Journal
BIOCHEMICAL JOURNAL
Volume 354, Issue -, Pages 717-725Publisher
PORTLAND PRESS
DOI: 10.1042/0264-6021:3540717
Keywords
capacitative Ca2+ entry; K+ channel; Kir; store-operated channel; Trp4
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Funding
- NIGMS NIH HHS [GM54235] Funding Source: Medline
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Drosophila transient receptor potential (Trp) and its mammalian homologues are postulated to form capacitative Ca2+ entry or store-operated channels. Were we show that expression of murine Trp4 in HEK 293 cells also leads to an increase in inwardly rectifying K+ currents. No similar increase was found in cell lines expressing Trp1, Trp3 or Trp6. Consistent with typical characteristics of inward rectifiers, the K+ currents in Trp4-expressing cells were blocked by low millimolar concentrations of Cs+ and Ba2+, but not by 1.2 mM Ca2+, and were only slightly inhibited by 5 mM tetraethylammonium. Single channel recordings of excised inside-out patches revealed the presence of two conducting states of 51 pS and 94 pS in Trp4-expressing cells. The outward current in the excised patches was blocked by 1 mM spermine, but not by 1 mM Mg2+. How Trp4 expression causes the increase in the K+ currents is not known. We propose that Trp4 either participates in the formation of a novel K+ channel or up-regulates the expression or activity of endogenous inwardly rectifying K+ channels.
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