Protemic Data Indicates Altered Steady State and De Novo Protein Expression in Fragile X Syndrome
- Description
Fragile X syndrome (FXS) is caused by changes in FMR1 gene, which leads to transcriptional silencing and loss of its protein product fragile X mental retardation protein (FMRP). For this study, proteomic experiments were performed to investigate the de novo translational profile in FXS model mice is altered at steady state and in response to metabotropic glutamate receptor (mGluR) stimulation. Altered proteins, hexokinase 1 (HK1) and RAS, are also expressed in the blood of FXS model mice and plasma levels of HK1 and RAS differ between FXS patients and healthy volunteers.
The dataset contains proteomic data as well as supplementary data tied to the publication. The supplementary data contains data about wild-type and knockout steady state results, top 20 DAVID GO clusters, complete mass spectrometry results, and top 20 DAVID GO table of top functional clusters for knockout mice. The supplementary data also contains data about steady state de novo proteome of wild-type and Fmr1 knockout mice, mGluR-stimulated de novo proteome of wild-type and Fmr1 knockout mice, steady state and mGluR-stimulated de novo proteomes in Fmr1 knockout mice, whole blood levels of RAS and HK1 in Fmr1 knockout mice, and BONLAC candidate proteins in human FXS patient plasma.
Access
- Restrictions
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Free to All
- Instructions
- All raw proteomic data can be found at MassIVE and DAVID original data can be found at Google Drive. All data needed to evaluate the conclusions in the paper are present in the Supplementary Materials.
- Grant Support
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FRAXA Research Foundation/FRAXA Research Foundation1507946/NSFCharles H. Revson Senior Biomedical Fellowship/Charles H. Revson Senior Biomedical FellowshipDepartment of Biotechnology, Government of India/Department of Biotechnology, Government of India