B6.129S1-Ahnak^tm1Vtm/J

Stock number: 007011
Product name: AHNAK KO
Research areas: Immunology, Inflammation and Autoimmunity Research

Description

Mice homozygous for this knock-out mutation exhibit decreased T cell proliferation and increased susceptibility to parasitic infection.

Detailed description

Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. Immunoblot analysis of heart ventricle RNA confirms the absence of expression. Defects in T cell activation and proliferation have been noted. This strain may also be useful in studies of cardiomyocyte physiology.

This allele involves many repeated sequences, making PCR distinction of homozygous and heterozygous genotypes impractical. Southern blot is recommended by the donating lab.

Development

A targeting vector was designed to replace a 5.3-kb genomic fragment containing a segment of the coding region, putative promoter and 5' UTR with a loxP-flanked neomycin resistance gene expression cassette. The targeting vector was linearized and electroporated into 129S1/Sv-p⁺ Tyr⁺ Kitl⁺-derived W9.5 embryonic stem (ES) cells. Clones resistant to G418 and gancyclovir were selected, and homologous recombination was confirmed by Southern blotting. Clones containing the targeted mutation were injected into C57BL/6 blastocysts. Resulting male chimeric mice were bred to C57BL/6 females to obtain heterozygous mice. Heterozygotes were intercrossed to generate homozygotes. This line has been backcrossed to C57BL/6 ten times by the donating laboratory.

Allele

Symbol: Ahnak^tm1Vtm
Name: targeted mutation 1, Vincent T Marchesi
MGI accession ID: MGI:3040870
Generation method: Targeted
Attributes: Null/Knockout
Marker symbol: Ahnak
Marker name: AHNAK nucleoprotein (desmoyokin)
Chromosome: 19
Strain of origin: 129S1/Sv-Oca2⁺ Tyr⁺ Kitl⁺
Molecular note: A floxed neo cassette replaced 5.3 kb of sequence encompassing the putative promoter, 5' UTR, and a segment of the coding region. Northern blot of mutant heart ventricles indicated no transcript was present, and absence of normal protein was confirmed by immunoblot.