TRPC channels: interacting proteins
K Kiselyov1, D M Shin, J Y Kim
1Department of Biological Sciences University of Pittsburgh, Pittsburgh, PA 15260, USA.
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 ofphospholipase 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.
Insights
Transient Receptor Potential (TRP) channels, including TRPC and TRPV, are key to calcium influx. This review explores why native TRP channels differ from recombinant ones, focusing on auxiliary protein interactions.
Area of Science:
- Molecular Biology
- Cell Physiology
- Biochemistry
Background:
- Transient Receptor Potential (TRP) channels, particularly TRPC and TRPV, are crucial for receptor-activated calcium (Ca2+) influx.
- These channels are activated by hormones, growth factors, and neurotransmitters via phospholipase C (PLC) signaling.
- Some TRPC channels also respond to calcium depletion in the endoplasmic reticulum (ER).
Purpose of the Study:
- To discuss the discrepancies between native and recombinant TRP channel properties.
- To investigate the role of auxiliary proteins in TRP channel function and regulation.
Main Methods:
- Literature review of studies on TRP channel function.
- Analysis of data comparing native and recombinant TRP channel characteristics.
- Examination of the impact of protein-protein interactions on TRP channel activity.
Main Results:
- Native TRP channels often exhibit different Ca2+ entry and store-operated current properties compared to their recombinant counterparts.
- Disparities suggest that native TRP channel function is modulated by interactions with other cellular proteins.
- Auxiliary proteins can significantly alter TRPC channel permeation and regulatory mechanisms.
Conclusions:
- The functional differences observed in native TRP channels are likely due to their association with auxiliary proteins.
- Understanding these interactions is vital for accurately characterizing TRP channel roles in cellular signaling.
- Further research into TRP channel-protein complexes will elucidate their precise physiological and pathophysiological functions.
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