These Bak1 knock-out mice have no phenotypic abnormalities, but are useful when bred with Bax knock-out mice to produce a double knock-out for purposes of studying defects in the regulation of apoptosis during development and tissue homeostasis, or with other specific knock-out mice for studies of autoimmune disease.
Tullia Lindsten, Memorial Sloan Kettering Cancer Center
Mice that are homozygous null for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. There were no statistically significant differences in apoptotic cell survival assays between the mutant and wild-type.
Used in conjunction with strain B6.129X1-Baxtm1Sjk (see Stock No. 002994), to generate the double knock-out Bak/Bax, a model for demonstrating severe defects in the regulation of apoptosis during development and tissue homeostasis.
When bred to a strain with loxP sites inserted into one Bax locus and a null allele at the other locus (Stock No. 006329) and a strain with a Cd19 null allele and expressing Cre recombinase during B lymphocyte development and differentiation (Stock No. 004126), this mutant mouse strain may be useful in studies of autoimmune disease.
When bred to a strain with loxP sites inserted into one Bax locus and a null allele at the other locus (Stock No. 006329) and a strain expressing interferon inducible Cre recombinase (Stock No. 003556), this mutant mouse strain may be useful in studies of autoimmune disease.
A targeting vector containing the neomycin resistance gene was used to remove exons III-VI of the Bak1 gene. The construct was electroporated into 129X1/SvJ x 129S1/Sv-derived R1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric animals were backcrossed to C57BL/6 mice.
|Allele Name||targeted mutation 1, Craig B Thompson|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Bak1, BCL2-antagonist/killer 1|
|Strain of Origin||(129X1/SvJ x 129S1/Sv)F1-Kitl+|
|Molecular Note||A neomycin resistance cassette replaced a genomic fragment containing exons 2-6. These exons encode the Bcl-2 homology domains of the encoded protein. Western blot analysis on spleen and thymus lysates derived from homozygous mice confirmed that no detectable protein is expressed from this allele.|
|Mutations Made By|| |
Craig Thompson, Memorial Sloan Kettering Cancer Center
Mice arose on a B6;129 background and has been backcrossed to C57Bl/6 for 5 generations before being made homozygous.
When using the bak- mouse strain in a publication, please cite the originating article(s) and include JAX stock #004183 in your Materials and Methods section.
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