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Caspase-3 regulates cell cycle in B cells: a consequence of substrate specificity.

Caspases are important for apoptosis but are also involved in mammalian cell survival and cell division. Here we report that caspase-3 is a negative regulator of B cell cycling. Mice deficient in caspase-3 (Casp3-/- mice) have increased numbers of splenic B cells that show normal apoptosis but enhanced proliferation in vivo and hyperproliferation after mitogenic stimulation in vitro. Cdkn1a encodes p21 (also called Waf1 or Cip1), a cyclin-dependent kinase (CDK) inhibitor. Although expression of p21 was increased, CDK activities and proliferating cell nuclear antigen (PCNA) were increased in Casp3-/- B cells. Using Casp3-/-Cdkn1a-/- mice, we show that the hyperproliferation of Casp3-/- B cells is abolished when Cdkn1a is also deleted. Our genetic and biochemical data demonstrate that caspase-3 is essential in the regulation of B cell homeostasis.

Pubmed ID: 12970760


  • Woo M
  • Hakem R
  • Furlonger C
  • Hakem A
  • Duncan GS
  • Sasaki T
  • Bouchard D
  • Lu L
  • Wu GE
  • Paige CJ
  • Mak TW


Nature immunology

Publication Data

October 29, 2003

Associated Grants


Mesh Terms

  • Animals
  • Apoptosis
  • B-Lymphocytes
  • Bromodeoxyuridine
  • Caspase 3
  • Caspases
  • Cell Cycle
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclin-Dependent Kinases
  • Cyclins
  • Flow Cytometry
  • Immunohistochemistry
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Proliferating Cell Nuclear Antigen
  • Spleen
  • Substrate Specificity