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anti-Human NOD2 Antibodies:
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Human Monoclonal NOD2 Primary Antibody for FACS, ICC - ABIN151959
McDonald, Chen, Ollendorff, Ogura, Marchetto, Lécine, Borg, Nuñez: A role for Erbin in the regulation of Nod2-dependent NF-kappaB signaling. in The Journal of biological chemistry 2005
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Human Polyclonal NOD2 Primary Antibody for ICC, IF - ABIN153051
Till, Rosenstiel, Bräutigam, Sina, Jacobs, Oberg, Seegert, Chakraborty, Schreiber: A role for membrane-bound CD147 in NOD2-mediated recognition of bacterial cytoinvasion. in Journal of cell science 2008
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Polyclonal NOD2 Primary Antibody for WB - ABIN540368
Abbott, Wilkins, Asara, Cantley: The Crohn's disease protein, NOD2, requires RIP2 in order to induce ubiquitinylation of a novel site on NEMO. in Current biology : CB 2004
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Human Polyclonal NOD2 Primary Antibody for ELISA, WB - ABIN251672
Keshav: Paneth cells: leukocyte-like mediators of innate immunity in the intestine. in Journal of leukocyte biology 2006
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Human Polyclonal NOD2 Primary Antibody for IHC (fro), IHC (p) - ABIN4340262
Lin, Song, Qin, Li, Li, Zhu, Zhang: Expression of nucleotide-binding oligomerization domain 2 in normal human dental pulp cells and dental pulp tissues. in Journal of endodontics 2009
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Human Polyclonal NOD2 Primary Antibody for IHC (fro), IF - ABIN541424
Inohara, Koseki, del Peso, Hu, Yee, Chen, Carrio, Merino, Liu, Ni, Núñez: Nod1, an Apaf-1-like activator of caspase-9 and nuclear factor-kappaB. in The Journal of biological chemistry 1999
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Human Polyclonal NOD2 Primary Antibody for IF, WB - ABIN541425
Hugot, Chamaillard, Zouali, Lesage, Cézard, Belaiche, Almer, Tysk, OMorain, Gassull, Binder, Finkel, Cortot, Modigliani, Laurent-Puig, Gower-Rousseau, Macry, Colombel, Sahbatou, Thomas: Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease. in Nature 2001
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Monoclonal NOD2 Primary Antibody for IHC (p), IP - ABIN534028
Lala, Ogura, Osborne, Hor, Bromfield, Davies, Ogunbiyi, Nuñez, Keshav: Crohn's disease and the NOD2 gene: a role for paneth cells. in Gastroenterology 2003
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Human Polyclonal NOD2 Primary Antibody for ELISA, ICC - ABIN4340247
Rahman, Midtling, Svingen, Xiong, Bell, Tung, Smyrk, Egan, Faubion: The pathogen recognition receptor NOD2 regulates human FOXP3+ T cell survival. in Journal of immunology (Baltimore, Md. : 1950) 2010
NOD2 is crucial to control intracellular infection caused by Leishmania spp. NOD2 receptor is important for Leishmania recognition, the control of intracellular killing, and the induction of innate and adaptive immune responses.
NOD1 and NOD2 mRNA was constitutively expressed in both tumor and adjacent healthy renal tissue, with NOD1 being significantly lower and in contrast NOD2 significantly higher expressed in tumor tissue compared to healthy tissues.
poor clinical healing outcome was associated with increased local expression of the pattern recognition receptor NOD2
A rare and, not yet, reported missense variation of the NOD2 gene, N1010K, was detected and co-segregated across affected patients. In silico evaluation and modelling highlighted evidence for an adverse effect of the N1010K variation with regard to Crohn's Disease (CD).
The frequency of NOD2/CARD15 gene mutations is high in Crohn's disease (CD) and ulcerative colitis among Bedouin Arab IBD patients and is associated with younger age at onset in CD and male gender.
NOD2 has unique expression sites in salivary glands, and they may synergistically activate autophagy in salivary glands under conditions of inflammation.
In this well-controlled study of NOD2 genotype and fecal microbiota, we identified no significant genotype-microbiota associations in Crohn's Disease patients
The aim of this study was to identify how genetic testing (NOD2/CARD15) can be used in patients with Crohn's disease to predict the need for surgical treatment.
The results support a role of guanylate cyclase C signaling and disturbed electrolyte homeostasis in development of IBD. Furthermore, downregulation of metallothioneins in the ileal mucosa of familial GUCY2C diarrhea syndrome patients may contribute to inflammatory bowel disease development, possibly alongside effects from NOD2 risk variants.
Mutations in the NOD2 gene are associated with a specific phenotype and lower anti-tumor necrosis factor trough levels in Crohn's disease.
In cirrhosis patients with ascites NOD2 gene variants were associated with an increased cumulative probability of spontaneous bacterial peritonitis (SBP) compared to wild-type. In cirrhosis, functional polymorphisms of Pattern recognition receptors did not improve the identification of patients with high risk of bacterial infections beyond SBP or progressive diseases course.
Study results showed no association between the single nucleotide polymorphism rs8057341 in NOD2 and leprosy in Brazilian population.
This first study on genetic susceptibility in sclerosing cholangitis in critically ill patients patients shows an extraordinary high frequency of NOD2 variation, pointing to a critical role of inherited impaired anti-bacterial defense in the development of this devastating biliary disease.
NOD1 and NOD2 expression and induced release of pro-inflammatory mediators were impaired in infants, contributing to the high susceptibility of infants to infection
NOD2 caspase recruitment domains (CARDs) bind to one end of the RIP2 CARD filament
ZNRF4 is a negative regulator of NOD2 signalling.NOD2 role in the protective host immunity.
