TRPC channels: Interacting proteins

K. Kiselyov; D. M. Shin; J. Y. Kim; J. P. Yuan; S. Muallem

doi:10.1007/978-3-540-34891-7_33

TRPC channels: Interacting proteins

K. Kiselyov, D. M. Shin, J. Y. Kim, J. P. Yuan, S. Muallem

Department of Oral Biology

Research output: Chapter in Book/Report/Conference proceeding › Chapter

17 Citations (Scopus)

Abstract

TRP channels, in particular the TRPC and TRPV subfamilies, have emerged as important constituents of the receptor-activated Ca²⁺ influx mechanism triggered by hormones, growth factors, and neurotransmitters through activation of phospholipase C (PLC). Several TRPC channels are also activated by passive depletion of endoplasmic reticulum (ER) Ca²⁺. Although in several studies the native TRP channels faithfully reproduce the respective recombinant channels, more often the properties of Ca²⁺ entry and/or the store-operated current are strikingly different from that of the TRP channels expressed in the same cells. The present review aims to discuss this disparity in the context of interaction of TRPC channels with auxiliary proteins that may alter the permeation and regulation of TRPC channels.

Original language	English
Title of host publication	Transient Receptor Potential (TRP) Channels
Editors	Veit Flockerzi, Bernd Nilius
Pages	559-574
Number of pages	16
DOIs	https://doi.org/10.1007/978-3-540-34891-7_33
Publication status	Published - 2007

Publication series

Name	Handbook of Experimental Pharmacology
Volume	179
ISSN (Print)	0171-2004
ISSN (Electronic)	1865-0325

All Science Journal Classification (ASJC) codes

Biochemistry
Pharmacology, Toxicology and Pharmaceutics(all)

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10.1007/978-3-540-34891-7_33

Cite this

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AU - Kiselyov, K.

AU - Shin, D. M.

AU - Kim, J. Y.

AU - Yuan, J. P.

AU - Muallem, S.

PY - 2007

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AB - TRP channels, in particular the TRPC and TRPV subfamilies, have emerged as important constituents of the receptor-activated Ca2+ influx mechanism triggered by hormones, growth factors, and neurotransmitters through activation of phospholipase C (PLC). Several TRPC channels are also activated by passive depletion of endoplasmic reticulum (ER) Ca2+. Although in several studies the native TRP channels faithfully reproduce the respective recombinant channels, more often the properties of Ca2+ entry and/or the store-operated current are strikingly different from that of the TRP channels expressed in the same cells. The present review aims to discuss this disparity in the context of interaction of TRPC channels with auxiliary proteins that may alter the permeation and regulation of TRPC channels.

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ER -

TRPC channels: Interacting proteins

Abstract

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