STIMulating store-operated Ca2+ entry

被引:341
作者
Cahalan, Michael D. [1 ,2 ]
机构
[1] Univ Calif Irvine, Dept Physiol & Biophys, Irvine, CA 92697 USA
[2] Univ Calif Irvine, Inst Immunol, Irvine, CA 92697 USA
关键词
STROMAL INTERACTION MOLECULE-1; CALCIUM SENSOR STIM1; CA2+-SELECTIVE ARC CHANNELS; PLASMA MEMBRANE JUNCTIONS; ACTIVATES CRAC CHANNELS; SMOOTH-MUSCLE-CELLS; CURRENT I-CRAC; ENDOPLASMIC-RETICULUM; TRPC CHANNELS; NEOINTIMA FORMATION;
D O I
10.1038/ncb0609-669
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Calcium influx through plasma membrane store-operated Ca2+ (SOC) channels is triggered when the endoplasmic reticulum (ER) Ca2+ store is depleted - a homeostatic Ca2+ signalling mechanism that remained enigmatic for more than two decades. RNA-interference (RNAi) screening and molecular and cellular physiological analysis recently identified STIM1 as the mechanistic 'missing link' between the ER and the plasma membrane. STIM proteins sense the depletion of Ca2+ from the ER, oligomerize, translocate to junctions adjacent to the plasma membrane, organize Orai or TRPC (transient receptor potential cation) channels into clusters and open these channels to bring about SOC entry.
引用
收藏
页码:669 / 677
页数:9
相关论文
共 108 条
[1]   STIM1 converts TRPC1 from a receptor-operated to a store-operated channel: Moving TRPC1 in and out of lipid rafts [J].
Alicia, Sampieri ;
Angelica, Zepeda ;
Carlos, Saldana ;
Alfonso, Salgado ;
Vaca, Luis .
CELL CALCIUM, 2008, 44 (05) :479-491
[2]   Store-operated Ca2+ channels and Stromal Interaction Molecule 1 (STIM1) are targets for the actions of bile acids on liver cells [J].
Aromataris, Edoardo C. ;
Castro, Joel ;
Rychkov, Grigori Y. ;
Barritt, Greg J. .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, 2008, 1783 (05) :874-885
[3]   RNA Interference Targeting STIM1 Suppresses Vascular Smooth Muscle Cell Proliferation and Neointima Formation in the Rat [J].
Aubart, Fleur C. ;
Sassi, Yassine ;
Coulombe, Alain ;
Mougenot, Nathalie ;
Vrignaud, Cedric ;
Leprince, Pascal ;
Lechat, Philippe ;
Lompre, Anne-Marie ;
Hulot, Jean-Sebastien .
MOLECULAR THERAPY, 2009, 17 (03) :455-462
[4]   Essential function for the calcium sensor STIM1 in mast cell activation and anaphylactic responses [J].
Baba, Yoshihiro ;
Nishida, Keigo ;
Fujii, Yoko ;
Hirano, Toshio ;
Hikida, Masaki ;
Kurosaki, Tomohiro .
NATURE IMMUNOLOGY, 2008, 9 (01) :81-88
[5]   Coupling of STIM1 to store-operated Ca2+ entry through its constitutive and inducible movement in the endoplasmic reticulum [J].
Baba, Yoshihiro ;
Hayashit, Kenji ;
Fujii, Yoko ;
Mizushima, Akiko ;
Watarai, Hiroshi ;
Wakamori, Minoru ;
Numaga, Takuro ;
Mori, Yasuo ;
Iino, Masamitsu ;
Hikida, Masaki ;
Kurosaki, Tomohiro .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2006, 103 (45) :16704-16709
[6]   An examination of the secretion-like coupling model for the activation of the Ca2+ release-activated Ca2+ current ICRAC in RBL-1 cells [J].
Bakowski, D ;
Glitsch, MD ;
Parekh, AB .
JOURNAL OF PHYSIOLOGY-LONDON, 2001, 532 (01) :55-71
[7]   Dynamic movement of the calcium sensor STIM1 and the calcium channel Orai1 in activated T-cells: Puncta and distal caps [J].
Barr, Valarie A. ;
Bernot, Kelsie M. ;
Srikanth, Sonal ;
Gwack, Yousang ;
Balagopalan, Lakshmi ;
Regan, Carole K. ;
Helman, Daniel J. ;
Sommers, Connie L. ;
Oh-hora, Masatsugu ;
Rao, Anjana ;
Samelson, Lawrence E. .
MOLECULAR BIOLOGY OF THE CELL, 2008, 19 (07) :2802-2817
[8]   Ca2+ handling is altered when arterial myocytes progress from a contractile to a proliferative phenotype in culture [J].
Berra-Romani, Roberto ;
Mazzocco-Spezzia, Amparo ;
Pulina, Maria V. ;
Golovina, Vera A. .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2008, 295 (03) :C779-C790
[9]   Orai, STIM1 and iPLA2β:: a view from a different perspective [J].
Bolotina, Victoria M. .
JOURNAL OF PHYSIOLOGY-LONDON, 2008, 586 (13) :3035-3042
[10]   STIM2 is a feedback regulator that stabilizes basal cytosolic and endoplasmic reticulum Ca2+ levels [J].
Brandman, Onn ;
Liou, Jen ;
Park, Wei Sun ;
Meyer, Tobias .
CELL, 2007, 131 (07) :1327-1339