期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 100, 期 5, 页码 2975-2980出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0536590100
关键词
hepatocytes; liver; inositol 1,4,5-trisphosphate; intracellular calcium signals; HepG2 cells
资金
- FIC NIH HHS [TW01452] Funding Source: Medline
- NIDDK NIH HHS [DK45710, P30 DK034989, DK57751, R01 DK045710, P01 DK057751] Funding Source: Medline
- NIGMS NIH HHS [GM51480] Funding Source: Medline
Nuclear calcium (Ca2+) regulates a number of important cellular processes, including gene transcription, growth, and apoptosis. However, it is unclear whether Ca2+ signaling is regulated differently in the nucleus and cytosol. To investigate this possibility, we examined subcellular mechanisms of Ca2+ release in the HepG2 liver cell line. The type II isoform of the inositol 1,4,5-trisphosphate (InsP(3)) receptor (InsP(3)R) was expressed to a similar extent in the endoplasmic reticulum and nucleus, whereas the type III InsP(3)R was concentrated in the endoplasmic reticulum, and the type I isoform was not expressed. Ca2+ signals induced by low InsP(3) concentrations started earlier or were larger in the nucleus than in the cytosol, indicating higher sensitivity of nuclear Ca2+ stores for InsP(3). Nuclear InsP(3)R channels were active at lower InsP(3) concentrations than InsP(3)R from cytosol. Enriched expression of type II InsP(3)R in the nucleus results in greater sensitivity of the nucleus to InsP(3), thus providing a mechanism for independent regulation of Ca2+-dependent processes in this cellular compartment.
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