The retinoblastoma tumour suppressor in development and cancer

By M. Classon, E. Harlow. Nature Reviews. Cancer, 2002

793 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Cancer genes and the pathways they control (2004, background): “The products of these genes include proteins as diverse as cdk4 (a kinase), cyclin D1 (which interacts with and activates cdk4), Rb (a transcription factor) and p16 (which interacts with and inhibits cdk4”
The E2F transcriptional network: old acquaintances with new faces (2005, background): “Further support comes from studies of mice carrying mutant alleles of RB and E2F family members (reviewed in Lipinski and Jacks, 1999; Nevins, 2001; Classon and Dyson, 2001; Classon and Harlow, 2002; DeGregori, 2002; Cam and Dynlacht, 2003).”
Cellular mechanisms of tumour suppression by the retinoblastoma gene (2008, background): “The role of RB in promoting cellular differentiation during embryonic development and in adult lineages has been well characterized in mutant mice and in vitro system”
Does the ribosome translate cancer? (2003, background): “Its function as tumour suppressor has been attributed to its ability to regulate the cell cycle, which involves modulation of the transcriptional activity of E2”
p38 MAP kinase inhibition enables proliferation of adult mammalian cardiomyocytes. (2005, background): “Finally, p38 inhibitor and FGF1, but neither factor alone, led to phosphorylation of Rb, a key cell cycle regulator (Fig. 1C,D; Classon and Harlow 2002).”