Evaluation of CamKII Dependent Regulation of mGluR5-Homer Scaffolds as a Potential Therapeutic for Fragile X Syndrome

With a $90,000 grant from FRAXA Research Foundation, Dr. Kimberly Huber and Dr. Weirui Guo at the University of Texas at Soutnwestern investigated the roles of Homer and CaMKII in Fragile X syndrome.

Kimberly Huber, Ph.D., FRAXA Investigator
$90,000 Grant
Kimberly Huber, PhD
Principal Investigator
University of Texas at Southwestern
2012-2013 FRAXA Research Grant
$90,000 over 2 Years
Funded with support from The Meadows Foundation of/for Texas

Developmental Study of FMRP Dependent Synapse Regulation in Fragile X Syndrome

Enhanced metabotropic glutamate receptor subunit 5 (mGluR5) function is causally associated with the pathophysiology of Fragile X syndrome. Little is known about the molecular mechanisms that cause overactive mGluR5 in Fragile X. mGluR5 is less associated with its intracellular scaffolding protein, Homer, in Fragile X syndrome mice (Fmr1 KO) which is linked with overactive mGluR5 and mGluR5 dysfunction in Fragile X. Drs. Guo and Huber tested their hypothesis that enhanced phosphorylation of Homer by a specific Homer kinase, CaMKII, occurs in the brains of Fmr1 KO mice and leads to enhanced mGluR5 function and Fragile X phenotypes. These experiments would determine if Homer kinases, such as CamKII, could be therapeutic targets for Fragile X syndrome.

Weirui Guo picture

Weirui Guo, PhD
Postdoctoral Fellow

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