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JCI early table of contents for July 16, 2012
Date:7/16/2012

of the ATR/CHK1 signaling pathway, known as HCLK2, associated with and was hydroxylated by prolyl hydroxylase domain protein 3 (PHD3). HCLK2 hydroxylation was necessary for its interaction with ATR and the subsequent activation of the DDR. Inhibiting PHD3 prevented activation of the ATR/CHK1/p53 pathway and decreased cell death induced by DNA damage. Consistent with these observations, they found that mice lacking PHD3 were resistant to the effects of ionizing radiation and had decreased thymic apoptosis, a biomarker of genomic integrity.

TITLE:

PHD3-dependent hydroxylation of HCLK2 promotes the DNA damage response

AUTHOR CONTACT:

Cam Patterson

University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

Phone: 919-843-6477; Fax: 9198434585; E-mail: cpatters@med.unc.edu

View this article at: http://www.jci.org/articles/view/62374?key=2f34187c2dec70f6cd0e

OPHTHALMOLOGY

Inflammation and age−related retinal degeneration | Back to top

Disruption of cellular processes affected by multiple genes and accumulation of numerous insults throughout life dictate the progression of age−related disorders, but their complex etiology is poorly understood. Post−mitotic neurons, such as photoreceptor cells in the retina, and the adjacent retinal pigmented epithelium that together maintain vision, are especially susceptible to age−related retinal degeneration (ARD). The multi-genic etiology of ARD in humans is reflected by the relative paucity of effective compounds for its early prevention and treatment. To understand the background genetic differences that drive the phenotypic progression of ARD, Dr. Krzysztof Palczewski and colleagues at Case Western University in Cleveland, OH studied a strain of mice that develop more pronounced AR
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Contact: Sarah Jackson
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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