期刊
PROGRESS IN BIOPHYSICS & MOLECULAR BIOLOGY
卷 98, 期 1, 页码 10-23出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pbiomolbio.2008.05.001
关键词
voltage-independent calcium channels; smooth muscle; TRP
资金
- Institut National de la Sante et de la Recherche Medicale, Fondation de France [2006005603]
- Agence National de la Recherche [ANR06-Physio-015-01]
in smooth muscle cells, agonists such as neurotransmitters or hormones can induce an increase in [Ca2+](i), via a release of intracellular stored calcium or/and an influx of extracellular Calcium. The calcium entry pathway operates through a variety of plasmalemmal calcium channels which involve voltage-dependent and voltage-independent calcium channels. Voltage-independent calcium channels include (1) receptor-ope rated channels (ROCs)activated by agonist-receptor interaction and, in the majority of cases, the downstream signal transduction proteins, (2) store-operated channels (SOCs) activated by the emptying of intracellular Ca2+ store (mainly the sarcoplasmic reticulum), (3) mechanosensitive or stretch-activated channels (SACs) activated by membrane stretch. Generally, voltage-independent calcium channels are calcium permeable non-selective cation channels with electrophysiological differences, complex regulatory mechanisms and pharmacology. Although the molecular identity of voltage-independent calcium channels is not yet fully elucidated, there are growing evidences that these channels correspond to a new family of membrane proteins encoded by mammalian homologues of specific transient receptor potential (TRP) genes. Several types of TRP proteins are ubiquitously expressed in smooth muscle cells and variations in the expression depend on tissue and species. More recently, other proteins such as Orai1 and STIM1 proteins have been also proposed as participating in the molecular identity of voltage-independent calcium channels. These channels control phenomena such as smooth muscle cells proliferation and/or contraction. (c) 2008 Elsevier Ltd. All rights reserved.
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