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JCI early table of contents for Nov. 12, 2012
Date:11/12/2012

s of our ancestors. Jones and colleagues found that HIV infection stimulated the expression of HERV proteins, effectively tagging HIV-infected cells. Immune cells targeted to these proteins specifically eliminated cells infected with several different strains of HIV in vitro. This study suggests that HERV-targeted immune responses should be considered in the development of HIV vaccines.

TITLE:
HERV-K-targeted T-cells eliminate diverse HIV-1/2 and SIV primary isolates

AUTHOR CONTACT:
Brad Jones
University of Toronto, Toronto, ON, CAN
Phone: 617-777-9151; E-mail: bjones.ut@gmail.com

View this article at: http://www.jci.org/articles/view/64560?key=6bb3867c449f3c243fb1


Researchers find abnormal dopamine signaling in a mouse model of Angelman syndrome

Angelman syndrome (AS) is a developmental disorder characterized by intellectual disability, seizures, sleep disturbances, hand flapping, and a happy demeanor. It is caused by deletion or mutation of a gene on a maternal chromosome in the UBE3A gene. Currently, there is no effective treatment for AS, but several studies have suggested that abnormal dopamine signaling might be an underlying cause of the disorder. In a study published in the Journal of Clinical Investigation, researchers led by C.J. Malanga at the University of North Carolina at Chapel Hill engineered mice lacking maternal Ube3a and found that they exhibit behavior that correlates with abnormal dopamine signaling characterized by increased dopamine release. This study elucidates AS-associated changes in dopamine signaling that should inform clinical trials utilizing dopamine replacement therapy in AS patients.

TITLE:
Pathway-specific dopaminergic deficits in a mouse model of Angelman syndrome

AUTHOR CONTACT:
C.J. Malanga
University o
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Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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