Living with or without cyclins and cyclin-dependent kinases.

By C. Sherr, J. M. Roberts. Genes & Development, 2004

1,169 citations recorded by the source corpus.

Entry into, progression through, and exit from the G1 phase of the mammalian cell cycle in response to extracellular mitogenic cues are presumed to be governed by cyclin-dependent kinases (Cdks) regulated by the D-type and E-type cyclins. Studies performed over more than a decade have supported the view that these holoenzymes are important, if not required, for these processes. However, recent experiments in which the genes encoding all three D-type cyclins, the two E-type cyclins, cyclin D-dependent Cdk4 and Cdk6, or cyclin E-dependent Cdk2 have been disrupted in the mouse germ line have revealed that much of fetal development occurs normally in their absence. Thus, none of these genes is strictly essential for cell cycle progression. To what extent is the prevailing dogma incorrect, and how can the recent findings be reconciled with past work?

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/8b0b0432c28be634f716005938cddfdf17a85dad

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In Cell Biology

1. E. Musgrove
2. J. Diehl
3. G. Shapiro

In Molecular Biology

1. J. León
2. G. Shapiro
3. G. Bretones
4. M. Delgado

In Oncology

1. E. Musgrove
2. G. Shapiro

Citations in the corpus

• Myc and cell cycle control. (2015, background): “Finally, B-type cyclins (B1 and B2) together with Cdk1 drive cells through mitosis [1,12].”
• The Role of the PERK/eIF2α/ATF4/CHOP Signaling Pathway in Tumor Progression During Endoplasmic Reticulum Stress (2016, background): “Collectively, exposure of cells to stress conditions and activation of UPR trigger PERK-dependent eIF2α phosphorylation which results in repression of protein translation, involving cyclin D1 – a prominent cell cycle regulator, which plays a key role in controlling G1/S transition [78].”
• Cyclin D as a therapeutic target in cancer (2011, background): “The synthesis of individual cyclins, and consequent cyclin-dependent kinase (CDK) activation at specific cell cycle stages, coordinates the sequential completion of DNA replication and cell divisio”
• Cyclin-dependent kinase pathways as targets for cancer treatment. (2006, background): “progression depicted in Figure 1.(77) For example, quiescent, serum-”