Regulatory mechanisms of the store-operated Ca2+ entry through Orai1 and STIM1 by an adaptor protein in non-excitable cells

서지정보

ㆍ발행기관 : 대한구강생물학회 ㆍ수록지정보 : International Journal of Oral Biology / 47권 / 3호
ㆍ저자명 : Jung Yun Kang, Yu-Mi Yang

목차

Introduction
Materials and Methods
1. 재료
2. 실험동물
3. 췌장의 선세포 분리
4. 세포 배양 및 플라즈미드 DNA 형질 주입(transfection)
5. [Ca2+]i 측정
6. 실험자료의 통계 분석
Results
1. 췌장 선세포에서 Homer2에 의한 SOCE 변화 양상
2. Homer2에 의한 CRAC 채널의 활성과 SOCE 반응의 조절
Discussion
Acknowledgements
Conflicts of Interest
References

영어 초록

Store-operated Ca2+ entry (SOCE) represents one of the major Ca2+ entry routes in non-excitable cells. It is involved in a variety of fundamental biological processes and the maintenance of Ca2+ homeostasis. The Ca2+ releaseactivated Ca2+ (CRAC) channel consists of stromal interaction molecule and Orai; however, the role and action of Homer proteins as an adaptor protein to SOCE-mediated Ca2+ 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 Ca2+ signaling induced by the interaction between CRACs and Homer2 proteins in non-excitable cells. The response to Ca2+ entry by thapsigargin-mediated Ca2+ 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 Ca2+ entry by the depletion in Ca2+ 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.

참고 자료

없음