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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

The FMR-1 protein is cytoplasmic, most abundant in neurons and appears normal in carriers of a fragile X premutation.

Fragile X mental retardation syndrome is caused by the unstable expansion of a CGG repeat in the FMR-1 gene. In patients with a full mutation, abnormal methylation results in suppression of FMR-1 transcription. FMR-1 is expressed in many tissues but its function is unknown. We have raised monoclonal antibodies specific for the FMR-1 protein. They detect 4-5 protein bands which appear identical in cells of normal males and of males carrying a premutation, but are absent in affected males with a full mutation. Immunohistochemistry shows a cytoplasmic localization of FMR-1. The highest levels were observed in neurons, while glial cells contain very low levels. In epithelial tissues, levels of FMR-1 were higher in dividing layers. In adult testis, FMR-1 was detected only in spermatogonia. FMR-1 was not detected in dermis and cardiac muscle except under pathological conditions.[1]

References

  1. The FMR-1 protein is cytoplasmic, most abundant in neurons and appears normal in carriers of a fragile X premutation. Devys, D., Lutz, Y., Rouyer, N., Bellocq, J.P., Mandel, J.L. Nat. Genet. (1993) [Pubmed]
 
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