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Same protein that fires up cancer-promoting Erk also blocks its activation
Date:4/19/2013

nts showed that Shc blocks Erk function by sequestering it away from the Ras-Raf-Mek MAPK pathway in the worms. Without the Shc-Erk connection, the MAPK pathway is activated, causing excessive Erk activation.

EGFR stimulation not only sets off the normal activation of Erk via Shc and the MAPK pathway, Ladbury said, but also frees Erk for greater availability for activation by breaking the tie to Shc.

Co-authors with Ladbury are first author Kin Man Suen and Chi-Chuan Lin, Ph.D., Fernando Melo, Ph.D., Zamal Ahmed, Ph.D., and Stefan Arold, Ph.D., all of MD Anderson's Department of Biochemistry and Molecular Biology; Roger George, Ph.D., of the London Research Institute of Cancer Research UK; Eleanor Biggs, of the University of Bath, Bath, UK; and Melanie Drake and Swathi Arur, Ph.D., of MD Anderson's Department of Genetics.

Suen is a graduate student in The University of Texas Graduate School of Biomedical Sciences, which is run jointly by MD Anderson and The University of Texas Health Science Center at Houston. Ladbury and Arold also are affiliated with the Center for Biomolecular Structure and Function at MD Anderson.


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Contact: Scott Merville
smerville@mdanderson.org
713-792-0661
University of Texas M. D. Anderson Cancer Center
Source:Eurekalert

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