These mice express Bmf (BCL2 modifying factor) with a targeted Ser74Ala mutation. They provide a model for defects in JNK(Mapk8)-induced apoptosis mediated by Bmf phosphorylation.
Roger J Davis, University of Massachusetts Medical Sch.
These mice express Bmf (BCL2 modifying factor) with a targeted Ser74Ala mutation. They provide a model for defects in JNK(Mapk8)-induced apoptosis mediated by Bmf phosphorylation. This mutation does not affect expression in the spleen.
A loxP-flanked neomycin resistance cassette was introduced to intron 3 and a Ser74Ala (S74A) mutation with novel Nae1 restriction site was created in codon 74/exon 3 (AGTCCA to GCGCCG). TC1 129S6/SvEvTac-derived embryonic stem (ES) cells were used to create the mutation. The floxed neomycin cassette was excised with germline protamine (Prm) PC3-cre recombinase on a C57BL/6 background, leaving a single loxP site. This strain was backcrossed to C57BL/6 for ten generations by the donating laboratory.
|Allele Name||targeted mutation 2.1, Roger J Davis|
|Allele Type||Targeted (Not Specified)|
|Allele Synonym(s)||BmfS74D; BmfSD|
|Gene Symbol and Name||Bmf, BCL2 modifying factor|
|Promoter||Bmf, BCL2 modifying factor, mouse, laboratory|
|Strain of Origin||129S6/SvEvTac|
|Molecular Note||A floxed neo cassette was inserted within intron 3, and specific nucleotide mutations in exon 3 were introduced by homologous recombination. Mutation resulted in the JNK protein kinase phosphorylation site (Ser-74) in exon 3 to be substituted with an Asp (S74D). The neo cassette was then excised with Cre mediated recombination leaving a single loxP site in intron 3.|
|Mutations Made By|| |
Roger Davis, University of Massachusetts Medical Sch.
When maintained as a live colony, homozygotes may be bred.
When using the B6.129S6-Bmftm2.1Rjd/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #011022 in your Materials and Methods section.