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- W2064202261 endingPage "894" @default.
- W2064202261 startingPage "887" @default.
- W2064202261 abstract "Fragile X syndrome (FXS) is a common form of mental disability and one of the known causes of autism. The mutation responsible for FXS is a large expansion of the trinucleotide CGG repeats that leads to DNA methylation of the fragile X mental retardation gene 1 (FMR1) and transcriptional silencing, resulting in the absence of fragile X mental retardation protein (FMRP), an mRNA binding protein. Although it is widely known that FMRP is critical for metabotropic glutamate receptor (mGluR)-dependent long-term depression (LTD), which has provided a general theme for developing pharmacological drugs for FXS, specific downstream targets of FMRP may also be of therapeutic value. Since alterations in potassium channel expression level or activity could underlie neuronal network defects in FXS, here we describe recent findings on how these channels might be altered in mouse models of FXS and the possible therapeutic avenues for treating FXS." @default.
- W2064202261 created "2016-06-24" @default.
- W2064202261 creator A5041305380 @default.
- W2064202261 creator A5048173084 @default.
- W2064202261 date "2012-10-01" @default.
- W2064202261 modified "2023-09-27" @default.
- W2064202261 title "Fragile X syndrome: mechanistic insights and therapeutic avenues regarding the role of potassium channels" @default.
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