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anti-Human NOD2 Anticorps:
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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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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 IHC (fro), WB - ABIN2475899
Goolamali, Evered, Shuster: Thyroid disease and sebaceous function. dans British medical journal 1976
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Human Monoclonal NOD2 Primary Antibody pour FACS, ICC - ABIN4340264
Subramanian, Bergman, Henriques-Normark: Vitamin D Promotes Pneumococcal Killing and Modulates Inflammatory Responses in Primary Human Neutrophils. dans Journal of innate immunity 2017
Human Polyclonal NOD2 Primary Antibody pour IP, WB - ABIN4340260
Chauhan, Marriott: Differential roles for NOD2 in osteoblast inflammatory immune responses to bacterial pathogens of bone tissue. dans Journal of medical microbiology 2010
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
The results confirmed that polymorphisms in NOD2 (Leu1007insC) and IRGM (Montrer IRGM Anticorps) genes are associated with increased risk of Crohn's disease; whereas the ORMDL3 (Montrer ORMDL3 Anticorps) variant is associated with susceptibility to ulcerative colitis in the Lithuanian early-onset inflammatory bowel disease population.
We found that D299G and T399I SNPs were associated with Crohn's Disease susceptibility in patients carrying NOD2 variants. The patients carrying any mutant TLR4 (Montrer TLR4 Anticorps) variant were predisposed to develop a stricturing disease, especially in the presence of NOD2 mutation.
Homology modeling shows how the R702W mutation in NOD2 found in Crohn's disease, lowers the muramyl dipeptide-dependent activity of NOD2, and suggests that the residue is involved in autoregulation through direct interaction with the leucine rich domain.
wild type NOD2 is involved in preserving intestinal barrier integrity and immune homeostasis, properly functioning autophagy and balancing the gut (Montrer GUSB Anticorps) microbiota composition; there is a high prevalence and effect size of NOD2 risk alleles in patients with Crohn's disease
NOD2 is an important mediator in the viral uptake and inflammatory response during the pathogenesis of CVB3 myocarditis.
We identified 2 missense mutations at 16q12 in NOD2 (p.Ala110Thr and p.Arg311Trp), which encodes nucleotide-binding oligomerization domain protein 2. We further examined 94 genetically unrelated AgP patients by targeted sequencing of NOD2 and found that 2 patients among them also carried the p.Arg311Trp variant. Furthermore, we found 3 additional missense mutations in this gene (p.His370Tyr, p.Arg459Cys, and p.Ala868Thr)
Performed genetic analysis in patients with Crohn's disease (CD) to determine effect of NOD2/CARD15 polymorphisms on treatment response to adalimumab and infliximab.
The study of the correlation between genotype and phenotypic expression showed that CARD15 mutation is associated with ileocecal Crohn's disease, with fistulizing and stenosing behavior in Crohn's disease as well as with severe evolution
Ligand-driven triggering of TLR-3 (Montrer TLR3 Anticorps), -4, NOD2, and DC-SIGN (Montrer CD209 Anticorps), despite reducing viral replication, markedly increased the capacity of infected dendritic cells to stimulate HIV-specific cytotoxic T-cells.
This work suggests that Crohn's Disease-associated Nod2 variants could be stabilized in vivo with a molecular chaperone (Montrer HSP90AA1 Anticorps).
we conclude that coordinate engagement of NOD2 and TLR2 (Montrer TLR2 Anticorps) 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 (Montrer NOD1 Anticorps) 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.
this study shows that the effect of the gut (Montrer GUSB Anticorps) microbiota on bone is dependent on NOD1 (Montrer NOD1 Anticorps) and NOD2 signaling
this study shows that microbial sensing by Nod2 is an important mechanism to regulate small intestinal mucosal damage following acute T cell activation
results demonstrate that the recognition of bacterial products by NOD2 inside the PLNs contributes to T1D development, establishing a new putative target for intervention during the early stages of the disease.
These results indicate glycine enhances muscle protein mass under an inflammatory condition. The beneficial roles of glycine on the muscle are closely associated with maintaining Akt (Montrer AKT1 Anticorps)-mTOR (Montrer FRAP1 Anticorps)-FOXO1 (Montrer FOXO1 Anticorps) signaling and suppressing the activation of TLR4 (Montrer TLR4 Anticorps) and/or NOD2 signaling pathways.
this study shows that innate immunity activation by muramyl peptides is mediated via an interaction between YB1 (Montrer YBX1 Anticorps) and NOD2
this study shows that NOD2 is important for osteoclast differentiation and inflammatory bone resorption in vivo and also for the macrophage response to Gram-negative bacteria
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.
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