Mice lacking a functional chk gene have no apparent defects in the hematopoietic system

Biochem Mol Biol Int. 1997 Sep;43(1):115-22. doi: 10.1080/15216549700203881.


Non-receptor tyrosine kinase Chk has been implicated in hematopoietic development. To study the function of Chk in vivo, we have generated chk-deficient mice using gene targeting. Overall development of mice homozygous for this mutation was apparently normal. Blood counts, FACS analysis of hematopoietic cell populations, CFU-C and CAFC assays showed no significant difference between wild type and mutant animals. Thus, the dispensability of Chk for mouse development and hematopoiesis suggests that its function may be redundant in vivo, and most likely be compensated by activity of a closely related protein tyrosine kinase Csk.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Cell Count
  • Bone Marrow Cells / cytology
  • CSK Tyrosine-Protein Kinase
  • Cell Differentiation
  • Colony-Forming Units Assay
  • Crosses, Genetic
  • Female
  • Gene Targeting
  • Hematopoiesis*
  • Hematopoietic Stem Cells / cytology
  • Hematopoietic Stem Cells / physiology
  • Homozygote
  • Male
  • Mice
  • Mutation
  • Protein-Tyrosine Kinases / genetics*
  • Protein-Tyrosine Kinases / metabolism
  • Proto-Oncogene Proteins pp60(c-src)*
  • src-Family Kinases


  • Matk protein, mouse
  • Protein-Tyrosine Kinases
  • CSK Tyrosine-Protein Kinase
  • Proto-Oncogene Proteins pp60(c-src)
  • src-Family Kinases