Nuclear Export of NF-ATc Enhanced by Glycogen Synthase Kinase-3-Reference-Cited by-同舟云学术

Nuclear Export of NF-ATc Enhanced by Glycogen Synthase Kinase-3

Published:1997-03-28 Issue:5308 Volume:275 Page:1930-1933
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Beals Chan R.¹,Sheridan Colleen M.²,Turck Christoph W.³,Gardner Phyllis²,Crabtree Gerald R.¹

Affiliation:

1. C. R. Beals and G. R. Crabtree, Howard Hughes Medical Institute, Department of Developmental Biology, Stanford University, Stanford, CA 94305, USA.

2. C. M. Sheridan and P. Gardner, Department of Molecular Pharmacology, Stanford University, Stanford, CA 94305, USA.

3. C. W. Turck, Howard Hughes Medical Institute, University of California, San Francisco, CA 94143, USA.

Abstract

The transcription factor NF-AT responds to Ca 2+ -calcineurin signals by translocating to the nucleus, where it participates in the activation of early immune response genes. Calcineurin dephosphorylates conserved serine residues in the amino terminus of NF-AT, resulting in nuclear import. Purification of the NF-AT kinase revealed that it is composed of a priming kinase activity and glycogen synthase kinase-3 (GSK-3). GSK-3 phosphorylates conserved serines necessary for nuclear export, promotes nuclear exit, and thereby opposes Ca 2+ -calcineurin signaling. Because GSK-3 responds to signals initiated by Wnt and other ligands, NF-AT family members could be effectors of these pathways.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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