期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
卷 1865, 期 7, 页码 981-994出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbamcr.2018.04.007
关键词
TRP channel; MAMs; Alternate transcription; ER calcium fluxes; Mitochondria; Prostate cancer
资金
- INSERM
- Ministere de l'Education Nationale
- Region Nord-Pas-de-Calais
- SIRIC OncoLILLE
- Association de Recherche sur les Tumeurs de la Prostate
- Institut National du Cancer [INCa-PLBIO14-213]
- Fondation pour la recherche medicale
- IHU OepRa within the program Investissements d'Avenir [ANR-10-IBHU-004]
- Agence Nationale de la Recherche, ANR [10-EQPX-04-01]
- Ligue Contre le Cancer
Calcium (Ca2+) release from the endoplasmic reticulum plays an important role in many cell-fate defining cellular processes. Traditionally, this Ca2+ release was associated with the ER Ca2+ release channels, inositol 1,4,5-triphosphate receptor (IP3R) and ryanodine receptor (RyR). Lately, however, other calcium conductances have been found to be intracellularly localized and to participate in cell fate regulation. Nonetheless, molecular identity and functional properties of the ER Ca2+ release mechanisms associated with multiple diseases, e.g. prostate cancer, remain unknown. Here we identify a new family of transient receptor potential melastatine 8(TRPM8) channel isoforms as functional ER Ca2+ release channels expressed in mitochondria-associated ER membranes (MAMs). These TRPM8 isoforms exhibit an unconventional structure with 4 transmembrane domains (TMs) instead of 6 TMs characteristic of the TRP channel archetype. We show that these 4TM-TRPM8 isoforms form functional channels in the ER and participate in regulation of the steady-state Ca2+ concentration ([Ca2+]) in mitochondria and the ER. Thus, our study identifies 4TM-TRPM8 isoforms as ER Ca2+ release mechanism distinct from classical Ca(2+)release channels.
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