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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 (show NOD2 ELISA Kits) receptors might play a role in the development of gastric cancer.
this study reveals that LRRK2 (show LRRK2 ELISA Kits) is a new positive regulator of Rip2 (show ARHGEF28 ELISA Kits) and promotes inflammatory cytokine induction through the Nod1/2-Rip2 (show ARHGEF28 ELISA Kits) pathway.
Finally, NOD1 agonist increased the formation of cranial and subintestinal vessel plexus in zebrafish, and this effect was abrogated by concurrent PPARgamma (show PPARG ELISA Kits) activation. Overall, these findings identify a PPARgamma (show PPARG ELISA Kits)-miR (show MLXIP ELISA Kits)-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 (show PVRL1 ELISA Kits) 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.
Brain pericytes can sense Gram-negative bacterial products by both NOD1 and TLR4 (show TLR4 ELISA Kits) receptors, acting through distinct pathways.
NOD1 And NOD2 (show NOD2 ELISA Kits) polymorphisms were associated with increased susceptibility to Guillain-Barre syndrome in a Northern Indian population.
over-expression of NOD1 and NOD2 (show NOD2 ELISA Kits) may be involved in the pathogenesis of Vogt-Koyanagi-Harada (VKH) Syndrome syndrome.
Porphyromonas gingivalis induced NOD1 overexpression in endothelial cells and that NOD1 played an important role in the process of VCAM-1 (show VCAM1 ELISA Kits) and ICAM-1 (show ICAM1 ELISA Kits) expression in endothelial cells infected with Porphyromonas gingivalis through the NF-kappaB (show NFKB1 ELISA Kits) signaling pathway.
NOD1 activation in cardiac fibroblasts induces myocardial fibrosis in a murine model of type 2 diabetes.
this study reveals that LRRK2 (show LRRK2 ELISA Kits) is a new positive regulator of Rip2 (show ARHGDIG ELISA Kits) and promotes inflammatory cytokine induction through the Nod1/2-Rip2 (show ARHGDIG ELISA Kits) 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 (show NLRP3 ELISA Kits) inflammasome that modulates NOD1 and pro-IL-1beta (show IL1B ELISA Kits) expression, while NOD2 (show NOD2 ELISA Kits) inversely promoted IL-1beta (show IL1B ELISA Kits) expression.
The results indicate that Nod1 cooperates with Nod2 (show NOD2 ELISA Kits) 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 (show CDX2 ELISA Kits) expression in gastric epithelial cells
NOD1 and NOD2 (show NOD2 ELISA Kits), play a collaborative role in T cell activation by alloantigen and that their blockade in vitro can inhibit T cell responses.
NOD1 and NOD2 (show NOD2 ELISA Kits), 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 (show NFKB1 ELISA Kits) activation.
Activation of NOD1 by DAP (show DAP ELISA Kits) 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