[HTML][HTML] Choosing anticancer drug targets in the postgenomic era

WG Kaelin - The Journal of Clinical Investigation, 1999 - Am Soc Clin Investig
WG Kaelin
The Journal of Clinical Investigation, 1999Am Soc Clin Investig
Simplified views of the pRB and p53 pathways. The cdk4 and cdk6 kinases are positively
regulated by G1 cyclins such as the D-type cyclins and negatively regulated by cdk inhibitors
such as p16/INK4A. Cdk4 and Cdk6 phosphorylate, and thus inhibit, the retinoblastoma
protein (pRB). pRB forms complexes with members of the E2F transcription factor family.
These complexes repress transcription from E2F-responsive promoters. p53 is a sequence-
specific DNA-binding protein that transcriptionally activates target genes such as p21/WAF1 …
Simplified views of the pRB and p53 pathways. The cdk4 and cdk6 kinases are positively regulated by G1 cyclins such as the D-type cyclins and negatively regulated by cdk inhibitors such as p16/INK4A. Cdk4 and Cdk6 phosphorylate, and thus inhibit, the retinoblastoma protein (pRB). pRB forms complexes with members of the E2F transcription factor family. These complexes repress transcription from E2F-responsive promoters. p53 is a sequence-specific DNA-binding protein that transcriptionally activates target genes such as p21/WAF1 and BAX. HDM2 silences the p53 transcriptional activation domain and targets p53 for degradation. ARF antagonizes HDM2. As indicated by the dashed lines, these apparently linear pathways are subject to cross-talk, which links them into a more complex regulatory network.
The Journal of Clinical Investigation