You are currently viewing the abstract.
View Full TextLog in to view the full text
AAAS login provides access to Science for AAAS members, and access to other journals in the Science family to users who have purchased individual subscriptions.
More options
Download and print this article for your personal scholarly, research, and educational use.
Buy a single issue of Science for just $15 USD.
Abstract
Data accumulated over more than three decades demonstrate that the assembly of macrocomplexes, mainly of dimers, is widespread among the members of the different tiers that constitute the RAS-ERK pathway. In this issue of Science Signaling, Yuan et al. report that MEK1 homodimerization is necessary for signal transduction through the RAF-ERK pathway and that cancer-related MEK1 mutations confer enhanced dimerization and resistance to MEK inhibitors. These findings endorse interference with RAS-ERK pathway–component dimerization as a potential therapeutic strategy in cancer patients.
This is an article distributed under the terms of the Science Journals Default License.
