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Nuclear calcium signalling

delete2000-03-01
delete94
PRE
AI
B
Bootman, MD *
D
David G. Thomas
S
Stephen C. Tovey
M
Michael J. Berridge
P
Peter Lipp
DOI：10.1007/PL00000699delete
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Abstract

Abstract

En 中文
The topic of nuclear Ca2+ signalling is beset by discrepant observations of substantial nuclear/cytoplasmic gradients. The reasons why some labs have recorded such gradients, whilst other workers see equilibration of Ca-cyt(2+) and Ca-nuc(2+) using the same cells and techniques, is unexplained. Furthermore, how such gradients could arise across the NE that possesses many highly-conductive NPCs is a mystery. Although nuclei may have the capacity to be autonomous signalling entities, with functional Ca2+ release channels and an inositide cycle, the balance of evidence suggests that Ca2+ release on the inner NE does not occur during physiological stimulation. Our work suggests that elementary Ca2+ release events originating in the cytoplasm can give rise to Ca-nuc(2+) signals without causing elevation of the bulk cytoplasm. Clearly, the many Ca2+ signalling mechanisms that may impinge on Ca-nuc(2+) will remain a topic of controversy and debate for some time.
Keywords:
INOSITOL 1,4,5-TRISPHOSPHATE
CYTOPLASMIC CALCIUM
CYTOSOLIC CA2+
HELA-CELLS
STARFISH OOCYTES
GENE-REGULATION
PORE COMPLEX
3T3 CELLS
ENVELOPE
STORES

Journal

Cellular and Molecular Life Sciences cover
Cellular and Molecular Life Sciences
IF:
6.2
Papers:
9.1K
Citations:
4.0W

Organization

No organization information available