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anti-Human NOD1 Antibodies:
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Human Polyclonal NOD1 Primary Antibody for IHC, IHC (p) - ABIN4340241
Swaan, Bensman, Bahadduri, Hall, Sarkar, Bao, Khantwal, Ekins, Knoell: Bacterial peptide recognition and immune activation facilitated by human peptide transporter PEPT2. in American journal of respiratory cell and molecular biology 2008
Show all 2 Pubmed References
Human Polyclonal NOD1 Primary Antibody for WB - ABIN1169390
Costello, Joyce, Abrahams: NOD protein expression and function in first trimester trophoblast cells. in American journal of reproductive immunology (New York, N.Y. : 1989) 2006
Human Polyclonal NOD1 Primary Antibody for IF (p), IHC (p) - ABIN872332
Arentsen, Qian, Gkotzis, Femenia, Wang, Udekwu, Forssberg, Diaz Heijtz: The bacterial peptidoglycan-sensing molecule Pglyrp2 modulates brain development and behavior. in Molecular psychiatry 2016
Human Polyclonal NOD1 Primary Antibody for IHC (fro), IHC (p) - ABIN537419
Necchi, Sommi, Vanoli, Manca, Ricci, Solcia: Proteasome particle-rich structures are widely present in human epithelial neoplasms: correlative light, confocal and electron microscopy study. in PLoS ONE 2011
Human Polyclonal NOD1 Primary Antibody for ELISA, WB - ABIN4235349
Lu, Zou, Feng, Yuan, Gu, Li, Li, Jin, Li: Association of NOD1 (CARD4) insertion/deletion polymorphism with susceptibility to IBD: a meta-analysis. in World journal of gastroenterology 2010
Human Polyclonal NOD1 Primary Antibody for IHC (p), WB - ABIN4340243
Scott, Chen, Sun, Billiar: Hepatocytes express functional NOD1 and NOD2 receptors: a role for NOD1 in hepatocyte CC and CXC chemokine production. in Journal of hepatology 2010
Human Polyclonal NOD1 Primary Antibody for ELISA, FACS - ABIN4340244
Hosokawa, Hirao, Yumoto, Washio, Nakanishi, Takegawa, Kitamura, Matsuo: Functional Roles of NOD1 in Odontoblasts on Dental Pulp Innate Immunity. in BioMed research international 2016
results demonstrate that Evodiamine (Evo) could induce apoptosis remarkably and the inhibitory effect of Evo on Hepatocellular cancer cells may be through suppressing the NOD1 signal pathway in vitro and in vivo.
Two Single-Nucleotide Polymorphisms associated with susceptibility to develop dengue in NOD1 or RIPK2 genes were observed Children from Colombia.
our work indicates that NOD1 plays a previously undetected protective role in larval survival through CD44a-mediated activation of the PI3K-Akt signaling.
Upregulation of miR-495 ameliorates the high glucose-induced inflammatory, cell differentiation and extracellular matrix accumulation of human CFs by modulating both the NF-kappaB and TGF-beta1/Smad signaling pathways through downregulation of NOD1 expression.
Study proposes that NOD1 contributes to inflammation not only by promoting pro-inflammatory processes, but also by suppressing anti-inflammatory pathways.
Overexpression of either NOD1 or NOD2 reduces cell proliferation and increases clonogenic potential in vitro in breast cancer cell lines.
NOD1 (rs6958571) SNP was associated with gram-positive blood stream infection in Caucasian infants and extremely low birth weight infants.
In transgenic mice expressing human NOD1 and deficient for the murine NOD1, we showed enhanced clearance of a lipl21- mutant of Leptospira interrogans compared to the complemented strain, or to what was observed in NOD1KO mice, suggesting that LipL21 facilitates escape from immune surveillance in humans.
The changes in the nucleotide-binding oligomerization domain-like receptors (NLRs) in human corneas with disease expression may reflect different susceptibility to infectious and non-infectious injuries in corneas with various diseases.
A role for NOD1 in HCMV control via RIPK2- IKKalpha-IRF3 signaling, NOD1 polymorphisms predict the risk of infection.
Bronchial epithelial overexpression of TLR4 and NOD1 in severe/very severe stable COPD, associated with increased bronchial inflammation and P. aeruginosa bacterial load, may play a role in the pathogenesis of COPD
study provides structural and dynamic insights into the NOD1-RIP2 oligomer formation, which will be crucial in understanding the molecular basis of NOD1-mediated CARD-CARD interaction in higher and lower eukaryotes
Based on molecular docking studies using PG ligands, we propose few residues - G825, D826 and N850 in hNOD1-LRR and L904, G905, W931, L932 and S933 in hNOD2-LRR, evolutionarily conserved across different host species, which may play a major role in ligand recognition.
