Ask about this productRelated genes to: NFKB2 antibody
- Gene:
- NFKB2 NIH gene
- Name:
- nuclear factor kappa B subunit 2
- Previous symbol:
- -
- Synonyms:
- LYT-10, p52, p105, NF-kB2, p49/p100
- Chromosome:
- 10q24.32
- Locus Type:
- gene with protein product
- Date approved:
- 1991-11-14
- Date modifiied:
- 2019-04-23
Related products to: NFKB2 antibody
Related articles to: NFKB2 antibody
- Neurogenic heterotopic ossification (NHO), which occurs within the periarticular musculature subsequent to a significant spinal cord injury (SCI) and traumatic brain injury (TBI), remains poorly understood with no effective preventative measures. Multiple studies have demonstrated that dysregulated inflammatory environments caused by macrophage activation and aberrant differentiation of FAPs are critical factors contributing to disease progression. However, the specific mechanisms mediating functional changes between these two cell types during NHO remain unclear. This study found that FAPs aggregate, proliferate, and undergo osteogenic differentiation in the pathological bone regions of NHO. Differential gene expression analysis in an NHO mouse model has shown that the OPN expression is elevated in muscles which develop NHO. Using techniques such as flow cytometry sorting with immunofluorescence staining, it has been shown that the primary cellular source of osteopontin (OPN) is the M2 macrophage (M2). The up-regulation of OPN expression is primarily controlled by the transcription factor NFKB2 within the macrophage. We also demonstrate that OPN induces the increased expression of the osteogenesis-related transcription factor RUNX2 in FAPs via the P38-MAPK signaling pathway. Together, these data show that M2-derived OPN promotes pathological bone formation after SCI, thus providing useful information relevant to a therapeutic strategy for treatment of NHO. - Source: PubMed
Zhang DiLi GangDeng YilongLai HongxiLong YuniWu XiaoyuKong GanggangWan YongWang LeLi Xiang - Magnetite nanoparticles (FeO NPs), due to their unique physicochemical properties, are considered as promising nanomaterials for multiple biomedical applications. However, the development of novel strategies for surface modification and coating of FeO NPs is needed to fabricate FeO NPs with improved biocompatibility. In the present study, two polymers, namely, poly(ε-caprolactone) (PCL) and poly(ethylene oxide) (PEO), were applied to produce PCL/PEO microfibers containing FeO NPs (PCL/PEO/FeO MFs) using the electrospinning method. Their physicochemical properties, especially magnetically induced hyperthermia effects, were compared to FeO NPs. The biocompatibility and immunocompatibility of PCL/PEO/FeO MFs were then tested using four types of human immune cells, namely, CD14+ monocytes, CD4+ helper, CD8+ cytotoxic T cells, and CD56+ NK cells. Monocytes were the most sensitive to PCL/PEO/FeO MFs as judged by the induction of cell death (apoptosis and necrosis) and micronuclei production, whereas other immune cells were less or not affected by the stimulation with PCL/PEO/FeO MFs. PCL/PEO/FeO MFs also did not lower the viability of normal human fibroblasts. Furthermore, a mild immunogenic response was revealed in PCL/PEO/FeO MF-treated helper T cells based on the analysis of transcriptional activity of 92 genes involved in the NFκB pathway. Observed elevated mRNA levels of , , , , and may have context-dependent immunomodulatory effects in PCL/PEO/FeO MF-stimulated helper T cells that should be taken into account while designing novel drug-delivery systems based on PCL/PEO and FeO NPs. - Source: PubMed
Publication date: 2026/04/15
Radoń AdrianDeręgowska AnnaCiuraszkiewicz AgnieszkaHawełek ŁukaszSpałek HannaWarski TymonHudecki AndrzejŁukowiec DariuszPiotrowski PiotrKrogul-Sobczak AgnieszkaRost-Roszkowska MagdalenaChajec ŁukaszPieszko WeronikaBukała JuliaRzeszutek JuliaWnuk MaciejLewińska Anna - Phospholipids are key regulators of immune metabolism, yet their specific influence on macrophage function remains incompletely defined. We investigated how phosphatidylethanolamine (PE) species with distinct acyl chains (PE18:0/22:6 and PE18:0/20:4) modulate RAW264.7 macrophages under resting and LPS-stimulated conditions using LC-MS/MS-based proteomics and metabolomics, followed by qPCR validation. LPS elicited a robust M1-like phenotype with strong upregulation of Ptgs2, Nos2, Nfkb1, and Nfkb2. PE supplementation alone did not induce a classical pro-inflammatory profile but significantly remodeled protein expression, enhancing antioxidant defenses, including catalase, Hmox1 and Prdx1. In the context of LPS activation, PE selectively attenuated inflammatory signaling by downregulating Nfkb1, Nfkb2, and Ptgs2 while further enhancing proteins linked to oxidative stress response (Prdx1 and Hmox1) and lipid metabolism (CD36 and Abcc1). qPCR corroborated these effects: both PE species reduced LPS-induced and mRNA levels while increasing , , and transcription. Metabolomics converged with these findings, indicating reinforced glutathione metabolism and context-dependent shifts in purine and amino-acid pathways consistent with a restrained inflammatory phenotype. Collectively, native PE species reprogram macrophage immunometabolism, mitigating LPS-driven inflammation while strengthening Nrf2-mediated antioxidant and immune-supportive pathways. - Source: PubMed
Publication date: 2026/04/08
Maurício TatianaNeves BrunoDomingues M RosárioDomingues Pedro - High Mobility Group Box 1 (HMGB1) and Procathepsin L (pCTS-L) are crucial inflammatory mediators, yet their immunomodulating properties in human immune cells have not been systematically compared. This study employed RNA-sequencing to comparatively analyze their transcriptional effects on primary human peripheral blood mononuclear cells (PBMCs). Our findings demonstrate that while both mediators elicited significant transcriptional changes indicative of robust inflammatory responses, HMGB1 consistently induced a more extensive and diversified inflammatory program. Specifically, at a lower concentration of 0.5 µg/ml, HMGB1 triggered nearly four times more differentially expressed genes (DEGs) than pCTS-L (2.0 µg/ml). Despite this quantitative difference, an overlap of 412 DEGs (272 upregulated, 140 downregulated) revealed shared core inflammatory pathways, including the extensive upregulation of pro-inflammatory cytokines (e.g., IL1A, IL1B, and IL6), chemokines (e.g., CCL2 and CXCL1), and S100 proteins (e.g., S100A8, S100A9, and S100A12). Both mediators also converged on activating the non-canonical NF-κB pathway, evidenced by NFKB2 and RELB upregulation, suggesting a common underlying regulatory mechanism. Notably, HMGB1 uniquely upregulated CASP4 and CASP5-key components of the non-canonical inflammasome pathway-and a broader spectrum of cytokines and chemokines (e.g., IL23A, CXCL5). These findings delineate the distinct yet overlapping roles of HMGB1 and pCTS-L in orchestrating immune responses, offering a foundation for targeted therapeutic development for inflammatory diseases. - Source: PubMed
Publication date: 2026/03/16
Lou LiQiang XiaolingZhu Cassie ShuXiong BrianChen WeiqiangLi JianhuaTracey Kevin JWang Haichao - Aberrant glycosylation is implicated in tumor progression. However, the role of β-1,3-N-acetylglucosaminyltransferase 3 (B3GNT3) in non-small cell lung cancer (NSCLC) remains poorly understood. - Source: PubMed
Publication date: 2026/03/16
Lin YingZhang YaoYu BoWang JialeiWu ZhengWang Huijie