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

Nature immunology | Oct 29, 2003

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 RIS Download

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

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