Abstract

The extracellular signal-regulated kinase (ERK1/2) cascade regulates a myriad of functions in multicellular organisms. Scaffold proteins provide critical spatial and temporal control over the specificity of signaling. Shoc2 is a scaffold that accelerates activity of the ERK1/2 pathway. Loss of Shoc2 expression in mice results in embryonic lethality, thus highlighting the essential role of Shoc2 in embryogenesis. In agreement, patients carrying mutated Shoc2 suffer from a wide spectrum of developmental deficiencies. Efforts to understand the mechanisms by which Shoc2 controls ERK1/2 activity revealed the intricate machinery that governs the ability of Shoc2 to transduce signals of the ERK1/2 pathway. Understanding the mechanisms by which Shoc2 contributes to a high degree of specificity of ERK1/2 signaling as well as deciphering the biological functions of Shoc2 in development and human disorders are major unresolved questions.

Document Type

Article

Publication Date

5-18-2016

Notes/Citation Information

Published in Communicative & Integrative Biology, v. 9, no. 4, article e1188241, p. 1-7.

© 2016 The Author(s). Published with license by Taylor & Francis.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

Digital Object Identifier (DOI)

https://doi.org/10.1080/19420889.2016.1188241

Funding Information

Support for this work was provided by the National Cancer Institute (R00CA126161 to EG), the National Institute of General Medical Sciences (R01GM113087 to EG) and the American Cancer Society (RSG-14-172-01-CSM to EG).

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