EXPERIMENTAL MODELS

Contributor Information
- Name Paul Crocker
- Institute University of Dundee
Tool Details
- Tool name: Siglec-F KO mouse
- Alternate names: Siglec-8, Sialic Acid Binding Ig Like Lectin 8, SAF-2,
- Tool type: Experimental models
- Tool sub-type: Mouse
- Model: Knock-Out
- Conditional: No
- Genetic background and cross history: 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
- Zygosity: Homozygous
- Strain: C57BL/6
- 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
- Research area: Cell biology; Immunology
- 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
- For Research Use Only
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.