Ask about this productRelated genes to: FBG2 antibody
- Gene:
- FBXO6 NIH gene
- Name:
- F-box protein 6
- Previous symbol:
- -
- Synonyms:
- FBX6, FBG2, FBS2, Fbx6b
- Chromosome:
- 1p36.22
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-27
- Date modifiied:
- 2015-09-01
Related products to: FBG2 antibody
Related articles to: FBG2 antibody
- Intestinal ischemia/reperfusion (I/R) injury is a critical clinical condition associated with high mortality, in which the ubiquitin‒proteasome system (UPS) plays a pivotal pathogenic role. Cullin-associated and neddylation-dissociated 1 (CAND1), a critical regulator of cellular protein homeostasis, governs the ubiquitination and degradation of abnormal protein substrates by regulating the assembly of SKP1‒Cullin1‒F-box (SCF) E3 ubiquitin ligase complexes. However, the mechanisms by which CAND1 regulates SCF complex assembly and its potential therapeutic role in intestinal I/R injury remain unclear. - Source: PubMed
Publication date: 2026/06/15
Qiang MiaomiaoZhao YanWang GuorongChen ZhaoZhang FengWang ZhanyuWang GuangzhiZhuang ChengjunNing ShiliYao JihongTian Xiaofeng - Hepatocellular carcinoma (HCC) is an extraordinarily heterogeneous tumor that poses a hazard to millions of people globally. Long intergenic noncoding RNAs (lincRNAs) have been recognized as key regulators influencing prognosis of HCC patients. However, their underlying mechanisms in HCC warrant further investigation. The role of the unreported lincRNA RP11-738E22.3 in HCC is still unknown. In this research, differentially expressed lincRNAs were identified using Arraystar long noncoding RNA (lncRNA) microarray sequencing, and the expression levels of RP11-738E22.3 were measured by RT-qPCR and FISH. The impact of RP11-738E22.3 on HCC cell autophagy, apoptosis, xenograft tumor growth, and metastasis were investigated in both in vitro and in vivo experiments. Furthermore, RNA sequencing, dual-luciferase reporter assays, and rescue tests were carried out to clarify its molecular process. We found that RP11-738E22.3 was substantially overexpressed in HCC tissues and linked to poor prognosis and unfavorable clinicopathological characteristics in HCC patients. Functionally, by upregulating FBXO6, an activator of the MAPK/ERK/mTOR signaling, RP11-738E22.3 stimulated HCC migration and proliferation in vitro and in vivo. Mechanically, RP11-738E22.3 regulated FBXO6 expression by competitively binding to miR-504-3p and miR-3135b, thereby activating the MAPK/ERK/mTOR pathway to suppress autophagy and apoptosis in HCC. In conclusion, lincRNA RP11-738E22.3 is a novel and promising biomarker for HCC progression, exerting its oncogenic effects through the inhibition of autophagy and apoptosis via activation of MAPK/ERK/mTOR signaling. Targeting RP11-738E22.3 may offer new therapeutic opportunities for HCC treatment. - Source: PubMed
Publication date: 2026/05/05
Chen YihongHu EryaTang ShiqiCui GuangzuMa JiayaoLi YinLiu HaicongZhou XinPeng QingpingTang DiyaWang XinwenHan YingCai ChangjingZeng ShanShen HongJiang Binyuan - Colorectal cancer (CRC) is the third most common malignant tumor worldwide, with high recurrence and metastasis rates significantly impacting outcomes. This study explores the role of FBXO6, a ubiquitination-related protein, in regulating CRC malignancy, particularly cell migration and invasion. Our analysis reveals that higher FBXO6 expression correlates with better prognosis in CRC patients, although its expression decreases in advanced-stage tumors. Functional studies demonstrate that FBXO6 overexpression suppresses the invasive and migratory abilities of HCT116 and RKO cells and reduces single-cell colony formation. In contrast, FBXO6 knockdown promotes these malignant traits. Immunoprecipitation and mass spectrometry analyses identified ITGB1 as a key substrate of FBXO6, with potential prognostic relevance in CRC. Subsequent in vitro assays confirmed this interaction, revealing that FBXO6 binds ITGB1 at its glycoprotein recognition site, thereby reducing ITGB1 stability and attenuating downstream FAK/PI3K/AKT/ERK signaling. ITGB1 overexpression counteracts the suppressive effects of FBXO6, restoring downstream signaling activity. In vivo xenograft models further validate these findings: FBXO6 overexpression reduces tumor growth, Ki67 levels, and ITGB1-associated signaling. Additional rescue experiments show that FBXO6 counteracts the tumor-promoting effects of ITGB1 overexpression. In conclusion, FBXO6 suppresses CRC cell proliferation, migration, and invasion by targeting ITGB1 for ubiquitination and disrupting key oncogenic signaling pathways, thereby supporting its potential as a prognostic biomarker and candidate therapeutic target in CRC. - Source: PubMed
Publication date: 2026/03/19
Ren NianshengCheng LongHuang ZijianHu XuchenChi FengxuZhu YuekunWang Gang - Ulcerative colitis (UC) is a chronic inflammatory disease characterized by mucosal immune activation and epithelial barrier breakdown. The pathogenic mechanisms underlying UC remain incompletely understood, and identifying key molecular drivers of disease onset and progression may provide new therapeutic opportunities. - Source: PubMed
Publication date: 2026/02/26
Dai LongfeiYu ChaoXu RonglinGe RuomuZhang LiangliangLi AlongXu XinjianZhang Zhen - Bone repair following large defects remains a significant clinical challenge due to limited osteogenic capacity. F-box only protein 6 (FBXO6), an E3 ubiquitin ligase known to promote degradation of downstream proteins, was highly expressed after osteogenic differentiation. Herein, the role of FBXO6 in osteoblastic differentiation and bone remodeling was explored. Rat bone marrow mesenchymal stem cells (BMSCs) were first isolated and characterized. Following 14 days of osteogenic induction, FBXO6 was significantly upregulated (approximately 4-fold increase). BMSCs overexpressing FBXO6 demonstrated enhanced osteogenic potential, evidenced by increased mRNA expression of osteogenic markers (runt-related transcription factor 2, osteocalcin, COL1A1), elevated alkaline phosphatase (ALP) activity, and greater formation of calcium nodules. Conversely, FBXO6-silenced BMSCs exhibited the opposite effects. FBXO6 overexpression activated the Wnt/β-catenin signaling pathway, a known mediator of osteogenic differentiation. This effect was reversed by treatment with the Wnt/β-catenin inhibitor DKK1. Furthermore, β-catenin overexpression rescued the impaired osteogenesis caused by FBXO6 silencing. Label-Free Quantitative Proteomics analysis identified 439 differentially expressed proteins in FBXO6-overexpressing cells (245 upregulated, 194 downregulated). STARD3 N-terminal like protein (STARD3NL) was prioritized for further investigation (log2FC = -0.97, p = 0.02). FBXO6 interacted with STARD3NL and promoted its destabilization. STARD3NL knockdown attenuated the effects of FBXO6 silencing on osteogenesis. In a 3-mm-diameter critical-size femoral defect model, implantation of collagen scaffolds seeded with FBXO6-downregulated BMSCs significantly suppressed osteogenesis. These findings demonstrate that FBXO6-modified BMSC implantation represents a promising therapeutic strategy for bone defect repair. - Source: PubMed
Publication date: 2026/01/01
Yang KerongYue XiWu JinliangChen GuanhaoYang ShuminMa HaojunTan Hongyu