ABHD5 knock out mouse

Useful model to study ABHD5 deficiency. Animals might be useful for studies, e.g. on energy metabolism or skin development/barrier function. Mice homozygous for the mutation die shortly after birth due to transepidermal water loss.

Contributors

Inventor Institute
Franz Radner ; Rudolf Zechner University of Graz
Cat. #: 160868
Research Fields: Developmental biology;Metabolism
Target: Abhydrolase domain containing 5, comparative gene identification-58, Chanarin-Dorfman, ichthyosis
Model: Knock-Out
Zygosity: Heterozygous
Strain: C57BL/6J
Phenotype: Homozygote mutants display a severe ichthyosis-type skin barrier dysfunction, which leads to increased transepidermal water loss after birth, and consequently, death of the animal within hours. Further, knockout animals display growth retardation as well as triacylglycerol accumulation in the liver. Triacylglycerol hydrolysis is impaired in various tissues. Omega-O-acylceramide biosynthesis is drastically decreased. In line, keratinocyte differentiation is abnormal.
Alternate name: ABHD5, CGI-58
Product description: Useful model to study ABHD5 deficiency. Animals might be useful for studies, e.g. on energy metabolism or skin development/barrier function. Mice homozygous for the mutation die shortly after birth due to transepidermal water loss.
Conditional: No
Production details: A loxP site was inserted upstream of exon 4 and a floxed neomycin resistance cassette was inserted downstream of exon 7. Cre-mediated recombination removed Abhd5 exon 4 – 7 and the selection cassette. Further details are available upon request.
References:

27725204

Radner et al. 2010. J Biol Chem. 285(10):7300-11. PMID: 20023287.

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