Organ-specific electrophoretic heterogeneity of lysosomal alpha-mannosidase has been observed within individual strains of inbred mice. Polymorphism between C57BL/6J and CBA/J for liver lysosomal alpha-mannosidase is determined by a single genetic locus on chromosome 5 and appears to be the result o
A second gene affecting the sialylation of lysosomal α-mannosidase in mouse liver
✍ Scribed by Mark Dizik; Rosemary W. Elliott
- Book ID
- 104783800
- Publisher
- Springer
- Year
- 1978
- Tongue
- English
- Weight
- 676 KB
- Volume
- 16
- Category
- Article
- ISSN
- 0006-2928
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✦ Synopsis
We have previously reported on a mouse liver-specific genetic polymorphism associated with altered sialylation of lysosomal alpha-mannosidase. A second electrophoretic polymorphism for liver lysosomal alpha-mannosidase has now been found and characterized. This variation, between SWR/J and SM/JCv inbred mice, is determined by a single genetic locus (Map-2) on chromosome 17 and appears to be the result of further differences in sialylation of the lysosomal enzyme. The Map-2 gene appears to affect the processing of liver, spleen, and lung lysosomal alpha-mannosidase, whereas the Map-1 gene appears to be specific to the processing of liver lysosomal alpha-mannosidase (Dizik and Elliott, 1977). The more negatively charged electrophoretic liver phenotype (MA-A) characteristic of the SM/JCv strain is recessive to the phenotype (MA-B) characteristic of the SWR/J strain. In contrast, at the Map-1 locus, the more negatively charged phenotype is dominant. The electrophoretic pattern of development of the liver enzyme from SM/JCv mice is described.
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