Mammalian cells cycle without the D-type cyclin-dependent kinases Cdk4 and Cdk6.

By Marcos Malumbres, R. Sotillo, David Santamaría, Javier Galán, Ana Cerezo, Sagrario Ortega, P. Dubus, M. Barbacid. Cell, 2004

857 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/08c7b80cbe9d1dc71c2b7d88aca60103352e83a5

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Citations in the corpus

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”
Mammalian cell-cycle regulation: several Cdks, numerous cyclins and diverse compensatory mechanisms (2009, background): “Cdk6 Hypoplasia of thymus and spleen and defects in hematopoiesis Viable Fertile Nucleus (Malumbres et al., 2004)”
Living with or without cyclins and cyclin-dependent kinases. (2004, background): “Malumbres et al. 2004 CDK4 and CDK6 Progressive embryonic lethality from E14.”
Cyclin-dependent kinase pathways as targets for cancer treatment. (2006, background): “All rights reserved. progression depicted in Figure 1.77 For example, quiescent, serumstarved cdk4/cdk6-null fibroblasts enter S phase with kinetics similar to those of wild-type MEFs (albeit with lower efficiency), and earlypassage double-mutant MEFs displayed a doubling time similar to that of wil”
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).”
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).”
Cyclin-dependent kinases (2014, background): “For instance, Cdk1 is thought to be activated mainly by A- and B-type cyclins but can also bind to, and be activated by, D- or E-type cyclins in the absence of Cdk4/Cdk6 or Cdk2, respectively [9,27,56].”
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.”
Mechanisms of stem cell self-renewal. (2009, background): “Similarly, mice lacking both CDK4 and CDK6 die with defective hematopoiesis, but not until late gestation (Malumbres et al. 2004).”
Cdks, cyclins and CKIs: roles beyond cell cycle regulation (2013, background): “For example, several groups have reported that interphase Cdks, which were deemed essential for mammalian cell cycle progression, are in fact dispensable in mice as their loss did not compromise viability but instead led to phenotypes in highly specialized cell types, including hematopoietic cells i”