Fragile X syndrome (FXS) is one of the most prevalent forms of heritable mental retardation and developmental delay in males. The syndrome is caused by the silencing of a single gene (fragile X mental retardation-1; FMR1) and the lack of expression of its protein product (fragile X mental retardation-1 protein; FMRP). Recent work has linked the high expression levels of FMRP in the magnocellular layers of lateral geniculate nucleus (M-LGN) of the visual system to a specific reduction of perceptual function known to be mediated by that neural structure. This finding has given rise to the intriguing notion that FMRP expression level may be used as an index of susceptibility of specific brain regions to the observed perceptual and cognitive deficits in FXS. We undertook a comprehensive expression profiling study of FMRP in the monkey to obtain further insight into the link between FMPR expression and the behavioural impact of its loss in FXS. We report here the first 3D whole-brain map of FMRP expression in the Old-World monkey and show that certain brain structures display high FMRP levels, such as the cerebellum, striatum, and temporal lobe structures. This finding provides support for the notion that FMRP expression loss is linked to behavioural and cognitive impairment associated with these structures. We argue that whole-brain FMRP expression mapping may be used to formulate and test new hypotheses about other forms of impairments in FXS that were not specifically examined in this study.
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http://dx.doi.org/10.1016/j.brainres.2009.01.059 | DOI Listing |
Cells
December 2024
Department of Biomedical Sciences, College of Medicine, Florida State University, Tallahassee, FL 32306, USA.
Fragile X Syndrome (FXS) presents with a constellation of phenotypes, including trouble regulating emotion and aggressive behaviors, disordered sleep, intellectual impairments, and atypical physical development. Genetic study of the X chromosome revealed that substantial repeat expansion of the 5' end of the gene fragile X messenger ribonucleoprotein 1 () promoted DNA methylation and, consequently, silenced expression of . Further analysis proved that shorter repeat expansions in also manifested in disease at later stages in life.
View Article and Find Full Text PDFBiochem Biophys Res Commun
January 2025
Department of Biology, Kyung Hee University, Seoul, 02447, South Korea. Electronic address:
Fragile X Mental Retardation Protein 1 (FMR1) is a translational repressor crucial for regulating genes in the central nervous system. While a lack of FMR1 expression causes Fragile X Syndrome (FXS), its overexpression is implicated in various cancers, necessitating tight regulation of FMR1 protein levels for normal cell physiology. In this study, we report that FMR1 is upregulated in gastric cancer patients.
View Article and Find Full Text PDFArch Biochem Biophys
December 2024
Department of Biochemistry and Immunology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil. Electronic address:
UBC13 is an orthologue of Homo sapiens ubiquitin-conjugation E2 enzymes described in Leishmania mexicana, a null mutant lacking this gene cannot be produced, suggesting essential functions in this parasite. Leishmania infantum is an etiological agent of visceral leishmaniasis, the most severe type of disease that is potentially fatal if untreated. The ubiquitination process has been targeted for leishmanicidal compounds, indicating its essential function in parasite homeostasis.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Department of Biomedicine, University of Basel, Mattenstrasse 28, 4058 Basel, Switzerland.
Fragile X Syndrome (FX) is the most common form of inherited cognitive impairment and falls under the broader category of Autism Spectrum Disorders (ASD). FX is caused by a CGG trinucleotide repeat expansion in the non-coding region of the X-linked () gene, leading to its hypermethylation and epigenetic silencing. Animal models of FX rely on the deletion of the gene, which fails to replicate the epigenetic silencing mechanism of the gene observed in human patients.
View Article and Find Full Text PDFAnn Hepatol
December 2024
Department of Internal Medicine, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil. Electronic address:
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