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Strain Detail: Cmah-KO(129) mice
|Institution||Clinical Laboratory Science / Biological Chemistry, Graduate School of Medicine, Kyoto University|
|Conditions of distribution||
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|Animal Health Report|
The Cmah-KO(129) mice are knockout mice deficient for the enzyme cytidine monophospho-N-acetylneuraminic acid hydroxylase (Cmah), which catalyzes the converting reaction from N-acetylneuraminic acid to N-glycolylneuraminic acid in sialylated molecules. Therefore, the mice have sialylated molecules with N-acetylneuraminic acid only. Systemic effect of the Cmah deficiency is not entirely revealed yet, but the Cmah-KO mice showed hyperresponsive B cell phenotypes in assays measuring B-cell functions, i.e., antibody production and proliferation. The mice also showed activation-dependent dynamic reduction of CD22 ligand expression, and great increase of ligand expression for sialoadhesin (Siglec-1, CD169).
Humans (Homo sapiens) lack the Cmah gene unlike chimpanzee and bonobo, in which the Cmah gene is conserved. The Cmah-KO mice can be used as models for humans in terms of the sialic acid species in sialylated molecules. In this sense, the Cmah-KO strain serves as a base strain for creating mouse models for medical research in human diseases.
Care should be taken for the proliferation of the mice because their reproductive performances are not good.
|From other institutions||Genotype|
|Cryopreserved embryo||In-house||Mating System||IVF|
|Genotype||heterozygous and homozygous|
|From other institutions||Mating System|
|Strain status / Availability||Cryopreserved sperm||Within 1 month|
|Cryopreserved embryo||Within 1 month|
|Live animals||Approx. 2 months|
|Gene name||cytidine monophospho-N-acetylneuraminic acid hydroxylase|