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- Title
Caspase-3 regulates cell cycle in B cells: a consequence of substrate specificity.
- Authors
Minna Woo; Hakem, Razqallah; Furlonger, Caren; Hakem, Anne; Duncan, Gordon S.; Sasaki, Takehiko; Bouchard, Denis; Liwei Lu; Wu, Gillian E.; Paige, Christopher J.; Mak, Tak W.
- 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.
- Subjects
B cells; CELL death; CELL proliferation; CYCLIN-dependent kinases; LABORATORY mice
- Publication
Nature Immunology, 2003, Vol 4, Issue 10, p1016
- ISSN
1529-2908
- Publication type
Article
- DOI
10.1038/ni976