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14-3-3 Proteins Regulate Akt Thr308 Phosphorylation in Intestinal Epithelial Cells

14-3-3 Proteins Regulate Akt Thr308 Phosphorylation in Intestinal Epithelial Cells

M Gómez-Suárez, I Z Gutiérrez-Martínez, J A Hernández-Trejo, M Hernández-Ruiz, D Suárez-Pérez, A Candelario, R Kamekura, O Medina-Contreras, M Schnoor, V Ortiz-Navarrete, N Villegas-Sepúlveda, C Parkos, etc.

Cell Death Differ. 2016 Jun;23(6):1060-72.

PMID: 26846144

Abstract:

Akt activation has been associated with proliferation, differentiation, survival and death of epithelial cells. Phosphorylation of Thr308 of Akt by phosphoinositide-dependent kinase 1 (PDK1) is critical for optimal stimulation of its kinase activity. However, the mechanism(s) regulating this process remain elusive. Here, we report that 14-3-3 proteins control Akt Thr308 phosphorylation during intestinal inflammation. Mechanistically, we found that IFNγ and TNFα treatment induce degradation of the PDK1 inhibitor, 14-3-3η, in intestinal epithelial cells. This mechanism requires association of 14-3-3ζ with raptor in a process that triggers autophagy and leads to 14-3-3η degradation. Notably, inhibition of 14-3-3 function by the chemical inhibitor BV02 induces uncontrolled Akt activation, nuclear Akt accumulation and ultimately intestinal epithelial cell death. Our results suggest that 14-3-3 proteins control Akt activation and regulate its biological functions, thereby providing a new mechanistic link between cell survival and apoptosis of intestinal epithelial cells during inflammation.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP292870532	BV02		292870-53-2	Price

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