TY - JOUR
T1 - Store-operated Ca2+ entry
T2 - Evidence for a secretion-like coupling model
AU - Patterson, Randen L.
AU - Van Rossum, Damian B.
AU - Gill, Donald L.
N1 - Funding Information:
We greatly thank Paul Luther for assistance in confocal microscopy; Andrjez Janecki for advice on immunostaining; Phillip Crews for generously providing JP and LatA; Mark Donowitz, Carmen Ufret-Vincenty, and Michele Stone for assistance early in the project; Molly-Rose Arnstein for expert graphics; and Sheila Burbidge for inspiration. The work was supported by National Institutes of Health grant HL55426 and a Grant-In-Aid from the American Heart Association, Maryland Affiliate.
PY - 1999/8/20
Y1 - 1999/8/20
N2 - The elusive coupling between endoplasmic reticulum (ER) Ca2+ stores and plasma membrane (PM) "store-operated" Ca2+ entry channels was probed through a novel combination of cytoskeletal modifications. Whereas coupling was unaffected by disassembly of the actin cytoskeleton, in situ redistribution of F-actin into a tight cortical layer subjacent to the PM displaced cortical ER and prevented coupling between ER and PM Ca2+ entry channels, while not affecting inositol 1,4,5-trisphosphate-mediated store release. Importantly, disassembly of the induced cortical actin layer allowed ER to regain access to the PM and reestablish coupling of Ca2+ entry channels to Ca2+ store depletion. Coupling is concluded to be mediated by a physical "secretion-like" mechanism involving close but reversible interactions between the ER and the PM.
AB - The elusive coupling between endoplasmic reticulum (ER) Ca2+ stores and plasma membrane (PM) "store-operated" Ca2+ entry channels was probed through a novel combination of cytoskeletal modifications. Whereas coupling was unaffected by disassembly of the actin cytoskeleton, in situ redistribution of F-actin into a tight cortical layer subjacent to the PM displaced cortical ER and prevented coupling between ER and PM Ca2+ entry channels, while not affecting inositol 1,4,5-trisphosphate-mediated store release. Importantly, disassembly of the induced cortical actin layer allowed ER to regain access to the PM and reestablish coupling of Ca2+ entry channels to Ca2+ store depletion. Coupling is concluded to be mediated by a physical "secretion-like" mechanism involving close but reversible interactions between the ER and the PM.
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U2 - 10.1016/S0092-8674(00)81977-7
DO - 10.1016/S0092-8674(00)81977-7
M3 - Article
C2 - 10481913
AN - SCOPUS:0033587804
SN - 0092-8674
VL - 98
SP - 487
EP - 499
JO - Cell
JF - Cell
IS - 4
ER -