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Human Monoclonal NOD2 Primary Antibody pour FACS, ICC - ABIN151959
McDonald, Chen, Ollendorff, Ogura, Marchetto, Lécine, Borg, Nuñez: A role for Erbin in the regulation of Nod2-dependent NF-kappaB signaling. dans The Journal of biological chemistry 2005
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Human Polyclonal NOD2 Primary Antibody pour 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. dans Journal of cell science 2008
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Human Polyclonal NOD2 Primary Antibody pour ELISA, WB - ABIN251672
Keshav: Paneth cells: leukocyte-like mediators of innate immunity in the intestine. dans Journal of leukocyte biology 2006
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Polyclonal NOD2 Primary Antibody pour 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. dans Current biology : CB 2004
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Human Polyclonal NOD2 Primary Antibody pour 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. dans Journal of endodontics 2009
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Human Polyclonal NOD2 Primary Antibody pour IF, WB - ABIN541425
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. dans The Journal of biological chemistry 1999
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Human Polyclonal NOD2 Primary Antibody pour IHC (fro), IF - ABIN541424
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. dans Nature 2001
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Monoclonal NOD2 Primary Antibody pour 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. dans Gastroenterology 2003
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Human Polyclonal NOD2 Primary Antibody pour ELISA, ICC - ABIN4340247
Rahman, Midtling, Svingen, Xiong, Bell, Tung, Smyrk, Egan, Faubion: The pathogen recognition receptor NOD2 regulates human FOXP3+ T cell survival. dans Journal of immunology (Baltimore, Md. : 1950) 2010
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.
Combination of polymorphisms in the NOD2, IL17RA, EPHA2 and KALRN genes could play a significant role in the development of sarcoidosis by maintaining a chronic pro-inflammatory status in macrophages
NOD2 mutation is associated with inflammatory bowel disease.
Overexpression of either NOD1 or NOD2 reduces cell proliferation and increases clonogenic potential in vitro in breast cancer cell lines.
To expand the computational strategy designed when studying XIAP, we have applied the molecular modeling tools to a list of 140 variants seen in CFTR associated with cystic fibrosis, and a list of undiagnosed variants in 17 different genes. Graphical abstract XIAP in Caspase 3 and NOD2 signaling pathways.
DNA sequencing revealed a previously unreported heterozygous mutation consisting of a G>A transition in exon 4 of the NOD2 gene. This resulted in a glutamic acid to lysine substitution in helical domain 2 of the nucleotide binding and oligomerization (NACHT) region, possibly reducing efficiency of auto-inhibition in NOD2 signaling.
The E600A mutation in the NOD2 gene may confer a higher penetrance of uveitis but a later onset of milder forms of non-ocular involvement.
the rarity and lack of association between common NOD2 mutations with IBD in our study seem to reveal a genetic characteristic of the population in our region.
novel mechanisms allowing Leptospira interrogans to escape recognition by the NOD1 and NOD2 receptors may be important in circumventing innate host responses
Studies results provide evidence that Crohn's disease patients have an impairment in mannose-binding lectin-mannose-associated serine protease functional activity and that this defect is associated with mannose-binding lectin 2 and NOD2 variants.
blockage of RhoA/ROCK repressed the TAK1/NOD2-mediated NF-kappaB pathway in HaCaT cells exposed to UVB.
this study reports the phenotype of a kindred with Blau syndrome caused by a novel NOD2 mutation
Results demonstrate that NOD2 contributes to the regulation of blood monocytes.
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.
Results show that the simultaneous absence of Nod1 and Nod2 is associated with accelerated T cell death upon alloantigen encounter, suggesting these proteins might provide new targets to ameliorate T cell responses in a variety of inflammatory states, including those associated with bone marrow or solid organ transplantation.
These data suggest that NOD2 contributes to bone loss in estrogen deficiency by elevating reactive oxygen species levels in OCs.
NOD2 is an important mediator in the viral uptake and inflammatory response during the pathogenesis of CVB3 myocarditis.
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