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Inositol hexakisphosphate kinase-1 regulates behavioral responses via GSK3 signaling pathways

Academic Article
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Overview

authors

  • Chakraborty, Anutosh
  • Latapy, C.
  • Xu, J.
  • Snyder, S. H.
  • Beaulieu, J. M.

publication date

  • March 2014

journal

  • Molecular Psychiatry  Journal

abstract

  • Glycogen synthase kinase 3 (GSK3), a prominent enzyme in carbohydrate metabolism, also has a major role in brain function. It is physiologically regulated by the kinase Akt, which phosphorylates GSK3 to inhibit catalytic activity. Inositol hexakisphosphate-1 (IP6K1) generates the inositol pyrophosphate diphosphoinositol pentakisphosphate (IP7), which physiologically inhibits Akt leading to enhanced GSK3 activity. We report that IP6K1 binds and stimulates GSK3 enzymatic activity in a non-catalytic fashion. Physiological relevance is evident in the inhibition of GSK3 activity in the brains of IP6K1-deleted mice. Behavioral alterations of IP6K1 knockout mice resemble those of GSK3 mutants. Accordingly, modulation of IP6K1-GSK3β interaction may exert beneficial effects in psychiatric disorders involving GSK3.

subject areas

  • Amphetamine
  • Animals
  • Glycogen Synthase Kinase 3
  • Male
  • Mice
  • Mice, Knockout
  • Motor Activity
  • Phosphotransferases (Phosphate Group Acceptor)
  • Protein Binding
  • Rotarod Performance Test
  • Signal Transduction
  • Social Behavior
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Research

keywords

  • GSK3
  • IP6K1
  • behavior
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Identity

International Standard Serial Number (ISSN)

  • 1476-5578 (Electronic) 1359-4184 (Linking)

Digital Object Identifier (DOI)

  • 10.1038/mp.2013.21

PubMed ID

  • 23439485
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Additional Document Info

start page

  • 284

end page

  • 293

volume

  • 19

issue

  • 3

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