Cdk2 Knockout Mice Are Viable

  title={Cdk2 Knockout Mice Are Viable},
  author={Cyril Berthet and Eiman Aleem and Vincenzo Coppola and Lino Tessarollo and Philipp Kaldis},
  journal={Current Biology},

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Cdk2 catalytic activity is essential for meiotic cell division in vivo.
The data indicate that the essential meiotic functions of Cdk2 depend on its kinase activity, without which the generation of haploid cells is disrupted, resulting in sterility of otherwise healthy animals.
Cyclin A2/Cdk1 is Essential for the in vivo S Phase Entry by Phosphorylating Top2a
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Cdk1 is sufficient to drive the mammalian cell cycle
It is shown that mouse embryos lacking all interphase Cdks undergo organogenesis and develop to midgestation and that in the absence of interphaseCdks, Cdk1 can execute all the events that are required to drive cell division.
Mammalian Cells Cycle without the D-Type Cyclin-Dependent Kinases Cdk4 and Cdk6
Cdk2 and Cdk4 cooperatively control the expression of Cdc2
It is considered that the balance between proliferation and differentiation is disturbed, which affects especially heart development and leads to embryonic lethality in Cdk2-/-Cdk4-/- mutants.
Cdc2–cyclin E complexes regulate the G1/S phase transition
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Dual Regulation of the Anaphase Promoting Complex in Human Cells by Cyclin A-Cdk2 and Cyclin A-Cdk1 Complexes
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Mammalian cyclin-dependent kinases.
Cdk2 Is Required for p53-Independent G2/M Checkpoint Control
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Delayed early embryonic lethality following disruption of the murine cyclin A2 gene
To address the possible redundancy between different cyclins in vivo and also the control of early embryonic cell cycles, the targeted deletion of the murine cyclin A2 gene was undertook, demonstrating that the cyclinA2 gene is essential.
Cyclin-Dependent Kinase-2 Controls Oligodendrocyte Progenitor Cell Cycle Progression and Is Downregulated in Adult Oligodendrocyte Progenitors
The data indicate that cyclin E/cdk2 activity plays a pivotal function in OP cell cycle decisions occurring at G1/S checkpoint; initiation of OP differentiation is independent of cyclinE/CDk2 checkpoint, and intrinsic differences in cyclin N/N expression and activity may underlie the slowly proliferative state that characterizes so-called “quiescent” adult OP cells in vivo.
Targeted Disruption of CDK4 Delays Cell Cycle Entry with Enhanced p27Kip1 Activity
Results suggest that at least part of CDK4’s participation in the rate-limiting mechanism for the G0-S transition consists of controlling p27 activity, which is opposite to those of p27-deficient mice.
S and G2 Phase Roles for Cdk2 Revealed by Inducible Expression of a Dominant-Negative Mutant in Human Cells
Evidence is provided for essential functions of Cdk2 during S and G2 phases of the mammalian cell cycle, as well as stable clones with inducible expression of wild-type and dominant-negative forms of the enzyme.
p21 Is a Critical CDK2 Regulator Essential for Proliferation Control in Rb-deficient Cells
Animals with the genotype Rb +/−;p21 −/− succumbed to tumors more rapidly than Rb -/− mice, suggesting that in certain contexts mutations in these two cell cycle regulators can cooperate in tumor development.
Cyclin-dependent kinase 2 is essential for meiosis but not for mitotic cell division in mice
CDK2 is essential for completion of prophase I during meiotic cell division in male and female germ cells, an unforeseen role for this cell cycle kinase.
Cyclin A1 is required for meiosis in the male mouse
Meiosis arrest in Ccna1–/– males was associated with increased germ cell apoptosis, desynapsis abnormalities and reduction of Cdc2 kinase activation at the end of meiotic prophase, indicating cyclin A1 is essential for spermatocyte passage into the first meiotic division in male mice, a function that cannot be complemented by the concurrently expressed B-type cyclins.
Cyclin E-CDK2 is a regulator of p27Kip1.
CDK inhibitors are thought to prevent cell proliferation by negatively regulating cyclin-CDK complexes. We propose that the opposite is also true, that cyclin-CDK complexes in mammmalian cells can
The Oncogenic Activity of Cyclin E Is Not Confined to Cdk2 Activation Alone but Relies on Several Other, Distinct Functions of the Protein*
This work shows that cyclin E mutants defective to form an active kinase complex with Cdk2 are unable to drive cells from G1 into S phase but can still malignantly transform rat embryo fibroblasts in cooperation with Ha-Ras, and proposes thatcyclin E harbors other functions, independent of Cdk 2 activation and p27Kip1 binding, that contribute significantly to its oncogenic activity.