TRP Channels

TRP Channels

New Book on TRP Channels

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Transient Receptor Potential Channels offers a unique blend of thoughtfully selected topics ranging from the structural biology of this fascinating group of ion channels to their emerging roles in human diseases. This single book covers TRP channels of yeasts, flies, fishes frogs and humans. And from the biophysics of primary thermo-sensory events in cells to the thermosensation at whole organism level, from physiology of pain to the development of pain-killers, from psychiatric illnesses to cancers, from skin cells to sperms, from taste buds to testes, from established facts to heated debates, this book contains something for every TRP enthusiasts, beginner and expert alike. It includes crucial background information, critical analysis of cutting edge research, and ideas and thoughts for numerous testable hypotheses. It also shows directions for future research in this highly dynamic field. It is a book readers will be just as eager to give to others as keep for themselves. Transient Receptor Potential Channels (Advances in Experimental Medicine and Biology) [Hard cover]. Md. Shahidul Islam (Editor). Publisher: Springer. 52 chapters, 125 authors, about 1115 pages

Chapter 24

AbstractsPosted by Md. Shahidul Islam Mon, February 07, 2011 17:48:24

Contribution of TRPC1 and Orai1 to Ca2+ Entry Activated by Store Depletion

Kwong Tai Cheng, Hwei Ling Ong, Xibao Liu, and Indu S. Ambudkar

Store-operated Ca2+ entry (SOCE) is activated in response to depletion of the ER-Ca2+ stores by the ER Ca2+ sensor protein, STIM1 which oligomerizes and moves to ER/PM junctional domains where it interacts with and activates channels involved in SOCE. Two types of channel activities have been described. ICRAC, via Ca2+ release-activated Ca2+ (CRAC) channel, which displays high Ca2+ selectivity and accounts for the SOCE and cell function in T lymphocytes, mast cells, platelets, and some types of smooth muscle and endothelial cells. Orai1 has been established as the pore-forming component of CRAC channels and interaction of Orai1 with STIM1 is sufficient for generation of the CRAC channel. Store depletion also leads to activation of relatively non-selective cation currents (referred to as ISOC) that contribute to SOCE in several other cell types. TRPC channels, including TRPC1, TRPC3, and TRPC4, have been proposed as possible candidate channels for this Ca2+ influx. TRPC1 is the best characterized channel in this regard and reported to contribute to endogenous SOCE in many cells types. TRPC1-mediated Ca2+ entry and cation current in cells stimulated with agonist or thapsigargin are inhibited by low [Gd3+] and 10–20 μM 2APB (conditions that block SOCE). Importantly, STIM1 also associates with and gates TRPC1 via electrostatic interaction between STIM1 (684KK685) and TRPC1 (639DD640). Further, store depletion induces dynamic recruitment of a TRPC1/STIM1/Orai1 complex and knockdown of Orai1 completely abrogates TRPC1 function. Despite these findings, there has been much debate regarding the activation of TRPC1 by store depletion as well as the role of Orai1 and STIM1 in SOC channel function. This chapter summarizes recent studies and concepts regarding the contributions of Orai1 and TRPC1 to SOCE. Major unresolved questions regarding functional interaction between Orai1 and TRPC1 as well as possible mechanisms involved in the regulation of TRPC channels by store depletion will be discussed.

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