Comment
doi: 10.1073/pnas.96.26.14669.
TRP, inositol 1,4,5-trisphosphate receptors, and capacitative calcium entry
Affiliations
- PMID: 10611268
- PMCID: PMC33952
- DOI: 10.1073/pnas.96.26.14669
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Comment
TRP, inositol 1,4,5-trisphosphate receptors, and capacitative calcium entry
Proc Natl Acad Sci U S A.
.
No abstract available
Figures
Model for regulation of capacitative calcium entry channels by
IP3 receptors. Agonist activation of a surface membrane
receptor (R), perhaps through a heterotrimeric G-protein (G),
activates phospholipase C (PLC), leading to the production of the
calcium-mobilizing messenger, IP3. IP3 releases
calcium from a critical endoplasmic reticulum store. The fall in
luminal calcium in this store causes a conformational change in an
IP3 receptor that interacts with a TRP subunit of the
capacitative calcium entry channel, causing it to open. A signaling
complex containing the PLC, TRP, and IP3 receptor may
require an as yet uncharacterized scaffolding protein, perhaps
similar to InaD. The close spatial arrangement of this signaling
complex results in a constant supply of IP3 from basal PLC
activity for the IP3 receptor, such that IP3
levels are not normally limiting; rather, it is depletion of calcium
from the specific intracellular store that provides the critical signal
for channel activation.
Comment on
-
Modulation of Ca(2+) entry by polypeptides of the inositol 1,4, 5-trisphosphate receptor (IP3R) that bind transient receptor potential (TRP): evidence for roles of TRP and IP3R in store depletion-activated Ca(2+) entry.Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):14955-60. doi: 10.1073/pnas.96.26.14955. Proc Natl Acad Sci U S A. 1999. PMID: 10611319 Free PMC article.
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