Cdk2 Knockout Mice Are Viable

By C. Berthet, E. Aleem, V. Coppola, L. Tessarollo, Philipp Kaldis. Current Biology, 2003

699 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/7376178711c70172e17581e1983038a8d836913e

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Citations in the corpus

Preventing re-replication of chromosomal DNA (2005, neutral): “The picture is further complicated by the observation that Cdk2 knockout mice — which lack the only known kinase partner of cyclin E — are viable, and produce MEFs that can exit normally from serum starvatio”
Myc and cell cycle control. (2015, positive): “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.”
Mammalian cells cycle without the D-type cyclin-dependent kinases Cdk4 and Cdk6. (2004, neutral): “PreviE-type cyclins are not required for mitotic cell divisionous studies have shown that Cdk4 is dispensable for has challenged this model (Berthet et al., 2003; Ortega etproliferation in most cell types, an observation attribal., 2003; Geng et al., 2003; Parisi et al., 2003).”
Long Noncoding RNA MALAT1 Controls Cell Cycle Progression by Regulating the Expression of Oncogenic Transcription Factor B-MYB (2013, neutral): “The in vivo cdk2 knock out mouse is viable and does not show any obvious defects in normal mitotic cell division cycles [89,90].”
Living with or without cyclins and cyclin-dependent kinases. (2004, positive): “Moreover, cyclin Aassociated kinase activity, while present in Cdk2-null splenocyte extracts from young mice or in early-passage MEFs, was no longer detected in Cdk2-deficient adult spleen cells and in immortalized MEFs (Berthet et al. 2003).”
Cyclin-dependent kinase pathways as targets for cancer treatment. (2006, positive): “In addition, cdk2 knockout mice are viable.(80,81) Although”
Cdks, cyclins and CKIs: roles beyond cell cycle regulation (2013, neutral): “These include cyclin A1 (Liu et al., 1998), Cdk2 (Berthet et al., 2003; Ortega et al., 2003) and Cdk4 (Rane et al., 1999; Tsutsui et al., 1999) knockouts.”
The Concept of Synthetic Lethality in the Context of Anticancer Therapy (2005, neutral): “, possibly because another catalytic partner can substitute for CDK2 in its absenc”
Mammalian cell-cycle regulation: several Cdks, numerous cyclins and diverse compensatory mechanisms (2009, positive): “Surprisingly, Cdk2 knockout mice are viable and develop normally with a reduced body size (Berthet et al., 2003; 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”
Cell cycle, CDKs and cancer: a changing paradigm (2009, neutral): “Mice without CDK2 do not display any detectable defects in mitotic cell”
Specific inhibition of cyclin-dependent kinase 4/6 by PD 0332991 and associated antitumor activity in human tumor xenografts. (2004, neutral): “In fact, Cdk2 knockout mice have been reported to be entirely viable (86).”
Cell cycle kinases as therapeutic targets for cancer (2009, positive): “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”