PMID- 18400989
OWN - NLM
STAT- MEDLINE
DCOM- 20080717
LR  - 20200930
IS  - 0363-6143 (Print)
IS  - 0363-6143 (Linking)
VI  - 294
IP  - 6
DP  - 2008 Jun
TI  - Enhanced exocytotic-like insertion of Orai1 into the plasma membrane upon 
      intracellular Ca2+ store depletion.
PG  - C1323-31
LID - 10.1152/ajpcell.00071.2008 [doi]
AB  - Ca+ release-activated Ca2+ (CRAC) channels are activated when free Ca2+ 
      concentration in the intracellular stores is substantially reduced and mediate 
      sustained Ca2+ entry. Recent studies have identified Orai1 as a CRAC channel 
      subunit. Here we demonstrate that passive Ca2+ store depletion using the 
      inhibitor of the sarcoendoplasmic reticulum Ca2+-ATPase, thapsigargin (TG), 
      enhances the surface expression of Orai1, a process that depends on rises in 
      cytosolic free Ca2+ concentration, as demonstrated in cells loaded with dimethyl 
      BAPTA, an intracellular Ca2+ chelator that prevented TG-evoked cytosolic free 
      Ca2+ concentration elevation. Similar results were observed with a low 
      concentration of carbachol. Cleavage of the soluble 
      N-ethylmaleimide-sensitive-factor attachment protein receptor, 
      synaptosomal-assiciated protein-25 (SNAP-25), with botulinum neurotoxin A 
      impaired TG-induced increase in the surface expression of Orai1. In addition, 
      SNAP-25 cleaving by botulinum neurotoxin A reduces the maintenance but not the 
      initial stages of store-operated Ca2+ entry. In aggregate, these findings 
      demonstrate that store depletion enhances Orai1 plasma membrane expression in an 
      exocytotic manner that involves SNAP-25, a process that contributes to 
      store-dependent Ca2+ entry.
FAU - Woodard, Geoffrey E
AU  - Woodard GE
AD  - National Institute of Diabetes and Digestive and Kidney Diseases, National 
      Institutes of Health, Bethesda, Maryland, USA.
FAU - Salido, Gines M
AU  - Salido GM
FAU - Rosado, Juan A
AU  - Rosado JA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080409
PL  - United States
TA  - Am J Physiol Cell Physiol
JT  - American journal of physiology. Cell physiology
JID - 100901225
RN  - 0 (Calcium Channels)
RN  - 0 (Chelating Agents)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (ORAI1 Protein)
RN  - 0 (ORAI1 protein, human)
RN  - 0 (Synaptosomal-Associated Protein 25)
RN  - 526U7A2651 (Egtazic Acid)
RN  - 67526-95-8 (Thapsigargin)
RN  - 8Y164V895Y (Carbachol)
RN  - EC 3.4.24.69 (Botulinum Toxins, Type A)
RN  - EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases)
RN  - K22DDW77C0 (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Botulinum Toxins, Type A/pharmacology
MH  - Calcium/*metabolism
MH  - Calcium Channels/*metabolism
MH  - Carbachol/pharmacology
MH  - Cell Membrane/drug effects/*metabolism
MH  - Chelating Agents/pharmacology
MH  - Egtazic Acid/analogs & derivatives/pharmacology
MH  - Enzyme Inhibitors/pharmacology
MH  - *Exocytosis/drug effects
MH  - HeLa Cells
MH  - Humans
MH  - ORAI1 Protein
MH  - Protein Transport
MH  - Sarcoplasmic Reticulum/drug effects/enzymology/*metabolism
MH  - Sarcoplasmic Reticulum Calcium-Transporting ATPases/antagonists & 
      inhibitors/metabolism
MH  - Synaptosomal-Associated Protein 25/metabolism
MH  - Thapsigargin/pharmacology
MH  - Time Factors
MH  - Up-Regulation
EDAT- 2008/04/11 09:00
MHDA- 2008/07/18 09:00
CRDT- 2008/04/11 09:00
PHST- 2008/04/11 09:00 [pubmed]
PHST- 2008/07/18 09:00 [medline]
PHST- 2008/04/11 09:00 [entrez]
AID - 00071.2008 [pii]
AID - 10.1152/ajpcell.00071.2008 [doi]
PST - ppublish
SO  - Am J Physiol Cell Physiol. 2008 Jun;294(6):C1323-31. doi: 
      10.1152/ajpcell.00071.2008. Epub 2008 Apr 9.