Nfkbiz polyclonal antibody
- Known as:
- Nfkbiz pab (anti-)
- Catalog number:
- PAB0226
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- Nfkbiz polyclonal antibody
Related genes to: Nfkbiz polyclonal antibody
- Gene:
- NFKBIZ NIH gene
- Name:
- NFKB inhibitor zeta
- Previous symbol:
- -
- Synonyms:
- MAIL, FLJ34463, INAP
- Chromosome:
- 3q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-29
- Date modifiied:
- 2016-10-05
Related products to: Nfkbiz polyclonal antibody
Related articles to: Nfkbiz polyclonal antibody
- Gastric cancer (GC) is a major global health challenge. This study explores the efficacy of linalool in GC and further elucidates its underlying mechanisms. Linalool inhibited the proliferation, migration, and invasion of GC cells and prevented transplanted tumor growth in nude mice. Linalool directly interacted with and stabilized the NR3C2 protein, inhibiting its proteasomal degradation. Functional rescue experiments demonstrated that knockdown of NR3C2 partially reversed the antitumor effects of linalool. Further studies revealed that NR3C2 transcriptionally activated NFKBIZ and inhibited NF-κB signaling, and restoring NFKBIZ expression reversed GC progression caused by NR3C2 deficiency. In clinical samples, the expression levels of NR3C2 and NFKBIZ were lower in GC tissues than in adjacent normal tissues, and the two markers were positively correlated in the tumor tissues. Furthermore, low expression of both NR3C2 and NFKBIZ was significantly associated with higher T stages and more advanced pTNM stages and was accompanied by NF-κB signaling activation and elevated levels of inflammatory cytokines in tumor tissues. Overall, linalool inhibits GC progression by upregulating NR3C2 and transcriptionally activating NFKBIZ, thereby suppressing NF-κB signaling. Low NR3C2/NFKBIZ expression is associated with adverse clinical and pathological features in GC. - Source: PubMed
Publication date: 2026/05/18
Hu YingChen ShunfengWang YuLiu LingZhang ChaoyiChen HongDuanmu YuanyuanSu ZhaotianMa Jun - To investigate the therapeutic potential of 4-Octyl itaconate (4-OI), a derivative of the endogenous immunomodulator itaconate (ITA), as a safe and effective anti-inflammatory agent for the treatment of dry eye disease (DED). - Source: PubMed
Publication date: 2026/01/14
Zhai ZimengLu YitengZhou XujiaoZhou XingtaoZhou FengHong Jiaxu - ( ) infects the gastric epithelium of approximately half of the global population, and is a well-known risk factor for developing gastric cancer. Despite the clinical significance of infection, many genetic factors that contribute to susceptibility remain unidentified. While it is well-established that infection can result in gastritis and peptic ulcers, which may progress to gastric cancer, its causal link to other diseases remains unclear. We performed the genome-wide association study (GWAS) for anti- IgG antibody titers, which were validated as a surrogate marker for infection by the correlation with clinical traits, followed by gene-based and pathway analyses, involving up to 140,863 individuals. This included 56,967 in the discovery phase, and 68,211 in the replication phase from Japanese cohorts, and an additional 15,685 from European populations in a cross-ancestry meta-analysis. We reveal significant associations between infection and polymorphisms in the Human Leukocyte Antigen (HLA) class II region within the Major Histocompatibility Complex (MHC), as well as genes related to innate immunity, including , , , , and . Mendelian randomization (MR) analysis revealed that genetic liability to infection has both positive and negative causal relationships with a variety of diseases, including autoimmune-related diseases such as Type 1 diabetes, Hashimoto's disease, atopic dermatitis, as well as traits like body height and weight. These genetic findings strongly support the notion that genetic liability to infection influences not only gastrointestinal diseases, but also a broader spectrum of health issues, thereby providing valuable insights for public health strategies and personalized medicine approaches. - Source: PubMed
Publication date: 2026/03/30
Kyosaka TomokiNarita AkiraKulski Jerzy KMinn Aye Ko KoMiyake AkimitsuKotsar YuriiHiraide KyogaOjima TakafumiNakatochi MasahiroNamba ShinichiYamaji TaikiSutoh YoichiSasaki YuBroer LindaFrost FabianKoyanagi Yuriko NKasugai YumikoIto HidemiSawada NorieNakano ShioriSuzuki SadaoHishida AsahiKoyama TeruhideKubo YokoFunayama TakamitsuMakino SatoshiShirota MatsuyukiTakayama JunGocho ChinatsuSugimoto SachiyoOtsuka-Yamasaki YayoiTanno KozoAbe YasuhikoNakajima OsamuSpaander Manon C WWeiss StefanLerch Markus MLevy DanielHwang Shih-JenWood Alexis CRich Stephen SRotter Jerome ITaylor Kent DTracy Russell PStocker HannahBrenner HermannLeja MārcisPeculis RaitisHozawa AtsushiKinoshita KengoShimizu AtsushiYamamoto MasayukiMatsuo KeitaroIwasaki MotokiWakai KenjiUeno YoshiyukiFuhler Gwenny MHomuth GeorgPeppelenbosch Maikel P Okada YukinoriKuriyama ShinichiMatsuzaki MotomichiTamiya Gen - Qi-Huang Decoction (QHD), a combined prescription of Buzhong Yiqi decoction and Dachengqi decoction, is used for gastrointestinal protection post-operation at present. Previously, we found that QHD could ameliorate Candida colitis through Dectin-1 associated pathway, but was rather weak against Candida albicans in vitro. - Source: PubMed
Publication date: 2026/04/09
Wang ZixuWang XueLuo QinaiLiu ChengchengZhu HanyuYang LiuWang ChangzhongPeng HuiYu QingshengHu MinShao Jing - Chikungunya virus (CHIKV) is a re-emerging arbovirus causing acute febrile illness and chronic debilitating arthritis, thereby imposing significant global public health and economic burdens. While robust immune responses involving inflammatory cytokines and immune cell infiltration characterize acute infection, the cellular mechanisms underlying pathogenesis and chronicity remain incompletely defined. In this study, we employed single-cell RNA sequencing (scRNA-seq) to comprehensively profile splenic and peripheral blood mononuclear cells (PBMCs) immune responses in rhesus macaques at day 7 post CHIKV infection, an acute phase. Splenic neutrophils marked recruitment, upregulation of , downregulation of interferon-stimulated genes (ISGs), and functional activation marked by degranulation, enhanced anti-apoptotic pathways, and neutrophil extracellular traps (NETs) formation, as visualized by multiplex immunofluorescence. Pseudotime trajectories delineated progressive states transitioning from proliferation to effector functions. Splenic T and B cells showed increased abundance with innate-to-adaptive transition signature. Splenic CD4 and CD8 T cell subsets and B cell subsets exhibited enrichment for innate immune pathways and translational machinery. In PBMCs, CD8 T cell subsets and B cell subsets exhibited activation of adhesion, cytokine signaling, and protein homeostasis pathways in infection group. Notably, CHIKV infection induced skewing of T cells toward states enriched for Th1 and Th17 differentiation (marked by expression) in PBMCs. These results delineate the spatiotemporal immune landscape during CHIKV acute phase, in this non-human primate model, identifying neutrophil-mediated inflammation, lymphocyte transcriptional adaptation, and Th1/Th17 polarization as hallmarks of acute phase, offering a detailed cellular map that may inform future investigations into CHIKV pathogenesis and therapeutic strategies. - Source: PubMed
Publication date: 2026/03/26
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