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Siglec-E KO mouse

Info

Catalogue Number 154181
Antigen/Gene or Protein Targets Siglec-E
Synonyms Siglec-9, Sialic Acid Binding Ig Like Lectin 9, CD329, Protein FOAP-9
Model Knock-Out
Relevance Siglecs are type 1 membrane proteins of the Ig superfamily that mediate sialic acid–dependent interactions with ligands via their N-terminal Ig domain. Siglec-E is the murine version of human Siglec-9, and is an inhibitory receptor expressed constitutively on neutrophils and is induced on macrophages during inflammation
Production Details Siglec E KO mice were generated by targeting the Siglec E gene in embryonic stem (ES) cells by homologous recombination. The Siglec E homology region was subcloned from a phage library of 129/Sv mouse genomic DNA. A targeting vector was constructed containing a 2.2kb XhoI/NdeI 5’ short homology arm, a 1.2kb neomycin cassette and a 6kb ClaI/HindIII 3’ long homology arm. After linearizing with NotI, E14 ES cells were transfected according to standard protocols. Clones resistant to G418 were screened for homologous recombination by Southern blotting of EcoRI digested genomic DNA and probed with a PCR product amplified from genomic DNA upstream of the short homology arm. Three clones were microinjected into CB6F1 blastocysts to generate chimeric mice. Siglec E KO mice were backcrossed to the C57Bl/6 background for >15 generations
Conditional No
Strain C57BL/6
Mouse Genetic Background/Cross History Backcrossed for fifteen generations to C57BL/6
Zygosity Homozygous
Research Area Adhesion, Immunology

References

There are 2 reference entries for this reagent.

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References: 2 entries

McMillan et al. 2013. Blood. 121(11):2084-94. PMID: 23315163.

Siglec-E is a negative regulator of acute pulmonary neutrophil inflammation and suppresses CD11b β2-integrin-dependent signaling.

Europe PMC ID: 23315163


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References: 2 entries

McMillan et al. 2013. Blood. 121(11):2084-94. PMID: 23315163.

Siglec-E is a negative regulator of acute pulmonary neutrophil inflammation and suppresses CD11b β2-integrin-dependent signaling.


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