Nod2
- Known as:
- Nod2
- Catalog number:
- 057116A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Nod2
Related genes to: Nod2
- 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
Related articles to: Nod2
- The function of the interferon-stimulated gene ISG15 in cervical cancer (CC) is complex and remains unclear. We analyzed the expression and clinical significance of ISG15 in the TCGA-CESC cohort. Its function was investigated in Caski cells using RNA-seq, siRNA, and pharmacological inhibition methods, and validated in vivo in a xenograft model. ISG15 was significantly overexpressed in cervical cancer tissues (P < 0.001). However, high ISG15 expression was associated with better overall survival (HR=0.67, 95% CI: 0.48-0.94, p = 0.02). Gene set enrichment analysis (GSEA) indicated that high ISG15 expression was associated with the NOD-like receptor signaling pathway. Mechanistically, ISG15 binds to and stabilizes the NOD2 protein via ISGylation. This binding promotes cell proliferation and invasion. The RIPK2 inhibitor (GSK583) eliminated the oncogenic effects of ISG15. In vivo experiments showed that ISG15 knockdown or GSK583 treatment inhibited tumor growth by approximately 50%. Our study reveals the dual nature of ISG15: it is both a prognostic biomarker and a functional oncoprotein in cervical cancer cells. Its pro-tumorigenic effect is mediated by the overactivation of the NLR pathway through ISGylation. The ISG15-NOD2/RIPK2 axis is a targetable vulnerability, suggesting that treatment strategies should be decoupled from its prognostic association. - Source: PubMed
Publication date: 2026/05/15
Jia ZongyangZhang JunhuaLiu XiaoliLiu ChangZhang Youzhong - NOD2-associated autoinflammatory syndrome or Yao syndrome was first described in 2011 in seven patients who were heterozygous for the :c.2717+158C>T (previously IVS8+158) variant, several of whom were also heterozygous for a second variant, NOD2:c.2023C>T;p.Arg675Trp (previously R702W). Since then, over 30 papers have been published either about or including mention of Yao syndrome, with the rate of publication increasing over recent years. The largest case series now includes 152 individuals, almost all heterozygous for one or both of the two mentioned variants. However, to date, there is insufficient evidence to link the broad phenotypes described in Yao syndrome to variants in . Approximately one in five people is heterozygous for c.2717+158C>T in the gnomAD database, while one in 12 is heterozygous for p.Arg702Trp in gnomAD. Thus, while it is conceivable that there is an association between very common variants in and the phenotypes referred to as Yao syndrome, this could only represent susceptibility with extremely low penetrance. Demonstrating such a link would require large-scale association studies, which have not been performed. As a result, given the current lack of evidence for the existence of Yao syndrome, this diagnosis should not be used. - Source: PubMed
Publication date: 2026/04/03
Gray Paul EMasters Seth LKirk Edwin P - Resistance to immune checkpoint blockade (ICB) often arises from immunologically cold tumors enriched in suppressive myeloid cells. Previous studies have implicated NOD2 signaling in antitumor immunity and in modulation of ICB responses, but approaches to engage this pathway effectively and durably within tumors remain limited. Here, single-cell transcriptomic analysis of colorectal cancer identified a tumor-associated macrophage (TAM) subset enriched for inflammatory and immune-activating programs. To therapeutically harness this state, we engineered an injectable manganese-containing alginate hydrogel encapsulating polyarginine-functionalized (MHY@PBCG) for sustained intratumoral delivery and localized coactivation of NOD2 and STING signaling in TAMs. Polyarginine enhanced BCG uptake by macrophages, whereas Mn stabilized the hydrogel and amplified STING activation. Local administration of MHY@PBCG reprogrammed TAMs toward an M1-like phenotype, increased inflammatory cytokine and interferon programs, converted cold tumors into immune-inflamed lesions, and restored responsiveness to anti-PD1 therapy in multiple models. Mechanistically, coordinated NOD2/STING activation established a self-reinforcing inflammatory circuit linking macrophage reprogramming to downstream T cell-mediated antitumor immunity. These findings establish a localized biomaterial strategy for overcoming checkpoint resistance through macrophage-centered remodeling of the tumor microenvironment. - Source: PubMed
Publication date: 2026/05/19
Xiao ZiyuanXu HuizhenMa NingyiLei LeiCong ChunyuSun NingyiWang GuodongChen XingmeiRen KeQiao Haishi - 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