B6.129-Selplg^tm1Rpmc/J

Stock number: 006336
Product name: PSGL-1 KO
Research areas: Cardiovascular Research, Immunology, Inflammation and Autoimmunity Research

Description

Homozygous PSGL-1 knock-out mice (Selplg^tm1Rpmc} exhibit elevated total leukocyte counts, and may be useful in studies relating to the inflammatory response.

Detailed description

Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by flow cytometry analysis of leukocytes. Homozygotes have elevated total leukocyte counts, with increased numbers of neutrophils, lympohcytes and eosinophils. Leukocytes isolated from homozygotes exhibit abnormal tethering and rolling (adhesion and migration) due to impaired attachment. This mutant mouse strain represents a model that may be useful in studies of leukocyte adhesion and migration in the inflammatory response.

This strain was transferred from the collection of the Consortium for Functional Glycomics.

Development

A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt the 5’ end of exon 2 and the ATG translational start site sequence. The construct was electroporated into 129S1/Sv-p⁺ Tyr⁺ Kitl^Sl-J/+ derived CJ7 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. The resulting chimeric animals were crossed to C57BL/6J mice. Heterozygotes were crossed to generate homozygotes. The mice were then backcrossed to C57BL/6J for 5 generations.

Allele

Symbol: Selplg^tm1Rpmc
Name: targeted mutation 1, Rodger P McEver
MGI accession ID: MGI:2180375
Generation method: Targeted
Attributes: Null/Knockout
Synonyms: PSGL-1-; PSGL-1 KO; Selpl^-
Marker symbol: Selplg
Marker name: selectin, platelet (p-selectin) ligand
Marker synonyms: CD162; CLA; Psgl1; PSGL-1; Selpl
Chromosome: 5
Strain of origin: 129S1/Sv-Oca2⁺ Tyr⁺ Kitl⁺
Molecular note: A neomycin resistance cassette replaced the 5' portion of exon 2, which includes the translation initiation start site, via homologous recombination. Flow cytometry was used to confirm the absence of gene expression in leukocytes of homozygous mutant animals.