These mutant mice, commonly referred to as NOD.scid12LOKO, combine the features of the NOD/ShiLtJ background, the severe combined immune deficiency mutation (scid), and Alox15 deficiency This mutant mouse strain may be useful for adoptive transfer studies to further investigate the role of Alox15 in autoimmunity.
Dr. Jerry L Nadler, Eastern Virginia Medical School
Mice homozygous for Alox15tm1Fun and Prkdcscid, commonly referred to as NOD.scid12LOKO, are viable and fertile. NOD.scid12LOKO mice injected with NOD/ShiLtJ, Stock No. 001976, splenocytes do not develop diabetes. This strain may be useful in adoptive transfer studies.
|Allele Name||severe combined immunodeficiency|
|Gene Symbol and Name||Prkdc, protein kinase, DNA activated, catalytic polypeptide|
|Site of Expression||T and B lymphocytes.|
|Strain of Origin||C.BKa-Ighb/Icr|
|Molecular Note||A T-to-A transversion point mutation at a position corresponding to codon 4046 (codon 4095 in transcript ENSMUST00000023352.8) created a premature stop codon (p.Y4046*).|
|Allele Name||targeted mutation 1, Colin D Funk|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||12/15-LO-; 12/15-LO KO; 12Lox KO; L-12/15-LOX KO; L-12LO-|
|Gene Symbol and Name||Alox15, arachidonate 15-lipoxygenase|
|Strain of Origin||129S2/SvPas|
|Molecular Note||Insertion of a neomycin resistance cassette into exon 3 disrupted the Alox15 gene. Northern blot analyses of resident peritoneal macrophages and of bone marrow-derived macrophages did not detect transcript in homozygous mutant mice. Western blot analysis of resident peritoneal macrophages did not detect ALOX15 in homozygous mutant mice.|
|Mutations Made By|| |
Colin Funk, Queen's University