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- W2149507105 abstract "Abstract In β-selection, surface-expression of a pre-T cell receptor (pre-TCR) induces thymocyte metabolic activation, proliferation, survival and differentiation. This pivotal αβ T cell fate-determining event requires co-stimulatory Notch signals. Here, we show that this Notch dependence is enforced through antagonistic signaling by inositol-trisphosphate 3-kinase B (Itpkb) and phosphoinositide 3-kinase (PI3K). Itpkb produces soluble inositol-tetrakisphosphate which competes with the PI3K lipid-product PIP3 for binding to the effector-kinase Akt. Itpkb-/- thymocytes are pre-TCR hyperresponsive, hyperactivate Akt, downstream mTOR and metabolism, undergo an accelerated β-selection and can develop to CD4+CD8+ cells without Notch. This is reversed by inhibition of Akt, mTOR or glucose-metabolism. Thus, Itpkb restricts pre-TCR induced metabolic activation to enforce coincidence-detection of pre-TCR expression and Notch-engagement, and to prevent premature thymocyte maturation." @default.
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- W2149507105 date "2015-05-01" @default.
- W2149507105 modified "2023-10-18" @default.
- W2149507105 title "Metabolic inhibition by inositol-tetrakisphosphate delays thymocyte β-selection and renders it Notch-dependent (HEM2P.241)" @default.
- W2149507105 doi "https://doi.org/10.4049/jimmunol.194.supp.51.11" @default.
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