Functional dissection of BCR signaling pathways

Curr Opin Immunol. 2000 Jun;12(3):276-81. doi: 10.1016/s0952-7915(00)00087-x.

Abstract

Signal transduction by the BCR is critical for progression through developmental checkpoints as well as for immune responses. Recent results obtained in mice deficient either in an adaptor molecule, BLNK (alternatively named SLP-65 or BASH), or in phosphatidylinositol 3-kinase have revealed similar - though not identical - phenotypes to those of Btk(-/-) mice, suggesting a functional link between BLNK, Btk and phosphatidylinositol 3-kinase.

Publication types

  • Review

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Agammaglobulinaemia Tyrosine Kinase
  • Animals
  • B-Lymphocytes / immunology*
  • Carrier Proteins / metabolism
  • Enzyme Precursors / metabolism
  • Intracellular Signaling Peptides and Proteins
  • Mice
  • Mice, Mutant Strains
  • Phosphatidylinositol 3-Kinases / metabolism
  • Phosphoproteins / metabolism
  • Protein-Tyrosine Kinases / metabolism
  • Receptors, Antigen, B-Cell / metabolism*
  • Signal Transduction
  • Syk Kinase

Substances

  • Adaptor Proteins, Signal Transducing
  • B cell linker protein
  • Carrier Proteins
  • Enzyme Precursors
  • Intracellular Signaling Peptides and Proteins
  • Phosphoproteins
  • Receptors, Antigen, B-Cell
  • Phosphatidylinositol 3-Kinases
  • Protein-Tyrosine Kinases
  • Agammaglobulinaemia Tyrosine Kinase
  • Syk Kinase
  • Syk protein, mouse