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Vol. 9, Issue 6, 1465-1478, June 1998
and
Rat basophilic leukemia (RBL-2H3) cells predominantly express the
type II receptor for inositol 1,4,5-trisphosphate
(InsP3), which operates as an InsP3-gated
calcium channel. In these cells, cross-linking the high-affinity
immunoglobulin E receptor (FcDepartment of Pathology and Cancer Research and
Treatment Center, University of New Mexico, Albuquerque, New Mexico
87131; and
Department of Pharmacology, College of
Medicine, State University of New York Health Science Center at
Syracuse, Syracuse, New York 13210
R1) leads to activation of
phospholipase C 
isoforms via tyrosine kinase- and
phosphatidylinositol 3-kinase-dependent pathways, release of
InsP3-sensitive intracellular Ca2+ stores, and
a sustained phase of Ca2+ influx. These events are
accompanied by a redistribution of type II InsP3 receptors
within the endoplasmic reticulum and nuclear envelope, from a diffuse
pattern with a few small aggregates in resting cells to large isolated
clusters after antigen stimulation. Redistribution of type II
InsP3 receptors is also seen after treatment of RBL-2H3
cells with ionomycin or thapsigargin. InsP3 receptor clustering occurs within 5-10 min of stimulus and persists for up to
1 h in the presence of antigen. Receptor clustering is independent of endoplasmic reticulum vesiculation, which occurs only at ionomycin concentrations >1 µM, and maximal clustering responses are dependent on the presence of extracellular calcium. InsP3 receptor
aggregation may be a characteristic cellular response to
Ca2+-mobilizing ligands, because similar results are seen
after activation of phospholipase C-linked G-protein-coupled receptors;
cholecystokinin causes type II receptor redistribution in rat
pancreatoma AR4-2J cells, and carbachol causes type III receptor
redistribution in muscarinic receptor-expressing hamster lung
fibroblast E36M3R cells. Stimulation of these three cell
types leads to a reduction in InsP3 receptor levels only in
AR4-2J cells, indicating that receptor clustering does not correlate
with receptor down-regulation. The calcium-dependent aggregation of
InsP3 receptors may contribute to the previously observed
changes in affinity for InsP3 in the presence of elevated
Ca2+ and/or may establish discrete regions within refilled
stores with varying capacity to release Ca2+ when a
subsequent stimulus results in production of InsP3.
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