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this study reports the molecular and functional identification of an NLRP1 homolog, Danio rerio NLRP1 (DrNLRP1) from a zebrafish (D. rerio) model
REVIEW: various mechanisms and pathways involved in H. pylori induction of NF-kappaB-dependent responses in gastric epithelial cells, including a 'state-of-the-art' review on the respective roles of NOD1 and ALPK1/TIFA pathways in these 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.
our results indicate that Columbianadin (CBN) suppressed the LPS-mediated inflammatory response by inhibiting NOD1/NF- kappa B activation. Further investigations are required to determine the mechanisms of action of CBN in the inhibition of NOD signaling: However, CBN may be employed as a therapeutic agent for multiple inflammatory diseases.
NOD1 expression seems to be modulated by 5-HT and other immune receptors as TLR2 and TLR4. This study could clarify the relation between both the intestinal serotonergic system and innate immune system, and their implications in intestinal inflammation.
NOD1 and NOD2 expression and induced release of pro-inflammatory mediators were impaired in infants, contributing to the high susceptibility of infants to infection
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).
Nod1-mediated lipolysis promoted accumulation of DAG, which engaged PKCdelta and IRAK1/4 to augment inflammation in 3T3-L1 adipocytes.
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 study reveals that LRRK2 is a new positive regulator of Rip2 and promotes inflammatory cytokine induction through the Nod1/2-Rip2 pathway.
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.
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