NOD1 (Nucleotide Binding Oligomerization Domain Containing 1)

NOD1 and NOD2 act as innate immune checkpoints that restrict donor HSPC reconstitution. Their simultaneous absence enhances chimerism without compromising immune defense or tolerance and reprograms stem cell metabolism to favor survival. Targeting NOD1/2 signaling may represent a novel strategy to improve hematopoietic stem cell transplantation outcomes.

NOD1 is an effective predictor of preoperative glioma grade and prognosis. It facilitates glioma progression by promoting microglial M2 polarization through the NOD1/RIP2 pathway.

In addition, IL-1β was associated with rs689466, LY96 with rs2228014, rs5743336 genotypes (P < 0.05). As a conclusion, the CCR3 gene rs4987053, COX-2 gene rs689466, and NOD1 gene rs5743336 variations were determined to be closely associated with prostate cancer risk.

MAPK1 gene mutation promotes the NLR signaling pathway and affects CHD development, providing new insights into the treatment of CHD.

The reduced expression and functional impairment of NOD-like receptors, such as NLRC3 and NOD1, in neonates, may contribute to their heightened susceptibility to severe infections. This finding indicates new avenues for the prevention and treatment of neonatal infections.

"Zhibian" (BL54)-toward-"Shuidao" (ST28) needling technique can alleviate the pain symptom of PD rats, and its action mechanism may be related to inhibiting the active expression of NOD1/RIP2/NF-κB signaling pathway in the uterine tissue, thereby reducing the inflammatory response.

We integrate functional genomics and tumor evolution reconstruction and infer immune escape trajectories across cancer types. Our results have important implications for developing biomarkers for immunoprevention and treatment strategies for immune escape of cancer.

Moreover, NOD1 expression was positively correlated with the expression of chemokine and immunomodulators in GBM. Overall, our findings suggest that NOD1 is a promising prognostic biomarker and is associated with immune cell infiltration in GBM, making it a potential diagnostic biomarker for this aggressive brain cancer.

Lastly, inhibiting NOD1 showed significant anti-PTC activity in vitro. Our results suggest that pyroptosis-related genes can be used for PTC diagnosis, and NOD1 could be a promising therapeutic target.

CCT3 knockdown suppressed the expression of NOD1 and p-IκBα/IκBα and the NOD1 agonist could reverse the effect of CCT3 suppression on BCa in vitro and in vivo. In summary, our findings demonstrate that silencing CCT3 inhibits BCa via induction of ferroptosis and suppression of the NOD1-NF-κB pathway.

The arginine supplementation increased nuclear factor kappa-B (NF-κB) protein level. In conclusion, arginine can alleviate LPS-induced inflammatory response and apoptosis as well as induce cd4 gene expression against LPS challenge via adjusting the expression of NODs signaling.

In conclusion, cigarette smoke significantly influences the development and progression of oral squamous cell carcinoma, based on the evidence highlighted in human oral cells. While previous studies have focused on specific carcinogens and pathways, this review added to our understanding of the overall impact of whole cigarette smoke on oral carcinogenesis at the molecular and cellular levels.