Ask about this productRelated genes to: FBXO28 antibody
- Gene:
- FBXO28 NIH gene
- Name:
- F-box protein 28
- Previous symbol:
- -
- Synonyms:
- FLJ10766, KIAA0483, Fbx28, CENP-30
- Chromosome:
- 1q42.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-15
- Date modifiied:
- 2016-10-05
Related products to: FBXO28 antibody
Related articles to: FBXO28 antibody
- Allergic airway inflammation (AA) is primarily driven by the activation of mast cells and eosinophils, with granular exocytosis serving as a key source of pro-allergic mediators that amplify pathological responses. This unmet need highlights the importance of identifying novel, pathway-specific therapeutic targets to improve disease management. A dust mite extract (DME)-induced murine model of AA was used to assess intranasal A13 (1 mg/kg daily) efficacy; human EoL-1 eosinophils and murine P815 mast cells were stimulated with PMA/ionomycin (P&I) to induce exocytosis. In DME-induced murine AA, intranasal A13 reduced lung inflammation by 58% (p < 0.01), serum sIgE by 73% (p < 0.001), and BALF Th2 cytokines (IL-4/IL-5/IL-13) by 65%-80% (p < 0.001), while restoring BALF IFN-γ (p < 0.01). A13 inhibited granular mediator release: in P&I-challenged WT mice, it reduced BALF eosinophil peroxidase (EPX) by 81% and mast cell protease-1 by 85%, but had no effect in APLNR⁻⁻ mice (p > 0.05). Mechanistically, P&I induced Rab27a upregulation (P815: 3.2-fold; EoL-1: 2.8-fold), which A13 reversed in vitro; in vivo, A13 lowered lung granulocyte Rab27a by 2.5-3.1-fold (p < 0.001). A13 engaged APLNR to recruit FBXO28, promoting K48-linked Rab27a ubiquitination and proteasomal degradation. APLNR knockdown or MG132 treatment abrogated A13's effects, while A13 enhanced FBXO28-Rab27a complex formation by 4.7-fold (p < 0.001)-an interaction undetectable in APLNR cells. Intranasal A13 exhibits localised action, effectively suppressing allergic inflammation without broad systemic immunosuppression, making it a promising candidate for development as a topical biologic to treat allergic airway diseases. - Source: PubMed
Publication date: 2026/05/01
Wu GaohuiYe YanyuDuan JiaqiLi MinyaoLiao YunYang PingchangHuang QinmiaoLiu Yu - Acute coronary syndrome (ACS) is a common emergency in the cardiovascular system. The prevention, diagnosis, and treatment of ACS are critical and continuous issues in the clinic. Identifying non-invasive and promising biomarkers for ACS is of great clinical significance. This study evaluated the significance of miR-885-5p in the early screening, severity evaluation, and prognosis prediction of ACS, aiming to explore novel biomarkers for its clinical management. - Source: PubMed
Publication date: 2026/04/30
Liu XinLi DanHuang LushuangChen NinaZhou ZhengLi Jingjing - Laryngeal squamous cell carcinoma (LSCC) is an aggressive cancer with poor quality of life. Understanding the somatic mutations in its genome can help us comprehend its occurrence and progression. Although somatic structural variations (SVs) have been documented in LSCC, conventional short-read sequencing lacks the sensitivity to effectively detect high-frequency SVs shared across multiple samples - variants that play a crucial role in tumorigenesis. Here, we presented SomaGauss-SV, a somatic SVs detection workflow leveraging nanopore long-read sequencing data. Benchmarking against five paired tumor cell line datasets showed SomaGauss-SV consistently achieves a balanced high precision and recall. SomaGauss-SV applied to 15 paired LSCC tumor-blood samples uncovered a comprehensive SVs landscape and a significant positive correlation between somatic deletion burden and smoking intensity. Furthermore, a high-frequency somatic simple repeat expansion was identified in 28/39 (71.79%) of LSCC patients, upregulating the expression of genes and through spatial proximity. These findings underscore the potential of long-read sequencing and SomaGauss-SV for uncovering recurrent somatic SVs in LSCC, providing valuable resources for biomarker discovery. - Source: PubMed
Publication date: 2026/04/08
Liu XuyanXia LinQiao YixinLi YangHuang YanYue BingyanLiang XiYang XinZhang HonghuiZhang JiaxunChen XiaoXie DanLiu Jifeng - KRAS, a frequently mutated oncogene, has been challenging to target therapeutically. Although covalent inhibitors like sotorasib against KRAS have been developed, their efficacy is often limited by acquired resistance. Targeted protein degradation offers a potential solution but has largely relied on large PROTAC molecules. Here, we report DJX-A-KM, a small-molecule degrader of KRAS, designed by incorporating an acrylamide warhead into the MRTX849 scaffold. It induces potent and sustained degradation of KRAS in cells and in vivo. Mechanistic investigation reveal that degradation is mediated by the ubiquitin-proteasome system, facilitated by covalent engagement with a E3 ligase, FBXO28, at cysteine 98. Antiproliferation assays demonstrate its potent inhibitory effects across multiple KRAS-mutant cancer models. This strategy also enables the development of pan-KRAS degraders against a broader spectrum of KRAS mutations. Our work presents a small-molecule degrader recruiting FBXO28 and provides a blueprint for exploring E3 ligases in protein degradation. - Source: PubMed
Publication date: 2026/03/26
Deng JianxiongShen ShujunHuang LeiXu FangHuang WeizhenHuang ChaomingZhang ZhangLiu TongzhengTan YiLi Zhengqiu - F-box protein 28 (FBXO28) plays a role in several malignancies; however, its association with gastric cancer (GC) remains uncertain. This study aimed to investigate the effects of FBXO28 on GC by bioinformatics analysis and molecular biology. - Source: PubMed
Publication date: 2026/01/27
Song WantingChen MinminLi ChenyanLi YilingSun Xuren