Homozygotes are viable, fertile, and exhibit normal development. The mutant mice are indistinguishable from normal controls in their responses to bacterial infectious challenge and endotoxin infusion. No differences are seen in monocyte recruitment into the peritoneum after thioglycollate injection. Epidermal wound healing is equivalent between homozygous mutants and wildtype controls. No obvious phenotype has been noted other than a mild decrease in blood platelet count and borderline significant low leukocyte count. Absence of protein synthesis has been confirmed in endotoxin-stimulated monocytes through Western blot analysis.
A targeting vector was designed to replace exons 3-8 with a neomycin resistance cassette. The targeting vector was introduced to 129S1-derived CJ7 embryonic stem (ES) cells. This line has been backcrossed to C57BL/6 for 20 generations by the donating laboratory.
|Allele Name||targeted mutation 1, David Ginsburg|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Serpinb2, serine (or cysteine) peptidase inhibitor, clade B, member 2|
|Strain of Origin||129S1/Sv-Oca2+ Tyr+ Kitl+|
|Molecular Note||A neomycin resistance cassette replaced exons 3-8. Western analysis of cultured monocytes did not detect immunoreactive protein in homozygous mutant mice.|
|Mutations Made By|| |
David Ginsburg, University of Michigan
When maintained as a live colony, this strain may be bred homozygously.
When using the B6.129S1-Serpinb2tm1Dgi/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #007234 in your Materials and Methods section.