Cx3cr1 Knockout

Constitutive Knock Out

Cx3cr1 Constitutive Knock Out Mouse Model
The NIAID Exchange Program has closed and live production of this model has ceased. This webpage is retained for historical reference, but this model is not available from Taconic.

C57BL/6 Background

  • Model #
  • Genotype
  • Nomenclature
  • 4167-F
  • 4167-M
CX3CR1 is the receptor for chemokine fractalkine (CX3CL1) and is expressed in monocytes, T cells, NK cells, as well as neurons, microglia cells, and astrocytes. Fractalkine mediates adhesion and chemotaxis of the cells expressing CX3CR1. An initial analysis indicates that Cx3cr1-/- mice on an atherogenic ApoE-/- background have reduced susceptibility to atherosclerosis.


Drs. Christopher Combadiere, Ji-Liang Gao and Philip Murphy in the Laboratory of Host Defenses, NIAID, made the Cx3cr1-/- mouse by targeted gene disruption in 1998. The Cx3cr1 gene was mutated by replacing a 0.6kb DNA fragment containing the Cx3cr1 start codon with a neomycin resistance gene. The disrupted 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 167 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.





Initial Publication:

Combadiere C, Potteaux S, Gao JL, Esposito B, Casanova S, Lee EJ, Debre P, Tedgui A, Murphy PM, Mallat Z. Decreased atherosclerotic lesion formation in CX3CR1/apolipoprotein E double knockout mice. Circulation. 2003; 107(7): 1009-16.