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Fragile X and Down syndromes share signalling pathway for intellectual disability
Date:8/3/2012

yndrome mice have difficulties with memory and brain function, and the formation of the heart is often compromised, symptoms that are also observed in humans with Down syndrome. Both model systems are very useful to scientists looking to dissect the molecular events that occur as the disorders take hold.

The scientists revealed that the Down syndrome critical region 1 protein (DSCR1) interacts with Fragile X mental retardation protein (FMRP) to regulate dendritic spine formation and local protein synthesis. By using specific antibodies that bind to the proteins as well as fluorescent labeling techniques they showed that DSCR1 specifically interacts with the phosphorylated form of FMRP. The overlapping molecular pathways of intellectual disability in both genetic disorders suggest that a common therapeutic approach might be feasible for both syndromes.

Min remarked: "We believe these experiments provide an important step forward in understanding the multiple roles of DSCR1 in neurons and in identifying a molecular interaction that is closely linked to intellectual disability for both syndromes."

DSCR1 interacts with FMRP and is required for spine morphogenesis and local protein synthesis


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Contact: Barry Whyte
barry.whyte@embo.org
49-622-188-91108
European Molecular Biology Organization
Source:Eurekalert  

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