Immunodeficiency diseases. Multiple roles for ZAP-70

Curr Biol. 1994 Aug 1;4(8):731-3. doi: 10.1016/s0960-9822(00)00162-7.

Abstract

Human patients with an immunodeficiency disease caused by mutations of the protein tyrosine kinase ZAP-70 show that this enzyme plays multiple important roles in T-cell differentiation and function.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Differentiation
  • Humans
  • Immunologic Deficiency Syndromes / enzymology*
  • Immunologic Deficiency Syndromes / genetics
  • Lymphocyte Activation
  • Lymphocyte Specific Protein Tyrosine Kinase p56(lck)
  • Membrane Proteins / physiology
  • Mice
  • Mice, Knockout
  • Phosphorylation
  • Point Mutation
  • Protein Processing, Post-Translational
  • Protein-Tyrosine Kinases / chemistry
  • Protein-Tyrosine Kinases / deficiency
  • Protein-Tyrosine Kinases / genetics
  • Protein-Tyrosine Kinases / physiology*
  • Proto-Oncogene Proteins / physiology
  • Proto-Oncogene Proteins c-fyn
  • Receptors, Antigen, T-Cell / physiology
  • Sequence Deletion
  • Signal Transduction
  • T-Lymphocytes / cytology
  • T-Lymphocytes / enzymology*
  • T-Lymphocytes / immunology
  • ZAP-70 Protein-Tyrosine Kinase

Substances

  • Membrane Proteins
  • Proto-Oncogene Proteins
  • Receptors, Antigen, T-Cell
  • antigen T cell receptor, zeta chain
  • Protein-Tyrosine Kinases
  • FYN protein, human
  • Fyn protein, mouse
  • Lymphocyte Specific Protein Tyrosine Kinase p56(lck)
  • Proto-Oncogene Proteins c-fyn
  • ZAP-70 Protein-Tyrosine Kinase
  • ZAP70 protein, human
  • Zap70 protein, mouse