Science Signaling Podcast: 23 October 2012
Stephen D. Nimer1,2 and
Annalisa M. VanHook3
1 Molecular Pharmacology and Chemistry Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.
2 Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, Florida 33136, USA.
3 Web Editor, Science Signaling, American Association for the Advancement of Science, 1200 New York Avenue, NW, Washington, DC 20005, USA.
Abstract:
This Podcast features an interview with Stephen Nimer, senior author of a Research Article published in the 23 October 2012 issue of Science Signaling. Nimer discusses his group’s finding that Akt signaling stimulates expression of the Ink4a-Arf locus, which encodes the cell cycle regulator p16 and the tumor suppressor p19. The kinase Akt, which is activated by growth signals and is often activated in cancer cells, phophorylated the transcriptional silencer Bmi1 to cause it to dissociate from the Ink4a-Arf locus. The resulting increase in abundance of p16 and p19 led to decreased cell proliferation, tumor growth, and self-renewal of stem and progenitor cells. Therefore, in addition to mediating growth signaling, Akt can also initiate a feedback loop that counteracts growth signaling.
