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PMID |
Sentence |
1 |
28424242
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mTORC1 Promotes T-bet Phosphorylation To Regulate Th1 Differentiation.
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2 |
28424242
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CD4+ T cells lacking the mTORC1 activator Rheb fail to secrete IFN-γ under Th1 polarizing conditions.
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3 |
28424242
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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.
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4 |
28424242
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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.
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5 |
28424242
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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.
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6 |
28424242
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The reduced activity of the triple mutant T-bet is associated with its failure to recruit chromatin remodeling complexes to the Ifng gene promoter.
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7 |
28424242
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These results establish a novel mechanism by which mTORC1 regulates Th1 differentiation, through control of T-bet phosphorylation.
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