Store-operated calcium channels and pro-inflammatory signals.
In non-excitable cells such as T lymphocytes, hepatocytes, mast cells, endothelia and epithelia, the major pathway for calcium [Ca2+] entry is through store-operated Ca2+ channels in the plasma membrane. These channels are activated by the emptying of intracellular Ca2+ stores, however, neither the gating mechanism nor the downstream targets of these channels has been clear established. Here, I review some of the proposed gating mechanisms of store-operated Ca2+ channels and the functional implications in regulating pro-inflammatory signals.
Chang
Wei-chiao
WC
Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK. wei-chiao.chang@physiol.ox.ac.uk
D000818:Animals; D001896:Boron Compounds / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism / Q000502:physiology*; D020013:Calcium Signaling / Q000502:physiology*; D002462:Cell Membrane / Q000378:metabolism; D006801:Humans; D015640:Ion Channel Gating / Q000502:physiology*; D008407:Mast Cells / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D050778:NFATC Transcription Factors / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D015398:Signal Transduction
D001896:Boron Compounds; D015220:Calcium Channels; D016328:NF-kappa B; D050778:NFATC Transcription Factors; C109986:2-aminoethoxydiphenyl borate; D052250:Nitric Oxide Synthase Type III; D002118:Calcium