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Yıl 2010, Cilt: 2 Sayı: 2, 79 - 86, 14.08.2013

Öz

Recent Progress in the Regulation of TRPC1 by Store Depletion

Yıl 2010, Cilt: 2 Sayı: 2, 79 - 86, 14.08.2013

Öz

Store-operated Ca entry (SOCE) is activated in response to depletion of the ER-Ca stores. The ER-Ca
2+
sensor protein, STIM1, oligomerizes when [Ca ] in the store is decreased and moves to ER/PM junctional
domains where it interacts with and activates channels involved in SOCE, namely Orai and TRPC channels.
2+
Orai1 is the primary pore-forming component of the highly Ca selective CRAC channel. It is recruited to ER/
PM junctional domains by STIM1 where it is gated via interaction with a specific C-terminal domain of STIM1.
Thus Orai1 and STIM1 are sufficient for generation of functional CRAC channels. Store depletion also leads
to activation of relatively non-selective cation channels, referred to as SOC channels that contribute to SOCE
in several other cell types. TRPC1 has been proposed as a possible candidate component of SOC channels.
2+
TRPC1 contributes to endogenous SOCE in many cells types. In these cells, TRPC1-mediated Ca entry and
3+
cation currents are stimulated with either agonist or thapsigargin, and inhibited by low [Gd ] and 10-20 µM
2APB (conditions that block SOCE). STIM1 also associates with and gates TRPC1 via electrostatic interaction
between STIM1 (684KK685) and TRPC1 (639DD640). Further, functional Orai1 is required for activation of
TRPC1-SOCE and this has been associated with recruitment of a TRPC1/STIM1/Orai1 complex. However,
there is ongoing debate regarding the activation of TRPC1 by store depletion as well as the role of Orai1 and
STIM1 in regulating its function. This chapter will summarize recent studies and concepts regarding the contri-
butions of Orai1 and TRPC1 to SOCE. We will discuss major unresolved questions regarding functional inter-
action between Orai1 and TRPC1 as well as possible mechanisms involved in the regulation of TRPC channels.

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Ayrıntılar

Birincil Dil İngilizce
Bölüm Derleme
Yazarlar

İndu Ambudkar Bu kişi benim

Hwei Ong Bu kişi benim

Kwong Cheng Bu kişi benim

Xibao Liu Bu kişi benim

Timothy Lockwich Bu kişi benim

Yayımlanma Tarihi 14 Ağustos 2013
Yayımlandığı Sayı Yıl 2010 Cilt: 2 Sayı: 2

Kaynak Göster

APA Ambudkar, İ., Ong, H., Cheng, K., Liu, X., vd. (2013). Recent Progress in the Regulation of TRPC1 by Store Depletion. Cell Membranes and Free Radical Research, 2(2), 79-86.
AMA Ambudkar İ, Ong H, Cheng K, Liu X, Lockwich T. Recent Progress in the Regulation of TRPC1 by Store Depletion. Cell Membranes and Free Radical Research. Ağustos 2013;2(2):79-86.
Chicago Ambudkar, İndu, Hwei Ong, Kwong Cheng, Xibao Liu, ve Timothy Lockwich. “Recent Progress in the Regulation of TRPC1 by Store Depletion”. Cell Membranes and Free Radical Research 2, sy. 2 (Ağustos 2013): 79-86.
EndNote Ambudkar İ, Ong H, Cheng K, Liu X, Lockwich T (01 Ağustos 2013) Recent Progress in the Regulation of TRPC1 by Store Depletion. Cell Membranes and Free Radical Research 2 2 79–86.
IEEE İ. Ambudkar, H. Ong, K. Cheng, X. Liu, ve T. Lockwich, “Recent Progress in the Regulation of TRPC1 by Store Depletion”, Cell Membranes and Free Radical Research, c. 2, sy. 2, ss. 79–86, 2013.
ISNAD Ambudkar, İndu vd. “Recent Progress in the Regulation of TRPC1 by Store Depletion”. Cell Membranes and Free Radical Research 2/2 (Ağustos 2013), 79-86.
JAMA Ambudkar İ, Ong H, Cheng K, Liu X, Lockwich T. Recent Progress in the Regulation of TRPC1 by Store Depletion. Cell Membranes and Free Radical Research. 2013;2:79–86.
MLA Ambudkar, İndu vd. “Recent Progress in the Regulation of TRPC1 by Store Depletion”. Cell Membranes and Free Radical Research, c. 2, sy. 2, 2013, ss. 79-86.
Vancouver Ambudkar İ, Ong H, Cheng K, Liu X, Lockwich T. Recent Progress in the Regulation of TRPC1 by Store Depletion. Cell Membranes and Free Radical Research. 2013;2(2):79-86.