Nod2
- Known as:
- Nod2
- Catalog number:
- 000055A
- 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
- 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 - Pyroptosis, a form of inflammatory programmed cell death, plays a dual role in tumor progression and anti-tumor immunity. Its comprehensive clinical and biological significance in intrahepatic cholangiocarcinoma (iCCA) remains to be elucidated. - Source: PubMed
Publication date: 2026/05/07
Zhao BinhanZhu YongjiJin ZiyangLi XiangLin KainanWang YifanLu YunkunHua Wen - Macrophage polarization and endoplasmic reticulum (ER) stress play critical yet incompletely understood roles in cancer progression and therapeutic resistance. - Source: PubMed
Publication date: 2026/04/30
Long ShengrongXiao KeweiHao Zhipeng - Interleukin-5 (IL-5) is central to eosinophil differentiation, survival, and activation. Subsequent studies confirmed IL-5 receptor expression and mapped downstream signaling, showing that IL-5 promotes not only survival but also trafficking and effector functions, including adhesion, degranulation, reactive oxygen species generation, mediator release (cytokines and cysteinyl leukotrienes), and extracellular trap formation. However, the roles of eosinophils vary across diseases and tissue compartments. Multi-omics analyses of blood and tissue eosinophils across transcriptomic, proteomic, and lipid-metabolic layers reveal disease- and site-specific molecular states. These data support two opposing classes of modulators that shape IL-5-driven programs: pro-inflammatory signals (IL-4/IL-13, IL-33, NOD2-mediated innate signaling, and IFN-γ) that drive inflammatory eosinophil changes and can cooperate in some settings, and counter-regulatory signals (IFN-α and all-trans retinoic acid [ATRA]) that restrain these changes. Such modulation may influence tissue retention, effector functions, and broader eosinophil activities, including antiviral and homeostatic roles. Clinical studies of anti-IL-5 and/or anti-IL-5Rα biologics in severe eosinophilic asthma, chronic rhinosinusitis with nasal polyps, eosinophilic granulomatosis with polyangiitis, hypereosinophilic syndromes, and other eosinophilic diseases have improved outcomes, underscoring that disease activity often depends on IL-5-driven eosinophil activation despite disease-specific IL-5-independent signals. In this review, we summarize IL-5 biology from mechanisms to therapy and discuss how integrated multi-omics signatures and clinical biomarkers may guide patient stratification, therapy selection, and treatment sequencing toward precision medicine for eosinophilic respiratory and systemic diseases. . - Source: PubMed
Publication date: 2026/04/14
Sasaki HisashiMiyata JunFukunaga Koichi - Inflammatory injury to the intestine triggers a reprogramming of the intestinal epithelium to a fetal-like state that drives rapid restoration of the epithelial barrier. Although the intestinal microbiota is a key modulator of inflammation, its role in influencing epithelial fetal-like stem cell reprogramming and consequent restitution remains unclear. Using irradiation (IR) injury as a model for small intestinal epithelium injury and repair, we found that the intestinal microbiota accelerated epithelial restitution by amplifying a repair-associated inflammatory response that promoted the emergence of fetal-like intestinal epithelial cells (IECs), marked by and . , the strongest genetic link to the development of Crohn's disease, was found to be expressed in fetal-like IECs following injury. Employing an ileal organoid model, we demonstrated that NOD2 activation by its peptidoglycan ligand potentiated an inflammatory gene signature characterized by interferon signaling, concurrent with enterocyte recovery. NOD2 deficiency exacerbated epithelial apoptosis following IR injury, whereas epithelial-specific NOD2 signaling promoted fetal-like IEC emergence and increased epithelial proliferation. Collectively, these findings reveal a pivotal role for the microbiota and NOD2-mediated microbial sensing in regulating fetal-like IEC fate after injury, thus contributing to the protective function of this microbial sensor during intestinal inflammation. - Source: PubMed
Publication date: 2026/04/29
Tsang Derek K LMaisonneuve CharlesAyyaz ArshadFoerster Elisabeth GNissan MarryBaerg LaurenTrcka DanielGhoshal BibaswanTsankov Boyan KBayer GiulianoDenney MadisonStreutker Catherine JWrana Jeffrey LGirardin Stephen EPhilpott Dana J