Science Signaling Podcast: 6 March 2012

John G. Albeck¹, Joan S. Brugge¹, and Annalisa M. VanHook²

¹ Department of Cell Biology, Harvard Medical School, Boston, MA, USA.
² Web Editor, Science Signaling, American Association for the Advancement of Science, 1200 New York Avenue, NW, Washington, DC 20005, USA.

Abstract: This Podcast features a conversation with authors of a Research Article published in the 6 March 2012 issue of Science Signaling. Joan Brugge and John Albeck discuss their work on a mechanism of crosstalk between growth factor signaling pathways that control proliferation in breast epithelial cells. Insulin-like growth factor 1 (IGF-1) and epidermal growth factor (EGF) both promoted proliferation of breast epithelial cells, but only EGF stimulated proliferation on its own. IGF-1 did not stimulate proliferation on its own, but instead enhanced the proliferative response to EGF. The signaling cascades stimulated by EGF and IGF-1, which are commonly used as indicators of oncogenic signaling, differentially regulated the activity of the cell cycle inhibitor p57. Thus, the status of p57 may indicate which pathway to inhibit in breast cancer.

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Cancer
Akt and ERK Control the Proliferative Response of Mammary Epithelial Cells to the Growth Factors IGF-1 and EGF Through the Cell Cycle Inhibitor p57^Kip2

Devin T. Worster, Tobias Schmelzle, Nicole L. Solimini, Eric S. Lightcap, Bjorn Millard, Gordon B. Mills, Joan S. Brugge, and John G. Albeck (6 March 2012)
Sci. Signal. 5 (214), ra19. [DOI: 10.1126/scisignal.2001986]
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Sci. Signal. 3 (124), ra43. [DOI: 10.1126/scisignal.2000876]
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Biochemistry
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MicroRNAs Differentially Regulated by Akt Isoforms Control EMT and Stem Cell Renewal in Cancer Cells

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Developmental Biology
Nedd4 Controls Animal Growth by Regulating IGF-1 Signaling

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