Ask about this productRelated genes to: Nod2 antibody
- Gene:
- NOD2 NIH gene
- Name:
- nucleotide binding oligomerization domain containing 2
- Previous symbol:
- IBD1, CARD15
- Synonyms:
- BLAU, CD, PSORAS1, CLR16.3, NLRC2
- Chromosome:
- 16q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-10
- Date modifiied:
- 2019-04-23
Related products to: Nod2 antibody
Related articles to: Nod2 antibody
- Biological sex influences immune function and inflammatory regulation, but its molecular role in periodontal disease remains insufficiently understood. This pilot study investigated sex-dependent differences in immune gene expression in patients with severe periodontitis. - Source: PubMed
Publication date: 2026/05/14
Dimitrov DDosseva-Panova VDimova INikolova D - is a leading cause of skin and soft tissue infections (SSTIs), which can escalate into systemic disease. While innate immune responses play a critical role in bacterial clearance, the bacterial components themselves can exacerbate inflammation. Here, we demonstrate that lipoproteins (Lpp) and polymeric peptidoglycan (PG) synergistically induce skin abscesses in mice, in a process that requires both the lipid moiety of Lpp and the intact polymeric structure of PG. This synergy is mediated by Toll-like receptor 2 (TLR2) and nucleotide-binding oligomerization domain-containing protein 2 (NOD2) and depends on infiltrating neutrophils and monocytes. Co-administration of Lpl1 and PG results in a 5-fold to 10-fold increase in macrophage inflammatory protein-2 (MIP-2) levels in the skin compared to either ligand alone, indicating a clear synergistic effect. Furthermore, we show that local alteration in coagulation and fibrinolysis contributes to the inflammatory response, as fibrinogen depletion significantly reduced lesion size. To extend these findings to a clinically relevant model, we employed an double mutant that lacked both lipidation (Δ) and peptidoglycan O-acetyltransferase (Δ). This strain exhibited markedly attenuated virulence in a murine skin infection model. Importantly, this attenuation was fully reversed by neutrophil depletion, indicating that neutrophils are essential mediators of the host responses to these bacterial structures. Our findings reveal a cooperative mechanism through which cell wall components drive skin lesion development, and we identify potential therapeutic targets for reducing the severity of SSTIs. - Source: PubMed
Publication date: 2026/05/15
Mohammad MajdHu ZhichengScheffler Julia MNega MulugetaLuqman ArifKrzyzowska MalgorzataSundqvist MartinaKopparapu Pradeep KumarPullerits RilleAli AbukarNguyen Minh-ThuGötz FriedrichJin Tao - Otitis media (OM) remains a prevalent and multifactorial inflammatory disease of the middle ear, especially in pediatric populations. The immune system, particularly pattern recognition receptors (PRRs), plays a central role in detecting microbial pathogens and initiating host defenses. TLR2 and TLR4 mediate bacterial clearance but exhibit subtype-specific dysregulation in chronic OM forms. NOD1, NOD2, and NLRP3 modulate intracellular pathogen sensing and inflammasome activation, while RIG-I governs antiviral immunity. C-type lectin receptors (CLRs) are emerging as modulators of both innate and adaptive responses, yet their mechanistic roles remain insufficiently explored. Cross-talk among PRRs and immune evasion by microbial biofilms contribute to chronicity and recurrence. Understanding these interactions and age- or genotype-related PRR variations may inform precision immunotherapies. This review summarizes current understanding of Toll-like receptors (TLRs), nucleotide-binding oligomerization domain-like receptors (NLRs), retinoic acid-inducible gene I-like receptors (RLRs), and CLRs in OM pathophysiology. By elucidating the PRR-mediated signaling landscape, this review highlights the intricate PRR-mediated signaling landscape in OM, offering insights into potential therapeutic targets and future translational strategies for improving OM management. - Source: PubMed
Publication date: 2026/04/28
Guo MingwenZhang ShaoyanLiao ZhenchengYan DaqingTan XinyuanLiu Chunling - Mesalazine () is a first-line therapy for inflammatory bowel disease (IBD); however, its clinical use is limited by variable patient response, intolerance, and reduced efficacy in severe cases. To address these challenges, we have designed and evaluated seventeen derivatives (-) using a comprehensive in silico strategy. Density functional theory with the B3LYP/6-311++G(d,p) basis set was employed to optimize geometries and explore electronic structure, stability, and reactivity. Structural characterization was further supported by FTIR and UV-visible spectral analysis. Molecular docking against five key IBD-associated targets (TNF, NOD2, ATG16L1, IL23R, and IL6) reveled that , -, , , , , and showed stronger binding affinities than , where the and showed the strongest binding affinity. was more toxic towards the human body, although some of its derivatives were less toxic compared to , while demonstrated an overall improved ADMET profile as an IBD medication. Molecular dynamics simulations of both -NOD2 and -NOD2 complexes revealed stable behavior in each system; however, reduced structural fluctuations, flexibility, and solvent exposure, whereas promoted a more compact and conformationally restricted state, indicating distinct stabilization mechanisms, with demonstrating superior dynamic control. Collectively, these findings identify as a promising drug candidate for IBD, warranting further experimental validation through in vitro and in vivo studies. - Source: PubMed
Publication date: 2026/05/11
Rana Md SohelRabbi Md FazlayRana Enamul HaqIslam Md TanvirHossain Md SanoarMatin Shamiha BinteFarjana MuhtadiWasick Intisar HussainKumar NeerajKudrat-E-Zahan Md - Intracranial aneurysm (IA) is a life-threatening cerebrovascular disorder, the underlying molecular mechanisms of which remain incompletely elucidated. Pyroptosis, a pro-inflammatory form of programmed cell death, has been implicated in various vascular pathologies. However, its role in the pathogenesis of IA remains largely unclear. In this study, we identified and validated a pyroptosis-related gene signature linked to IA using GEO dataset. Differential expression analysis and pathway enrichment methods revealed key pyroptosis-related markers, including CASP8, NOD2, PYCARD, which were strongly associated with IA progression. Functional analysis highlighted their involvement in inflammatory and immune pathways, particularly in promoting vascular remodeling through pyroptosis-driven mechanisms. Machine learning approaches refined these markers into a robust predictive signature. Validation in independent cohorts confirmed their diagnostic and prognostic potential for IA. Moreover, we validated the upregulation of these genes and found the activation of CASP8 in clinical IA samples. Our findings provide novel insights into the molecular underpinnings of IA, offering a framework for the development of pyroptosis-based biomarkers and therapeutic strategies aimed at early detection and targeted intervention in IA management. - Source: PubMed
Publication date: 2026/05/07
Liu YangCheng YuanchiLi QianWang Delong