Action of TFII-I outside the nucleus as an inhibitor of agonist-induced calcium entry
- PMID: 17023658
- DOI: 10.1126/science.1127815
Action of TFII-I outside the nucleus as an inhibitor of agonist-induced calcium entry
Abstract
TFII-I is a transcription factor and a target of phosphorylation by Bruton's tyrosine kinase. In humans, deletions spanning the TFII-I locus are associated with a cognitive defect, the Williams-Beuren cognitive profile. We report an unanticipated role of TFII-I outside the nucleus as a negative regulator of agonist-induced calcium entry (ACE) that suppresses surface accumulation of TRPC3 (transient receptor potential C3) channels. Inhibition of ACE by TFII-I requires phosphotyrosine residues that engage the SH2 (Src-homology 2) domains of phospholipase C-g (PLC-g) and an interrupted, pleckstrin homology (PH)-like domain that binds the split PH domain of PLC-g. Our observations suggest a model in which TFII-I suppresses ACE by competing with TRPC3 for binding to PLC-g.
Comment in
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Cell signaling. The double life of a transcription factor takes it outside the nucleus.Science. 2006 Oct 6;314(5796):64-5. doi: 10.1126/science.1133757. Science. 2006. PMID: 17023638 No abstract available.
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