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JCI early table of contents for March 25, 2013
Date:3/25/2013

key=94b8b0c4a137ae990970

ACCOMPANYING ARTICLE

TITLE:
Striking the target in iron overload disorders

AUTHOR CONTACT:
Karin Finberg
Duke University Medical School, Durham, NC, USA
Phone: +1 919.684.3491; Fax: ; E-mail: karin.finberg@duke.edu

View this article at: http://www.jci.org/articles/view/68889?key=c5c95c5b3a8b1b1152ed

Protein pair promotes skin regeneration

Because skin protects our bodies from pathogens and harsh environmental conditions, it must undego constant renewal. The cells that form the top most layer of the skin, known as cornified keratinocytes, are shed constantly and must be resupplied. Repression of a cellular signaling pathway mediated by ERK proteins is required for differentiation of keratinocytes, but this pathway is hyperactivated in a group of disorders known as RASopathies. In this issue of the Journal of Clinical Investigaiton, researchers led by Kathleen Green at Northwestern University, identified a pair of proteins that function to suppress ERK activation and drive the development of keratinocytes. In skin cells, two proteins, RAS and SHOC2 form a complex that activates ERK. Green and colleagues found that the proteins Erbin and DSG1 disrupt SHOC2/RAS complexes and prevent ERK activation. These findings reveal a previously unknown role for DSG1/Erbin in skin disorders. In a companion commentary, John Stanley of the University of Pennsylvania discusses how these findings contribute to our understanding of how skin is maintained.

TITLE:
Desmoglein-1/Erbin interaction suppresses ERK activation to support epidermal differentiation

AUTHOR CONTACT:
Kathleen J. Green
Professor, Chicago, IL, USA
Phone: 312-503-5300; Fax: 312-503-8240; E-mail: kgreen@northwestern.edu
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Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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