Scheid Signalling Lab @ York University

A study published March 22 in the New England Journal of Medicine shows how a monoclonal antibody reactive to a serine protease (PCSK9) may have significant therapeutic potential. Developed by Regeneron and Sanofi.

Evan A. Stein, M.D., Ph.D., Scott Mellis, M.D., Ph.D., George D. Yancopoulos, M.D., Ph.D., Neil Stahl, Ph.D., Douglas Logan, M.D., William B. Smith, M.D., Eleanor Lisbon, M.D., M.P.H., Maria Gutierrez, M.D., Cheryle Webb, M.D., Richard Wu, Ph.D., Yunling Du, Ph.D., Therese Kranz, R.N., M.B.A., Evelyn Gasparino, B.S., and Gary D. Swergold, M.D., Ph.D.   N Engl J Med 2012; 366:1108-1118. March 22, 2012.

Link to paper here.

PTEN continues to be a hot topic with a Science Signaling paper from Tibarewal and coworkers describing their work isolating the lipid and protein phosphatase activities on gene expression effects and cell invasion . See the Editors comments and article here.

P. Tibarewal, G. Zilidis, L. Spinelli, N. Schurch, H. Maccario, A. Gray, N. M. Perera, L. Davidson, G. J. Barton, N. R. Leslie, PTEN Protein Phosphatase Activity Correlates with Control of Gene Expression and Invasion, a Tumor-Suppressing Phenotype, But Not with AKT Activity. Sci. Signal. 5, ra18 (2012).

Big week in the lipid phosphatase world. The Pandolfi group reports in Cell the physiology of transgenic mice that express elevated PTEN. Surprising effects on metabolism. Click below on the graphical summary from the Cell website to reach the full article.

Cell, 06 March 2012 Copyright © 2012 Elsevier Inc. All rights reserved.

A recent paper by Worster and colleagues have provided some clues as to why PKB/Akt-dependent proliferation requires ERK activity, in this weeks edition of Science Signaling. See the Editors comments here with a link to the full citation.

D. T. Worster, T. Schmelzle, N. L. Solimini, E. S. Lightcap, B. Millard, G. B. Mills, J. S. Brugge, J. G. Albeck, 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. Sci. Signal. 5, ra19 (2012).