Regulatory mechanisms of the store-operated Ca 2+ entry through Orai1 and STIM1 by an adaptor protein in non-excitable cells
10.11620/IJOB.2022.47.3.33
- Author:
Jung Yun KANG
1
;
Yu-Mi YANG
Author Information
1. Department of Dental Hygiene, College of Software Digital Healthcare Convergence, Yonsei University, Wonju 26493, Republic of Korea
- Publication Type:Original Article
- From:International Journal of Oral Biology
2022;47(3):33-40
- CountryRepublic of Korea
- Language:English
-
Abstract:
Store-operated Ca 2+ entry (SOCE) represents one of the major Ca 2+ entry routes in non-excitable cells. It is involved in a variety of fundamental biological processes and the maintenance of Ca 2+ homeostasis. The Ca 2+ releaseactivated Ca 2+ (CRAC) channel consists of stromal interaction molecule and Orai; however, the role and action of Homer proteins as an adaptor protein to SOCE-mediated Ca 2+ signaling through the activation of CRAC channels in non-excitable cells still remain unknown. In the present study, we investigated the role of Homer2 in the process of Ca 2+ signaling induced by the interaction between CRACs and Homer2 proteins in non-excitable cells. The response to Ca 2+ entry by thapsigargin-mediated Ca 2+ store depletion remarkably decreased in pancreatic acinar cells of Homer2 –/– mice, as compared to wild-type cells. It also showed critical differences in regulated patterns by the specific blockers of SOCE in pancreatic acinar cells of Homer2 –/–mice. The response to Ca 2+ entry by the depletion in Ca 2+ store markedly increased in the cellular overexpression of Orai1 and STIM1 as compared to the overexpression of Homer2 in cells; however, this response was remarkably inhibited by the overexpression of Orai1, STIM1, and Homer2. These results suggest that Homer2 has a critical role in the regulatory action of SOCE activity and the interactions between CRAC channels.
