Mouse development and cell proliferation in the absence of D-cyclins.

By K. Kozar, M. Ciemerych, V. I. Rebel, H. Shigematsu, A. Zagozdzon, E. Sicinska, Y. Geng, Qunyan Yu, S. Bhattacharya, R. Bronson and 2 more. Cell, 2004

705 citations recorded by the source corpus.

Subfields: Biotechnology, Cancer Research, Oncology

View Paper: https://www.semanticscholar.org/paper/de7806edc122c818f278b5f55947dbbf96a8b16f

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Citations in the corpus

Mammalian cells cycle without the D-type cyclin-dependent kinases Cdk4 and Cdk6. (2004, methodology): “Genotyping of manuscript, Sicinski and coworkers (Kozar et al., 2004 Cdk6-null mice was carried out by PCR amplification using specific [this issue of Cell]) report that MEFs lacking the three oligonucleotides for the normal or mutant allele (primer sequences are available from the authors upon…”
Mammalian cell-cycle regulation: several Cdks, numerous cyclins and diverse compensatory mechanisms (2009, background): “The majority of the cell types including mouse embryonic fibroblasts (MEFs) proliferated relatively normally, though MEFs displayed higher dependence on serum than wild-type cells (Kozar et al., 2004).”
Mechanisms of stem cell self-renewal. (2009, background): “In the absence of D cyclins, HSCs are unable to divide normally and become depleted during fetal development (Kozar et al. 2004).”
Pocket proteins and cell cycle control (2005, neutral): “S progression in mouse fibroblasts (Berthet et al., 2003; Geng et al., 2003; Ortega et al., 2003; Kozar et al., 2004; Malumbres et al., 2004).”
G1 cell-cycle control and cancer (2004, background): “Mice that are defective in all three cyclin D genes die at mid/late gestation of severe anaemia, but not without having normally developed many organs and tissue”
The E2F transcriptional network: old acquaintances with new faces (2005, background): “…of the cell cycle to perturbation during animal development (Berthet et al., 2003; Geng et al., 2003; Ortega et al., 2003; Parisi et al., 2003; Kozar et al., 2004). cdk4 cycD1 p16/Ink4a RB E2F Pathway componentsAlterations in tumors melanoma, colon cancer,mesothelioma, biliary tract,…”
Cyclin D as a therapeutic target in cancer (2011, background): “Many of the non-catalytic effects of the D-type cyclins have been elucidated using cell culture models, and simultaneous knockout of all three D-type cyclins has a very similar phenotype to knockout of both Cdk4 and Cdk6 (REF”
FoxOs cooperatively regulate diverse pathways governing neural stem cell homeostasis (2009, background): “…cycle/quiescence, apoptosis, and intracellular redox status in the maintenance and fate determination within tissue stem cell compartment (Cheng et al., 2000a, 2000b; Doetsch et al., 2002b; Ito et al., 2004, 2006; Kippin et al., 2005; Kozar et al., 2004; Malumbres et al., 2004; Yuan et al., 2004).”
Myc and cell cycle control. (2015, background): “Cyclins D1−/−/D2−/−/D3−/− mouse fibroblasts proliferate normally although they require increased mitogenic stimulation for cell cycle re-entry [22].”
Living with or without cyclins and cyclin-dependent kinases. (2004, methodology): “MEFs can be propagated in culture with decreased ability to enter the cell cycle from quiescence; they express aberrantly high levels of p21 C1p1 and resist transformation by oncogenic Ras + DN-p53.”
Cell cycle, CDKs and cancer: a changing paradigm (2009, background): “Concomitant ablation of the three D-type cyclins results in embryonic lethality owing to haematopoietic defects similar to those observed in mice lacking CDK4 and CDK6, suggesting that the D-type cyclins are the functional activators of these G1 kinase”