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Gimap5-dependent inactivation of GSK3β is required for CD4

Nature communications (2018-02-01)
Andrew R Patterson, Mehari Endale, Kristin Lampe, Halil I Aksoylar, Aron Flagg, Jim R Woodgett, David Hildeman, Michael B Jordan, Harinder Singh, Zeynep Kucuk, Jack Bleesing, Kasper Hoebe
ABSTRACT

GTPase of immunity-associated protein 5 (Gimap5) is linked with lymphocyte survival, autoimmunity, and colitis, but its mechanisms of action are unclear. Here, we show that Gimap5 is essential for the inactivation of glycogen synthase kinase-3β (GSK3β) following T cell activation. In the absence of Gimap5, constitutive GSK3β activity constrains c-Myc induction and NFATc1 nuclear import, thereby limiting productive CD4

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BIO, ≥98% (HPLC)