Nod2

Constitutive Knockout

Nod2 - Constitutive knockout
EZcohort® Models
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This model is cryopreserved and available for immediate cryorecovery.

  • Model #
  • Genotype
  • Nomenclature
  • 16476
    C57BL/6NTac-Nod2em2Tac
  • Carries a deletion of exon 3 and 4 of Nod2 gene
  • The deletion removes part of the NACHT domain, resulting in a frame-shift leading to a premature stop codon in exon 5. Additionally, the resulting transcript may be a target for nonsense-mediated RNA decay and may therefore not be expressed at significant level.
  • Homozygous mice should not produce any Nod2 protein.
  • Useful in inflammatory bowel disease, microbiome, Parkinson's disease, immunology and inflammation research.
  • Nod2 is involved in gastrointestinal immunity, it is associated with inflammatory bowel disease (IBD) (Scientific Reports 2015, 5 (1), 12018, Science 2005, 307 (5710), 734-738). Mutations in Nod2 are also found in Blau and Yao syndrome patients.
  • Nod2 knockout mice have altered microbial community in the colonic mucosa when compared to Nod1 KO and wild type mice (Gut 2011, 60 (10), 1354-1362). Gut-associated lymphoid tissue (GALT) is also altered in Nod2 knockout mice resulting in increased epithelial permeability.
  • A host carrying mutant NOD2 alleles may have a diminished epithelial defense against enteric bacteria (Journal of Crohns and Colitis 2016, 10 (12), 1428-1436, Nature Medicine 2016, 22 (5), 524-530).
  • Loss of Nod2 gene also enhances epithelial dysplasia following chemically induced injury (Journal of Clinical Investigation 2013, 123 (2), 700-711).
  • Nod2 deficiency can protect neurons against 6-hydroxydopamine (6-OHDA) induced cell death, which mimics Parkinson's disease pathology (Journal of Neuroinflammation 2018, 15 (1), 243).

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 Nod2 knockout mouse was developed by Taconic Biosciences. The model was created through CRISPR/Cas9-mediated gene editing to delete exons 3 and 4 of Nod2. Targeting occurred in C57BL/6NTac embryos. The selected G1 founder was screened for off-target effects and the targeted locus was sequenced to confirm targeting specificity. Heterozygous animals were intercrossed to generate homozygous mice. Homozygous matings are possible.

Color:

Black

Species:

Mouse

Initial Publication:

There is no specific publication describing the generation of these mice, but multiple publications exist demonstrating applications using similar models. See reference list.

Other Publications:


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This model is sold under terms which grant perpetual use rights.