Siglec-F KO mouse

Siglecs-8 and -F are paralogous membrane proteins highly expressed on human and mouse eosinophils respectively.

Contributors

Inventor Institute
Paul Crocker University of Dundee
Cat. #: 154182
Research Fields: Cell biology;Immunology
Target: Siglec-F
Model: Knock-Out
Zygosity: Homozygous
Strain: C57BL/6
Alternate name: Siglec-8, Sialic Acid Binding Ig Like Lectin 8, SAF-2,
Product description: Siglecs-8 and -F are paralogous membrane proteins highly expressed on human and mouse eosinophils respectively. They are members of the CD33-related sialic acid binding Ig-like lectin family and contain immunoreceptor tyrosine based inhibitory motifs (ITIM) and ITIM-like motifs in their cytoplasmic tails that are implicated in negative regulatory functions
Conditional: No
Genetic background: Siglec FR114D knock in mice, carrying an Arg114 to Asp mutation in the Siglec F gene predicted to abolish sialic acid binding were generated by Taconic Artemis using C57Bl/6 ES cells (targeting strategy illustrated in PMID: 24698729). Further crossing of homozygous Siglec FR114D mice with Tg (Nes-Cre)1Wme/J(Bal1-Cre) mice produced offspring with mosaicism/partial deletion of exons 6-9 in adult organs (including germline) resulting in the truncated Siglec F knock out allele. Mosaic offspring were then used to generate Siglec F KO mice
Production details: Siglec FR114D knock in mice, carrying an Arg114 to Asp mutation in the Siglec F gene predicted to abolish sialic acid binding were generated by Taconic Artemis using C57Bl/6 ES cells (targeting strategy illustrated in PMID: 24698729). Further crossing of homozygous Siglec FR114D mice with Tg (Nes-Cre)1Wme/J(Bal1-Cre) mice produced offspring with mosaicism/partial deletion of exons 6-9 in adult organs (including germline) resulting in the truncated Siglec F knock out allele. Mosaic offspring were then used to generate Siglec F KO mice
Shipping conditions: Embryo/Spermatoza- Dry Ice
References:

McMillan et al. 2014. Immunol Lett. 160(1):11-16. PMID: 24698729.

Siglec-F-dependent negative regulation of allergen-induced eosinophilia depends critically on the experimental model.

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