Disease relevance of gt

• Moreover, the transmissible agent of gt disease differs from both Cas-Br-M MuLV and scrapie in its disease-inducing properties in NFS/N mice [1].
• A comparison of the pathology of gt to that caused by unconventional agents and neurotropic retroviruses suggests that gt may be valuable in conceptually unifying the whole class of noninflammatory spongiform lesions [2].

High impact information on gt

• Scrapie-associated fibrils, readily identifiable in subcellular fractions of brains from scrapie-inoculated NFS/N mice, were not detected in similar brain fractions from NFS/N mice inoculated with gt brain homogenates [1].
• Gray tremor (gt) is an autosomal recessive mutation in the mouse linked to caracul (Ca) on chromosome 15 [3].
• The heterozygote (+/gt) is phenotypically normal but develops a mild spongiform encephalopathy from 2 months of age onward [3].
• The present study describes the histopathology, topography, developmental sequence, and ultrastructure of the inherited spongiform encephalopathy in the gray tremor homozygote (gt/gt) [2].
• Further analyses using vimentin chemically cleaved by 2-nitro-5-thio-cyanobenzoic acid, and lambda gt 11 cDNA which encoded a partial sequence of vimentin indicated that six mAbs recognized epitopes between amino acids 1 and 313 and the other four mAbs recognized epitopes in the area between residues 314 and 326 [4].

Anatomical context of gt

• We describe the partial cloning and sequencing of the Ki-1/57 cDNA from a lambda gt 11-cDNA library derived from the Hodgkin-analogous cell line L540 [5].

References