Orders by weight:
- 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).
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.
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.