title: The cyclin D3 knockout: a pound of redundancy with a dash of tissue specificity.
abstract: Progression through each phase of the cell division cycle is driven by specific cyclin/CDK holoenzymes complexes, each complex having a discrete subset of critical substrates. Phosphorylation of these substrates by the appropriate cyclin/CDK complex in turn directs regulated cell cycle progression. Based on this notion, a reasonable assumption is that elimination of any one of these complexes would be catastrophic with regard to cellular and organismal development. Over the past year however, we have witnessed elegant work that challenges the notion that cyclin/CDK holoenzymes target unique and specific substrates. Indeed in the most recent work, Sicinska et al. report that targeted deletion of the G1 cyclin, cyclin D3, disrupts proliferation of immature T lymphocytes, but does not provide a function essential for organismal development or survival.
authors.affiliation: The Leonard and Madlyn Abramson Family Cancer Research Institute and Cancer Center, Department of Cancer Biology, 21 Curie Boulevard, 454 BRB II/III, Philadelphia, Pennsylvania 19104, USA. adiehl@mail.med.upenn.edu
authors.forename: J Alan
authors.initials: JA
authors.lastname: Diehl
mesh_terms: D000818:Animals; D002453:Cell Cycle; D056743:Cyclin D3; D016213:Cyclins / Q000235:genetics / Q000502:physiology*; D006801:Humans; D015458:Leukemia, T-Cell / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D008214:Lymphocytes / Q000378:metabolism*; D051379:Mice; D018345:Mice, Knockout
chemical_list: C534696:CCND3 protein, human; C534697:Ccnd3 protein, mouse; D056743:Cyclin D3; D016213:Cyclins