Strain Detail: Cmah-KO(129) mice

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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.

1. Naito Y, Takematsu H, Koyama S, Miyake S, Yamamoto H, Fujinawa R, Sugai M, Okuno Y, Tsujimoto G, Yamaji T, Hashimoto Y, Itohara S, Kawasaki T, Suzuki A, and Kozutsumi Y. (2007) Germinal center marker GL7 probes activation-dependent repression of N-glycolylneuraminic acid, a sialic acid species involved in the negative modulation of B-cell activation. Mol Cell Biol 27(8):3008-22. [PMID:17296732]