Action of TFII-I Outside the Nucleus as an Inhibitor of Agonist-Induced Calcium Entry-Reference-Cited by-同舟云学术

Action of TFII-I Outside the Nucleus as an Inhibitor of Agonist-Induced Calcium Entry

Published:2006-10-06 Issue:5796 Volume:314 Page:122-125
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Caraveo Gabriela¹²³⁴,van Rossum Damian B.¹²³⁴,Patterson Randen L.¹²³⁴,Snyder Solomon H.¹²³⁴,Desiderio Stephen¹²³⁴

Affiliation:

1. Department of Molecular Biology and Genetics, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

2. Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

3. Pharmacology and Molecular Science, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

4. Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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