| Model No. | Nomenclature | Genotype |
|---|---|---|
| 4169 | C57BL/6NTac-Fpr1tm1Gao N6 | Inquire for genotype |
Fpr1 Knockout
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Overview
Nomenclature: C57BL/6NTac-Fpr1tm1Gao N6
N-formylpeptides derive from bacterial and mitochondrial proteins, and bind to specific receptors on mammalian phagocytes. Since binding induces chemotaxis and activation of phagocytesin vitro, it has been postulated that N-formylpeptide receptor signaling in vivo may be important in antibacterial host defense, although direct proof has been lacking. Mice genetically deficient in formyl peptide receptor (FPR-/-) have no obvious developmental defects and do not develop spontaneous infection when derived in specific pathogen-free conditions. This suggests that, under these conditions, FPR is dispensable. However, when challenged with Listeria monocytogenes, FPR-/- mice have accelerated mortality and increased bacterial burden in liver and spleen early after infection, which suggests a role for FPR in host defense, specifically through regulation of innate immunity.
Origin
Drs. Ji-Liang Gao and Philip Murphy in the Laboratory of Molecular Immunology, NIAID, made the FPR-/- mouse by targeted gene disruption in 1999. The Fpr1 gene was mutated by replacing a 150 bp DNA fragment in the Fpr1 open reading frame with a neomycin resistance gene. The disrupted Fpr1 gene was introduced to 129/Sv ES cells to create chimeric mice, and then the chimeric founders were backcrossed to C57BL/6NAi mice for 10 generations in the NIAID barrier facility at Taconic. At this point, it was discovered that the C57BL/6NAi line had become contaminated with the IFNγ knockout gene. Line 4169 was then backcrossed to C57BL/6NTac (Taconic B6) for 5 generations in order to eliminate the contaminating gene and put the strain onto the Taconic C57BL/6 subline background.
This model is cryopreserved and available for recovery. Models can typically be recovered and delivered to customers within 14-16 weeks after order receipt. Purchase of this model includes perpetual use rights and a deliverable of four mutant animals at the Murine Pathogen Free™ health standard along with a genotyping protocol. For models which include a recombinase gene or multiple alleles, all alleles will be provided, but individual animals may not contain all mutant alleles.
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Genetics
Guides & Publications
Initial Publication:
Gao J-L, Lee E, and Murphy PM. (1999) Impaired anti-bacterial host defense in mice lacking the N-formylpeptide receptor. J. Exp. Med., 189: 657-662.
Applications & Therapeutic Areas
- Immunology
- Inflammation
Transit, Housing & Welfare
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