| First Author | Woo M | Year | 2003 |
| Journal | Nat Immunol | Volume | 4 |
| Issue | 10 | Pages | 1016-22 |
| PubMed ID | 12970760 | Mgi Jnum | J:85809 |
| Mgi Id | MGI:2677082 | Doi | 10.1038/ni976 |
| Citation | Woo M, et al. (2003) Caspase-3 regulates cell cycle in B cells: a consequence of substrate specificity. Nat Immunol 4(10):1016-22 |
| abstractText | 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. |
