Inositol trisphosphate 3-kinases: Focus on immune and neuronal signaling

Michael J. Schell

Research output: Contribution to journalReview articlepeer-review


The localized control of second messenger levels sculpts dynamic and persistent changes in cell physiology and structure. Inositol trisphosphate [Ins(1,4,5)P 3] 3-kinases (ITPKs) phosphorylate the intracellular second messenger Ins(1,4,5)P 3. These enzymes terminate the signal to release Ca2+ from the endoplasmic reticulum and produce the messenger inositol tetrakisphosphate [Ins(1,3,4,5)P 4]. Independent of their enzymatic activity, ITPKs regulate the microstructure of the actin cytoskeleton. The immune phenotypes of ITPK knockout mice raise new questions about how ITPKs control inositol phosphate lifetimes within spatial and temporal domains during lymphocyte maturation. The intense concentration of ITPK on actin inside the dendritic spines of pyramidal neurons suggests a role in signal integration and structural plasticity in the dendrite, and mice lacking neuronal ITPK exhibit memory deficits. Thus, the molecular and anatomical features of ITPKs allow them to regulate the spatiotemporal properties of intracellular signals, leading to the formation of persistent molecular memories.

Original languageEnglish (US)
Pages (from-to)1755-1778
Number of pages24
JournalCellular and Molecular Life Sciences
Issue number11
StatePublished - Jun 2010


  • Dendritic spines
  • F-actin
  • Inositol phosphates
  • Integration
  • Intracellular Ca
  • Lymphocyte
  • Neutrophil
  • Pyramidal neuron
  • Rho GTPase

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology
  • Pharmacology
  • Cellular and Molecular Neuroscience
  • Cell Biology


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