STIM1 controls calcineurin/Akt/mTOR/NFATC2-mediated osteoclastogenesis induced by RANKL/M-CSF.

ABSTRACT: Store-operated Ca²⁺ entry (SOCE) is the stable calcium channel influx in most cells. It consists of the cytoplasmic ion channel ORAI and endoplasmic reticulum receptor stromal interaction molecule 1 (STIM1). Abolition of SOCE function due to ORAI1 and STIM1 gene defects may cause non-perspiration, ectoderm dysplasia and skeletal malformations with severe combined immunodeficiency (CID). Calcineurin/mammalian target of rapamycin (mTOR)/nuclear factor of activated T cells 2 (NFATC2) is an important signalling cascade for osteoclast development. Calcineurin is activated by Ca²⁺ via SOCE during osteoclastogenesis, which is induced by receptor activator of NF-κB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). However, the underlying mechanism has remained

SUBMITTER: Huang Y 

PROVIDER: S-EPMC7388407 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature