of the transcription factor T-bet in CD8(+) T cells, predominantly via STAT1, and that T-bet is required for the induction of cytolytic molecules, including perforin and granzyme B in response to IL-21.
30	23479229	Finally, we show that IL-21-induced CTL function is T-bet dependent, as T-bet deficiency results in defective IL-21-dependent cytotoxicity in CD8(+) T cells in vitro and in vivo.
31	23479229	Thus, IL-21 drives CD8(+) CTL differentiation via the actions of the transcription factor T-bet.
32	23562076	Improved insulin sensitivity despite increased visceral adiposity in mice deficient for the immune cell transcription factor T-bet.
33	23562076	We report that mice deficient in the immune cell transcription factor T-bet have lower energy expenditure and increased visceral fat compared with wild-type mice, yet paradoxically are more insulin sensitive.
34	23562076	Indeed, adoptive transfer of T-bet-deficient, but not wild-type, CD4(+) T cells to Rag2(-/-) mice improved insulin sensitivity.
35	23562076	Our results reveal a role for T-bet in metabolic physiology and obesity-associated insulin resistance.
36	23562076	Improved insulin sensitivity despite increased visceral adiposity in mice deficient for the immune cell transcription factor T-bet.
37	23562076	We report that mice deficient in the immune cell transcription factor T-bet have lower energy expenditure and increased visceral fat compared with wild-type mice, yet paradoxically are more insulin sensitive.
38	23562076	Indeed, adoptive transfer of T-bet-deficient, but not wild-type, CD4(+) T cells to Rag2(-/-) mice improved insulin sensitivity.
39	23562076	Our results reveal a role for T-bet in metabolic physiology and obesity-associated insulin resistance.