Fcgr2b - Model 579

Constitutive Knockout

Fcgr2b (Model 579)  Constitutive Knockout Mouse Model
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BALB/c Background

  • Model #
  • Genotype
  • Nomenclature
  • 579-F
    C.129S4(B6)-Fcgr2btm1TtK/cAnNTac N12
  • 579-M
    C.129S4(B6)-Fcgr2btm1TtK/cAnNTac N12
  • Deficient in FcgRIIB protein, which is a low affinity immunoglobulin G receptor
  • The FcgRIIB protein inhibits the activation of disparate effector functions such as phagocytosis, antibody dependent cytotoxicity and release of inflammatory mediators and it is known to function as an inhibitory receptor on B cells and mast cells
  • This inhibitory pathway for activation of several immune effector responses is dysfunctional, resulting in the inability to regulate antibody levels in response to antigenic stimuli dependent on IgG immune complexes
  • Useful for studying the feedback inhibition pathways that regulate antibody production and in studies of allergic and autoimmune disorders
  • The mice are fertile and develop normally
  • These mice carry the H2d haplotype
Orders by weight: Taconic cannot accept orders by weight for this model. Please note that shipments may contain animals with a larger weight variation.

Origin:

The Fcgr2b mouse was developed in the laboratory of T. Takai of Okayama University in 1995. The model was created by targeting the Fcgr2b gene in J1 ES cells. Taconic received pregnant females from Okayama University in November 1996 for use by the laboratory of J.V. Ravetch. Heterozygotes on a hybrid 129 x C57BL/6 background were intercrossed to generate homozygous targeted mutation mice. The mice were then backcrossed twelve generations (N12) to BALB/cAnNTac. The mice were embryo transfer derived and were maintained by incrossing of homozygous mice.

Availability:

Cryopreserved at Taconic Biosciences

Genetics:

Wildtype for Nnt mutation

Color:

Albino

Species:

Mouse

Initial Publication:

Takai, T, Ono, M, Hikida, M, Ohmori, H, Ravetch, J. (1996) Augmented humoral and anaphylactic responses in FcgRII-deficient mice. Nature, 379: 346-349.


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