Immunodeficiencies caused by genetic defects in protein kinases

Curr Opin Immunol. 1996 Aug;8(4):448-53. doi: 10.1016/s0952-7915(96)80028-8.

Abstract

The recognition that defects of ZAP-70 and, more recently, of JAK3 kinase in humans result in severe combined immunodeficiency, and the demonstration that targeting of these and other protein-kinase genes in mice also leads to immunodeficiency, have highlighted the crucial role that these proteins play in T-cell differentiation and activation.

Publication types

  • Review

MeSH terms

  • Animals
  • DNA-Activated Protein Kinase
  • DNA-Binding Proteins*
  • Humans
  • Immunologic Deficiency Syndromes / enzymology*
  • Immunologic Deficiency Syndromes / genetics*
  • Immunologic Deficiency Syndromes / immunology
  • Janus Kinase 3
  • Nuclear Proteins
  • Protein Serine-Threonine Kinases / deficiency
  • Protein-Tyrosine Kinases / deficiency*
  • Severe Combined Immunodeficiency / enzymology
  • Severe Combined Immunodeficiency / genetics
  • Severe Combined Immunodeficiency / immunology
  • Signal Transduction / immunology
  • ZAP-70 Protein-Tyrosine Kinase

Substances

  • DNA-Binding Proteins
  • Nuclear Proteins
  • Protein-Tyrosine Kinases
  • JAK3 protein, human
  • Janus Kinase 3
  • ZAP-70 Protein-Tyrosine Kinase
  • ZAP70 protein, human
  • DNA-Activated Protein Kinase
  • PRKDC protein, human
  • Protein Serine-Threonine Kinases