The retinoblastoma protein RB and the transcription factor p53 are central tumor
suppressors. They are often found inactivated in various tumor types. Both proteins play …

Cellular senescence is a stable cell cycle arrest that can be triggered in normal cells in
response to various intrinsic and extrinsic stimuli, as well as developmental signals …

Cell cycle-dependent gene transcription is tightly controlled by the retinoblastoma (RB): E2F
and DREAM complexes, which repress all cell cycle genes during quiescence. Cyclin …

Ki-67 serves as a prominent cancer marker. We describe how expression of the MKI67 gene
coding for Ki-67 is controlled during the cell cycle. MKI67 mRNA and Ki-67 protein are …

Activation of the p53 tumor suppressor can lead to cell cycle arrest. The key mechanism of
p53-mediated arrest is transcriptional downregulation of many cell cycle genes. In recent …

The DNA-repair capacity in somatic cells is limited compared with that in germ cells. It has
remained unknown whether not only lesion-type-specific, but overall repair capacities could …

Limitless cell proliferation, evasion from apoptosis, dedifferentiation, metastatic spread and
therapy resistance: all these properties of a cancer cell contribute to its malignant phenotype …

The dimerization partner, RB-like, E2F and multi-vulval class B (DREAM) complex provides
a previously unsuspected unifying role in the cell cycle by directly linking p130, p107, E2F …

The precise timing of cell cycle gene expression is critical for the control of cell proliferation;
de-regulation of this timing promotes the formation of cancer and leads to defects during …

The tumor suppressor p53 functions predominantly as a transcription factor by activating and
downregulating gene expression, leading to cell cycle arrest or apoptosis. p53 was shown to …