NOD2 is a target gene of miR-320 and is regulated by XIST.
The CTLA-4 gene +49 A/G polymorphism and the NOD2/CARD15 gene N852S polymorphism were not associated with CD or UC in a Turkish population
genetic deficiency of NOD2 plays a protective role during Aspergillus infection.
Results show that homozygotes carrying 3020insC gene mutations in NOD2 represent a high risk group for Crohn Disease.
Nod2 contributes to the early lung defense against A. baumannii infection through reactive oxygen/nitrogen species production as Nod2(-/-) mice showed significantly reduced production of ROS/RNS in the lungs following A. baumannii infection. A. baumannii-induced neutrophil recruitment, cytokine/chemokine response and lung pathology was also exacerbated in Nod2(-/-) mice at early time points post-infection.
NOD2(-/-) mice are more prone to intestinal inflammation due to deregulated immune response and increased susceptibility to colitogenic bacteria.
This study provides a complete overview of the polyubiquitins in NOD2:RIP2 signaling and reveal MYSM1 as a central negative regulator restricting these polyubiquitins to prevent excessive inflammation.
The results of the present study demonstrated an understanding of the role of NOD2 in diabetesinduced cardiomyopathy, which provides a novel target and therapies for the prevention and treatment of DCM.
Overall, our results suggest that activation of NOD2 receptor could be an appealing approach to control pulmonary inflammation in patients infected with Influenza A virus.
The loss of bacterial muramyl dipeptide tolerance results in enhanced NOD2-dependent recruitment of inflammatory monocytes that is associated with the induction of several interferon-stimulated genes, including IFIT2 that was found to protect from an attaching-and-effacing bacterial pathogen.
This study provides the direct evidence that NOD2 is related to 6-OHDA-induced DA degeneration through NOX2-mediated oxidative stress.
We show that lactobacilli differentially utilize innate immune pathways and highlight NOD2 as a key mediator of macrophage function and antigen-specific humoral responses to a Lactobacillus acidophilus mucosal vaccine platform.
NOD-like receptors are implemented in first-line protective immune responses against filarial nematodes
In conclusion, the study indicates that Nod2-dependent responses account for Neospora caninum elimination. On the other hand, the inflammatory milieu induced by this innate receptor provoked pathogenesis and death in severe experimental neosporosis.
Results demonstrate that NOD2 contributes to the regulation of blood monocytes
Loss of function mutations in the nucleotide oligomerization domain 2 gene are the main genetic risk factor for Crohn's disease.
Study for the first time demonstrates a novel role of NOD-2 signaling in differentiating bone marrow precursors to highly immunogenic dendritic cells.
NOD2 plays a critical role in the suppression of inflammation and tumorigenesis in the colon via downregulation of the TLR signaling pathways.
our data suggest that Nod2 plays a role in T1DM development. the role of the Nod2 gene contributes to alteration of the gut microbiota, nod2 acts as a recessive modulator in T1DM susceptibility.
Nod2 deletion improved both chronic cobblestone ileitis, as well as acute dextran sodium sulfate colitis in a murine model of spontaneous ileitis
Nod2-signaling is essentially involved in the well-balanced innate and adaptive immune responses upon Campylobacter jejuni infection of IL-10(-/-) mice.
Chlamydophila pneumoniae cpn0423-induced cytokine response is mediated by host NOD2 during the infection.
we conclude that coordinate engagement of NOD2 and TLR2 constitutes a key step in the genesis of Lp-mediated protection from a lethal respiratory virus infection, and represents a critical target for modulation of virus-induced inflammatory pathology.
These results revealed that thermal stress increased the expression levels of NOD1/2 genes and acute inflammatory cytokines which sheds some light on their role on immune response of the host cells during thermal stress.These preliminary studies indicated that the immune-related genes differentially expressed during thermal stress among native and crossbred cattle.
Data indicate six single-nucleotide polymorphisms (SNPs) in the caspase recruitment domain 15 protein (CARD15) gene associated with susceptibility to bovine tuberculosis (BTB) in Chinese Holstein cows.
Data indicate that the Nod2 signaling adaptor protein (NOD2) G-->A at position 1594 bp plays a critical role in increasing 305-day milk yields.
Genetic variation and putative regulatory regions in bovine CARD15.
This study indicates that SNP c.3020A>T might play a role in the host response against mastitis and further detailed studies are needed to understand its functional mechanisms
A significant association was found between two polymorphisms of CARD15 and paratuberculosis status; cows with the heterozygous genotype were 3.35 times more likely to be infected than cows with the reference genotype.
This gene is a member of the Nod1/Apaf-1 family and encodes a protein with two caspase recruitment (CARD) domains and six leucine-rich repeats (LRRs). The protein is primarily expressed in the peripheral blood leukocytes. It plays a role in the immune response to intracellular bacterial lipopolysaccharides (LPS) by recognizing the muramyl dipeptide (MDP) derived from them and activating the NFKB protein. Mutations in this gene have been associated with Crohn disease and Blau syndrome.
caspase recruitment domain 15 protein
, NLR family, CARD domain containing 2
, NOD-like receptor C2
, caspase recruitment domain family, member 15
, caspase recruitment domain protein 15
, caspase recruitment domain-containing protein 15
, inflammatory bowel disease protein 1
, nucleotide-binding oligomerization domain 2
, nucleotide-binding oligomerization domain, leucine rich repeat and CARD domain containing 2
, nucleotide-binding oligomerization domain-containing protein 2