Alternative roles for Cdk5 in learning and synaptic plasticity

Ammar H. Hawasli, James A. Bibb

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Protein kinases mediate the intracellular signal transduction pathways controlling synaptic plasticity in the central nervous system. While the majority of protein kinases achieve this function via the phosphorylation of synaptic substrates, some kinases may contribute through alternative mechanisms in addition to enzymatic activity. There is growing evidence that protein kinases may often play structural roles in plasticity as well. Cyclin-dependent kinase 5 (Cdk5) has been implicated in learning and synaptic plasticity. Initial scrutiny focused on its enzymatic activity using pharmacological inhibitors and genetic modifications of Cdk5 cofactors. Quite recently Cdk5 has been shown to govern learning and plasticity via regulation of glutamate receptor degradation, a function that may not dependent on phosphorylation of downstream effectors. From these new studies, two roles emerge for Cdk5 in plasticity: one in which it controls structural plasticity via phosphorylation of synaptic substrates, and a second where it regulates functional plasticity via protein-protein interactions.

Original languageEnglish (US)
Pages (from-to)941-948
Number of pages8
JournalBiotechnology Journal
Volume2
Issue number8
DOIs
StatePublished - Aug 2007

Fingerprint

Cyclin-Dependent Kinase 5
Neuronal Plasticity
Learning
Protein Kinases
Phosphorylation
Glutamate Receptors
Signal Transduction
Proteins
Phosphotransferases
Central Nervous System
Pharmacology

Keywords

  • Cdk5
  • Cyclin-dependent kinase 5
  • Learning
  • Plasticity

ASJC Scopus subject areas

  • Applied Microbiology and Biotechnology
  • Molecular Medicine

Cite this

Alternative roles for Cdk5 in learning and synaptic plasticity. / Hawasli, Ammar H.; Bibb, James A.

In: Biotechnology Journal, Vol. 2, No. 8, 08.2007, p. 941-948.

Research output: Contribution to journalArticle

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