![Disruptions in protein-protein interactions between HTT, PRPF40B, and MECP2 are involved in Lopes-Maciel-Rodan syndrome](/rails/active_storage/representations/proxy/eyJfcmFpbHMiOnsibWVzc2FnZSI6IkJBaHBBajBMIiwiZXhwIjpudWxsLCJwdXIiOiJibG9iX2lkIn19--ae2a1e4948187afbdcf0aa1470f507e7befdf765/eyJfcmFpbHMiOnsibWVzc2FnZSI6IkJBaDdCem9MWm05eWJXRjBTU0lJYW5CbkJqb0dSVlE2QzNKbGMybDZaVWtpRFRZd01IZzJNREErQmpzR1ZBPT0iLCJleHAiOm51bGwsInB1ciI6InZhcmlhdGlvbiJ9fQ==--a3b53ba1a0f83efef18f6e75a8d4ce784384bee2/Figure_5_JEI-21-180.jpg)
In an extensive study of gene mutations, and their resulting effect on protein-protein interactions, Desai and Stork found that HTT-PRPF40B-MECP2 interactions are weakened with progression of Lopes-Maciel-Rodan syndrome.
Read More...Disruptions in protein-protein interactions between HTT, PRPF40B, and MECP2 are involved in Lopes-Maciel-Rodan syndrome
In an extensive study of gene mutations, and their resulting effect on protein-protein interactions, Desai and Stork found that HTT-PRPF40B-MECP2 interactions are weakened with progression of Lopes-Maciel-Rodan syndrome.
Read More...The Effect of the Human MeCP2 gene on Drosophila melanogaster behavior and p53 inhibition as a model for Rett Syndrome
In this study, the authors observe if the symptoms of Rett Syndrome, a neurodegenerative disease in humans, are reflected in Drosophila melanogaster. This was achieved by differentiating the behavior and physical aspects of wild-type flies from flies expressing the full-length MeCP2 gene and the mutated MeCP2 gene (R106W). After conducting these experiments, some of the Rett Syndrome symptoms were recapitulated in Drosophila, and a subset of those were partially ameliorated by the introduction of pifithrin-alpha.
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