#151588

MRP-14 (S100a9 -/-) Knockout Mouse

Cat. #151588

MRP-14 (S100a9 -/-) Knockout Mouse

Cat. #: 151588

Sub-type: Mouse

Availability: 6-8 weeks

Disease: Inflammatory disease

Model: Knock-Out

This fee is applicable only for non-profit organisations. If you are a for-profit organisation or a researcher working on commercially-sponsored academic research, you will need to contact our licensing team for a commercial use license.

Contributor

Inventor: Nancy Hogg

Institute: Cancer Research UK, London Research Institute: Lincoln's Inn Fields

Tool Details
Handling
Target Details
References

Tool Details

*FOR RESEARCH USE ONLY

  • Tool name: MRP-14 (S100a9 -/-) Knockout Mouse
  • Alternate name: Myeloid-related protein 14 (MRP-14)
  • Tool sub type: Mouse
  • Disease: Inflammatory disease
  • Model: Knock-Out
  • Description: S100a9 and its heterodimeric partner, S100a8, are a cytosolic calcium-binding protein, highly expressed in neutrophils and monocytes. This knockout mice generated by targeted disruption of the gene is useful for understanding the function of S100a9 and the dispensability of both S100a8 and S100a9 for myeloid cell functions.
  • Genetic background: The S100a9 gene was disrupted in ES cells with a replacement-type targeting vector and the strategy shown in the publication. ES cells were electroporated, and of 196 neomycin (G418)-resistant clones, 13 were correctly targeted. Two targeted clones were injected into C57BL/6 mouse blastocysts, and two independent strains of S100a9 -/- mice were established. The S100a9 -/- wild-type and mutant alleles were distinguished both by Southern hybridization with probe E following BglII digestion of mouse tail DNA and by a PCR-based assay. Interbreeding of S100a9 heterozygotes yielded the proportions of 1.0:1.9:1.0 for wild-typeheterogeneousnull mice, approximating the expected ratio for Mendelian inheritance.
  • Phenotype: No phenotype as yet
  • Zygosity: Homozygous
  • Strain: C57BL/6
  • Production details: The S100a9 gene was disrupted in ES cells with a replacement-type targeting vector and the strategy shown in the publication. ES cells were electroporated, and of 196 neomycin (G418)-resistant clones, 13 were correctly targeted. Two targeted clones were injected into C57BL/6 mouse blastocysts, and two independent strains of S100a9 -/- mice were established. The S100a9 -/- wild-type and mutant alleles were distinguished both by Southern hybridization with probe E following BglII digestion of mouse tail DNA and by a PCR-based assay. Interbreeding of S100a9 heterozygotes yielded the proportions of 1.0:1.9:1.0 for wild-type–heterogeneous–null mice, approximating the expected ratio for Mendelian inheritance.

Handling

  • Shipping conditions: Embryo/Spermatoza- Dry Ice

Target Details

  • Target: S100a9

References

  • De Filippo et al. 2014. FASEB J. 28(8):3600-8. PMID: 24776746.
  • McNeill et al. 2014. Int J Cancer. 135(4):798-808. PMID: 24436096.
  • A new protective role for S100A9 in regulation of neutrophil recruitment during invasive pneumococcal pneumonia.
  • S100A9 has a protective role in inflammation-induced skin carcinogenesis.
  • Croce et al. 2009. Circulation. 120(5):427-36. PMID: 19620505.
  • Myeloid-related protein-8/14 is critical for the biological response to vascular injury.
  • Hobbs et al. 2003. Mol Cell Biol. 23(7):2564-76. PMID: 12640137.
  • Myeloid cell function in MRP-14 (S100A9) null mice.