The STIM1-Orai1 pathway of store-operated Ca2+ entry controls the checkpoint in cell cycle G1/S transition.

ABSTRACT: Ca(2+) signaling is important to trigger the cell cycle progression, while it remains elusive in the regulatory mechanisms. Here we show that store-operated Ca(2+) entry (SOCE), mediated by the interaction between STIM1 (an endoplasmic reticulum Ca(2+) sensor) and Orai1 (a cell membrane pore structure), controls the specific checkpoint of cell cycle. The fluctuating SOCE activity during cell cycle progression is universal in different cell types, in which SOCE is upregulated in G1/S transition and downregulated from S to G2/M transition. Pharmacological or siRNA inhibition of STIM1-Orai1 pathway of SOCE inhibits the phosphorylation of CDK2 and upregulates the expression of cyclin E, resulting in autophagy accompanied with cell cycle arrest in G1/S transition. The subsequently transient exp

SUBMITTER: Chen YW 

PROVIDER: S-EPMC4768259 | biostudies-literature | 2016 Feb

REPOSITORIES: biostudies-literature