- 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:
- Kim, H.; Zhao, Q.; Zheng, H.; Li, X.; Zhang, T.; Ma, X. Scientific Reports 2015, 5 (1), 12018.
- Maeda, S.; Hsu, L.C.; Liu, H.; Bankston, L.A.; Iimura, M.; Kagnoff, M.F.; Eckmann, L.; Karin, M. Science 2005, 307 (5710), 734-738.
- Rehman, A.; Sina, C.; Gavrilova, O.; Hasler, R.; Ott, S.; Baines, J. F.; Schreiber, S.; Rosenstiel, P. Gut 2011, 60 (10), 1354–1362.
- Nabhani, Z. A.; Lepage, P.; Mauny, P.; Montcuquet, N.; Roy, M.; Roux, K. L.; Dussaillant, M.; Berrebi, D.; Hugot, J.-P.; Barreau, F. Journal of Crohns and Colitis 2016, 10 (12), 1428–1436.
- Couturier-Maillard, A.; Secher, T.; Rehman, A.; Normand, S.; Arcangelis, A. D.; Haesler, R.; Huot, L.; Grandjean, T.; Bressenot, A.; Delanoye-Crespin, A.; Gaillot, O.; Schreiber, S.; Lemoine, Y.; Ryffel, B.; Hot, D.; Nùñez, G.; Chen, G.; Rosenstiel, P.; Chamaillard, M. Journal of Clinical Investigation 2013, 123 (2), 700-711.
- Kim, D.; Kim, Y.-G.; Seo, S.-U.; Kim, D.-J.; Kamada, N.; Prescott, D.; Chamaillard, M.; Philpott, D. J.; Rosenstiel, P.; Inohara, N.; Núñez, G. Nature Medicine 2016, 22 (5), 524–530.
- Cheng, L.; Chen, L.; Wei, X.; Wang, Y.; Ren, Z.; Zeng, S.; Zhang, X.; Wen, H.; Gao, C.; Liu, H. Journal of Neuroinflammation 2018, 15 (1), 243.
