Calmodulin regulates Ca2+-dependent feedback inhibition of store-operated interaction with a site in the Ca2+ influx by C terminus of TrpC1

被引：112

作者：

Singh, BB

Liu, XB

Tang, JS

Zhu, MX

Ambudkar, IS ^{[1
]}

机构：

[1] Natl Inst Dent & Craniofacial Res, Secretory Physiol Sect, Gene Therapy & Therapeut Branch, NIH, Bethesda, MD 20892 USA

[2] Ohio State Univ, Neurobiotechnol Ctr, Columbus, OH 43210 USA

来源：

MOLECULAR CELL | 2002年 / 9卷 / 04期

关键词：

D O I：

10.1016/S1097-2765(02)00506-3

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The mechanism involved in [Ca2+](i)-dependent feedback inhibition of store-operated Ca2+ entry (SOCE) is not yet known. Expression of Call-insensitive calmodulin (Mut-CaM) but not wild-type CaM increased SOCE and decreased its Call-dependent inactivation. Expression of TrpC1 lacking C terminus aa 664-793 (TrpC1DeltaC) also attenuated Ca2+-dependent inactivation of SOCE. CaM interacted with endogenous and expressed TrpC1 and with GST-TrpC1 C terminus but not with TrpC1DeltaC. Two CaM binding domains, aa 715749 and aa 758-793, were identified. Expression of TrpC1Delta758-793 but not TrpC1Delta715-749 mimicked the effects of TrpC1DeltaC and Mut-CaM on SOCE. These data demonstrate that CaM mediates Ca2+-dependent feedback inhibition of SOCE via binding to a domain in the C terminus of TrpC1. These findings reveal an integral role for TrpC1 in the regulation of SOCE.

引用

页码：739 / 750

页数：12

共 43 条

[21] Trp1, a candidate protein for the store-operated Ca2+ influx mechanism in salivary gland cells [J].

Liu, XB ;

Wang, WC ;

Singh, BB ;

Lockwich, T ;

Jadlowiec, J ;

O'Connell, B ;

Wellner, R ;

Zhu, MX ;

Ambudkar, IS .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (05) :3403-3411

[22] Characteristics of a store-operated calcium-permeable channel - Sarcoendoplasmic reticulum calcium pump function controls channel gating [J].

Liu, XB ;

Ambudkar, IS .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (32) :29891-29898

[23] Stabilization of cortical actin induces internalization of transient receptor potential 3 (Trp3)-associated caveolar Ca2+ signaling complex and loss of Ca2+ influx without disruption of Trp3-inositol trisphosphate receptor association [J].

Lockwich, T ;

Singh, BB ;

Liu, XB ;

Ambudkar, IS .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (45) :42401-42408

[24] Assembly of Trp1 in a signaling complex associated with caveolin-scaffolding lipid raft domains [J].

Lockwich, TP ;

Liu, XB ;

Singh, BB ;

Jadlowiec, J ;

Weiland, S ;

Ambudkar, IS .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (16) :11934-11942

[25] Visual transduction in Drosophila [J].

Montell, C .

ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, 1999, 15 :231-268

[26]

MONTELL C, 2001, PHYSL PHYLOGENY FUNC

[27] Competitive regulation of CaT-like-mediated Ca2+ entry by protein kinase C and calmodulin [J].

Niemeyer, BA ;

Bergs, C ;

Wissenbach, U ;

Flockerzi, V ;

Trost, C .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (06) :3600-3605

[28] Slow feedback inhibition of calcium release-activated calcium current by calcium entry [J].

Parekh, AB .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (24) :14925-14932

[29] DEPLETION-ACTIVATED CALCIUM CURRENT IS INHIBITED BY PROTEIN-KINASE IN RBL-2H3 CELLS [J].

PAREKH, AB ;

PENNER, R .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (17) :7907-7911

[30] Store depletion and calcium influx [J].

Parekh, AB ;

Penner, R .

PHYSIOLOGICAL REVIEWS, 1997, 77 (04) :901-930

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