期刊
CELL CALCIUM
卷 39, 期 1, 页码 65-73出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.ceca.2005.09.010
关键词
ryanodine receptor; nuclear signaling; nucleoplasmic reticulum; C2Cl2; channel
类别
资金
- FIC NIH HHS [TW01451] Funding Source: Medline
- NIDDK NIH HHS [DK57751, DK45710, DK61747] Funding Source: Medline
- NIGMS NIH HHS [GM63496] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK061747, P01DK057751, R01DK045710, R29DK045710] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM063496] Funding Source: NIH RePORTER
Ca2+ signals control DNA synthesis and repair, gene transcription, and other cell functions that occur within the nucleus. The nuclear envelope can store Ca2+ and release it into the nucleus via either the inositol 1,4,5-trisphosphate receptor (InsP3R) or the ryanodine receptor (RyR). Furthermore, many cell types have a reticular network within their nuclei and InsP3Rs on this nucleoplasmic reticulum permit local subnuclear control of Ca2+ signals and Ca2+-dependent intranuclear events. However, it is unknown whether RyR similarly is expressed on the nucleoplasmic reticulum and can control subnuclear Ca2+ signals. Here we report that the type 1 RyR is expressed on intranuclear extensions of the sarcoplasmic reticulum of C2C12 cells, a skeletal muscle derived cell line. In addition, two-photon photorelease of caged Ca2+ in the region of the nucleoplasmic reticulum evoked Ca2+-induced Ca2+ release (CICR) within the nucleus, which could be suppressed by the RyR inhibitor dantrolene. These results show that intranuclear extensions of the nuclear envelope have functional RyR and provide a possible mechanism whereby cells expressing RyR can regulate Ca2+ signals in discrete regions within the nucleus. (c) 2005 Elsevier Ltd. All rights reserved.
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