Cyclin-dependent kinase 2 is essential for meiosis but not for mitotic cell division in mice

By Sagrario Ortega, I. Prieto, Junko Odajima, Alberto Martin, P. Dubus, R. Sotillo, J. Barbero, Marcos Malumbres, M. Barbacid. Nature Genetics, 2003

833 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/02b31517afbc2725eaecd55008c2553a2de27cd6

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Citations in the corpus

Living with or without cyclins and cyclin-dependent kinases. (2004, background): “…compensatory processes achieved during early embryonic development, since acute ablation of " floxed " Cdk2 alleles by Cre-mediated recombination did not compromise their continuous proliferation in vitro, although it was not reported whether exit from quiescence was affected (Ortega et al. 2003).”
Model organisms: The mighty mouse: genetically engineered mouse models in cancer drug development (2006, positive): “Recent GEMM experiments, however, have explained why: CDK2 activity is dispensable for proliferation in general and some cancers in particula”
Mouse development and cell proliferation in the absence of D-cyclins. (2004, neutral): “In wild-type cells, knockdown of CDK2 resulted in a slight delay of Response of Cyclin D1 / D2 / D3 / Cells to the Extracellular Environment the S phase entry, consistent with the published results (Berthet et al., 2003; Ortega et al., 2003).”
Cyclin-dependent kinase pathways as targets for cancer treatment. (2006, background): “For example, cdk4 can phosphorylate Rb even at cdk2preferred sites, including Thr821.”
Mammalian cell-cycle regulation: several Cdks, numerous cyclins and diverse compensatory mechanisms (2009, background): “Surprisingly, Cdk2 knockout mice are viable and develop normally with a reduced body size (Berthet et al., 2003; Ortega et al., 2003).”
The Concept of Synthetic Lethality in the Context of Anticancer Therapy (2005, background): “, possibly because another catalytic partner can substitute for CDK2 in its absenc”
Cyclin-dependent kinases (2014, background): “Like its yeast ortholog, Cdk1 is the only CDK essential for the cell cycle in mammals [9], whereas both Cdk2 and Cdk3 are dispensable [3,10].”
Mammalian cells cycle without the D-type cyclin-dependent kinases Cdk4 and Cdk6. (2004, methodology): “Cdk4 and Cdk2 mutantD-type cyclins grow well in culture and can be rescued mice were genotyped as previously described (Rane et al., 1999;from quiescence by mitogenic stimulation with kinetics Ortega et al., 2003).similar to those observed in Cdk4/Cdk6-deficient MEFs.”
Cell cycle, CDKs and cancer: a changing paradigm (2009, background): “Mice without CDK2 do not display any detectable defects in mitotic cell”
Specific arrests of spermatogenesis in genetically modified and mutant mice (2004, background): “In Cdk2-deficient mice spermatogenesis proceeds to the end of the prophase I of the meiotic divisions (Ortega et al., 2003).”
Myc and cell cycle control. (2015, background): “Nevertheless, systematic knockout of Cdk loci in themouse germline has shown that Cdk2 [16,17], Cdk4 [18,19] and Cdk6 [20] are not essential for cell cycle progression of most cell types, although loss of each of these Cdks results in particular developmental defects.”
Cell cycle kinases as therapeutic targets for cancer (2009, background): “Studies in genetically engineered mouse models support the concept that CDKs that act during interphase (CDK2, CDK4 and CDK6) have compensatory roles in the control of the mammalian cell cycl”