Nucleotide-binding oligomerization domain (NOD1) was the most significantly associated gene when analyzing exonic rare variants (RVs) in chromosome 7p to carotid bifurcation intima-media thickness (bIMT).
Fusion of human SGT1 (hSGT1) to NOD1 LRR significantly enhanced the solubility, and the fusion protein was stabilized by coexpression of mouse Hsp90alpha.
the results suggest that the chronic activation of NOD1 and NOD2 receptors might play a role in the development of gastric cancer.
this study reveals that LRRK2 is a new positive regulator of Rip2 and promotes inflammatory cytokine induction through the Nod1/2-Rip2 pathway.
Finally, NOD1 agonist increased the formation of cranial and subintestinal vessel plexus in zebrafish, and this effect was abrogated by concurrent PPARgamma activation. Overall, these findings identify a PPARgamma-miR-125a-NOD1 signaling axis in endothelial cells that is critical in the regulation of inflammation-mediated angiogenesis.
NOD1/2 gene variants are not linked with T2DM and IR.
findings show that NOD1, a PRR that normally senses bacterial peptidoglycans, is activated by HCV viral polymerase, probably through an interaction with dsRNA, suggesting that NOD1 acts as an RNA ligand recognition receptor.
Our studies establish the miR-146a/NOD1 axis as a key determinant of gammadelta T cell effector functions and plasticity.
Nod1(+/+) mice with chronic H. pylori infection exhibited significantly increased gastric IL-33 and splenic IL-13 responses, but decreased IFN-gamma responses, when compared with Nod1(-/-) animals. Collectively, our data identify NOD1 as an important regulator of mucosal IL-33 responses in H. pylori infection. We suggest that NOD1 may play a role in protection against excessive inflammation.
the absence of Nod1 does not impair the recruitment of neutrophils in response to P. aeruginosa
These findings reveal macrophage NOD1 as a cell-specific target to combat diet-induced inflammation past the step of macrophage infiltration, leading to insulin resistance.
The studies establish chronic pancreatitis as an IL-33-dependent inflammation resulting from synergistic interactions between the NOD1 and CCKR signaling pathways.
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.
this study shows that the effect of the gut microbiota on bone is dependent on NOD1 and NOD2 signaling
we propose that NOD1 signaling in mesenchymal stromal cells serves as an important pathway underlying the requirement for microbiota in the maintenance of steady-state hematopoiesis
results suggest a previously unappreciated role for the innate immune receptor Nod1 in suppressing colitis-associated tumorigenesis through a T cell-mediated mechanism
NOD1 activation in cardiac fibroblasts induces myocardial fibrosis in a murine model of type 2 diabetes.
this paper shows that deletion of NOD1 aggravated bone resorption induced by Gram-negative bacteria, accompanied by an increase in the numbers of osteoclasts
Sertoli cells have a functional NALP3 inflammasome that modulates NOD1 and pro-IL-1beta expression, while NOD2 inversely promoted IL-1beta expression.
contributes to fetal growth retardation and death through vascular inflammation
The results indicate that Nod1 cooperates with Nod2 or TLRs to produce cytokines in macrophages in response to M. tuberculosis infection.
findings illuminated a role for NOD1 signaling in attenuating H. pylori-induced Cdx2 expression in gastric epithelial cells
NOD1 and NOD2, play a collaborative role in T cell activation by alloantigen and that their blockade in vitro can inhibit T cell responses.
NOD1 and NOD2, two members of the NOD-like receptor family of pattern recognition receptors, are important mediators of ER-stress-induced inflammation in mouse and human cells
NOD1 activation induces cardiac dysfunction associated with excitation-contraction coupling impairment through NF-kappaB activation.
Activation of NOD1 by DAP contributes to reperfusion injury via multiple signaling pathways.
This gene encodes a member of the NOD (nucleotide-binding oligomerization domain) family. This member is a cytosolic protein. It contains an N-terminal caspase recruitment domain (CARD), a centrally located nucleotide-binding domain (NBD), and 10 tandem leucine-rich repeats (LRRs) in its C terminus. The CARD is involved in apoptotic signaling, LRRs participate in protein-protein interactions, and mutations in the NBD may affect the process of oligomerization and subsequent function of the LRR domain. This protein is an intracellular pattern-recognition receptor (PRR) that initiates inflammation in response to a subset of bacteria through the detection of bacterial diaminopimelic acid. Multiple alternatively spliced transcript variants differring in the 5' UTR have been described, but the full-length nature of these variants has not been determined.
NLR family, CARD domain containing 1
, caspase recruitment domain family, member 4
, caspase recruitment domain-containing protein 4
, nucleotide-binding oligomerization domain, leucine rich repeat and CARD domain containing 1
, nucleotide-binding oligomerization domain-containing protein 1
, caspase recruitment domain 4