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. 2003 Oct;4(10):1016-22.
doi: 10.1038/ni976. Epub 2003 Sep 14.

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

Minna Woo  1 , Razqallah Hakem, Caren Furlonger, Anne Hakem, Gordon S Duncan, Takehiko Sasaki, Denis Bouchard, Liwei Lu, Gillian E Wu, Christopher J Paige, Tak W Mak
Affiliations

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

Minna Woo et al. Nat Immunol. 2003 Oct.

Abstract

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.

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