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
- The high incidence of posttraumatic osteoarthritis after anterior cruciate ligament (ACL) injury and reconstruction suggests that biological mechanisms beyond joint instability contribute to disease progression. After injury, ACL-resident cells are exposed to inflammatory mediators within the joint and may influence the local inflammatory microenvironment; however, their global transcriptomic responses to inflammatory stimuli remain underexplored. - Source: PubMed
Publication date: 2026/08/17
Cai LeiBrophy Robert HTycksen Eric DRai Muhammad Farooq - Idiopathic inflammatory myopathy (IIM) is a systemic autoimmune disease targeting muscle and extramuscular organs, but the molecular mechanisms driving IIM pathogenesis remain largely undefined. Muscle fibroblasts are central to orchestrating inflammation in myositis. Here, we investigated muscle fibroblast dynamics using a single-cell RNA sequencing approach in an established murine model of anti-histidyl-tRNA synthetase (HRS, also known as Jo-1)-induced myositis. In fibroblasts, there was a robust activation of an IL-17 gene signature during disease. Among the induced genes was Nfkbiz, which encodes IκBζ, a noncanonical NF-κB transcriptional coactivator known to be key for pathologic IL-17 signaling in a variety of autoimmune settings. In muscle fibroblasts, IκBζ was potently activated by IL-17 in vitro and was essential for IL-17 signaling responsiveness. Surprisingly, however, the IL-17-IκBζ signaling axis was dispensable for the histopathological phenotype in HRS-induced myositis. Thus, despite a prominent IL-17 transcriptional signature, IL-17 and IκBζ are not required for autoantibody production or tissue inflammation in this model system. - Source: PubMed
Li DechengReay Daniel PLi YangVyas Shachi PYamamoto KentaAscherman Dana PGaffen Sarah L - Dry eye disease (DED) is a prevalent disorder affecting millions worldwide, fueled by both the aging population and extensive use of electronic devices. Yet, current treatments for moderate-to-severe DED fail to fully meet the clinical needs due to the lack of effective therapeutics and delivery systems for topical application. Based on the concept of "Barrier to Target," an siRNA-embedded nucleic acid hydrogel modified with a mucin-1 (MUC1) aptamer is developed to actively target the ocular surface for DED treatment. Upon distillation, the adhesive feature and aptamer-mucin recognition of the hydrogel enhance its retention on the ocular surface. Over time, tear dilution and the shear force of blinking lead the hydrogel to degrade into nanosized gel particles, facilitating drug uptake by corneal cells. Subsequently, the embedded siRNA targeting the nuclear factor of kappa-B inhibitor, zeta (NFKBIZ) gene can effectively silence the target gene expression, initiating a cascade of inflammation-related gene suppression. This comprehensive gene regulation effectively reshapes the inflammatory corneal environment to a normal state and alleviates the severity of DED in a mouse model. With the sequence-dependent nature of siRNA drugs, our targeting hydrogel may serve as a general platform for treating various ocular surface diseases. - Source: PubMed
Publication date: 2026/07/15
Liu YuheZhai ZimengHuang YangyangWang FujunWang ZifeiZhu LijuanJiang KaZhou XujiaoZhou XingtaoJie YingJin XiumingZhang ChuanHong Jiaxu - Inflammatory diseases arise from complex interactions between immune signaling and cellular stress. Although endoplasmic reticulum (ER) stress is a key modulator of immunity, the mechanisms by which it promotes inflammatory pathology remain incompletely understood. Notably, ER stress-induced NF-κB activation alone is insufficient to account for robust IL-6 production, thus suggesting the involvement of additional regulators. Using bone marrow-derived macrophages and sepsis model mice, we identified the inducible transcription factor IκBζ as a critical mediator of this response, with ER stress synergizing with TLR signaling to markedly upregulate IκBζ. Mechanistically, ER stress triggered calcium-dependent signaling that led to IκB kinase-mediated degradation of the RNase Regnase-1, likely stabilizing Nfkbiz mRNA and promoting the accumulation of IκBζ, which was found to cooperate with the ER stress factor XBP1s to drive transcription of selected secondary-response genes, particularly Il6 and Nos2. Importantly, this synergy was required for excessive IL-6 production in septic mice, highlighting a gene-specific amplification pathway. Together, these findings identify a dual mechanism in which transcriptional synergy between IκBζ and XBP1s is coupled to posttranscriptional mRNA stabilization via Regnase-1 degradation, thereby linking proteotoxic stress to hyperinflammatory responses. Our results establish ER stress-mediated IκBζ accumulation as a key driver of inflammatory pathogenesis and a potential therapeutic target in ER stress-associated inflammatory disorders. - Source: PubMed
Nakaminami YuriRuengsinpinya LerdluckSakihara RikoTakahata YoshifumiHata KenjiIwawaki TakaoNishimura RikoMurakami Tomohiko - Objective To investigate the early transcriptomic characteristics of neutrophils and monocytes stimulated by the major surface protein 2 (MSP2) of anaplasma phagocytophilum(AP), to preliminarily explore their functional differences and potential common pro-inflammatory mechanisms of these two cell types in the inflammatory response, and to provide a theoretical basis for understanding the inflammatory pathogenesis of Human Granulocytic Anaplasmosis (HGA) and for developing anti-inflammatory strategies. Methods HL60 cells (rHL60) differentiated with dimethyl sulfoxide (DMSO) for 8 days were used as a neutrophil-like cell model, and human acute monocytic leukemia (THP-1) cells were used as a monocyte model. Both cells were stimulated with recombinant MSP2 (rMSP2) for 2 hours. Differentially expressed genes (DEGs) were identified by transcriptome sequencing, and their biological functions and related signaling pathways were analyzed via Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment. The mRNA expression levels of key DEGs were validated by real-time quantitative PCR (qPCR), and the concentrations of cytokines in cell supernatants were measured by ELISA. Results Transcriptome analysis showed that in rHL60 cells, DEGs were mainly enriched in inflammation. qPCR confirmed the up-regulation of C-C motif chemokine receptor 7 (CCR7) and oxidized low-density lipoprotein receptor 1 (OLR1), while CD1D molecule and C-X-C motif chemokine receptors 1/2 (CXCR1/2) were down-regulated. In THP-1 cells, DEGs were primarily enriched in transcriptional regulation. qPCR validated the up-regulation of nuclear factor kappa B inhibitor zeta (NFKBIZ) and nuclear receptor subfamily 4 group A member 3 (NR4A3), whereas thioredoxin-interacting protein (TXNIP) and interleukin-16 (IL-16) were down-regulated. ELISA results demonstrated that both cell types significantly secreted C-C motif chemokine ligands 3/4/20 (CCL3/4/20) following MSP2 stimulation. Conclusion In the early phase of MSP2 stimulation, neutrophils serve as the primary cells initiating the inflammatory response, whereas monocytes focus on immune regulation. The co-secretion of CCL3, CCL4, and CCL20 may represent a potential molecular mechanism by which these two innate immune cell types jointly promote inflammatory responses during AP infection. - Source: PubMed
Chen ShihuaWang FengYue LeiYan Min