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
- 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 - Current targeted therapies for gastric cancer have limited efficacy, and recently discovered markers have not significantly improved survival rates in patients with gastric cancer. Therefore, it is imperative to identify more specific genes associated with the occurrence and progression of gastric cancer to achieve prevention and treatment. The aim of this study is to discover high-risk genes for gastric cancer by integrating single-cell transcriptomics and Mendelian randomization (MR) analysis. - Source: PubMed
Publication date: 2025/09/20
Qi LiChen HaoyuHao XinyuGao TianyuZhou PingpingLi WenboWang ChenLi KunfengLiu ShaoweiWang YuhuaRen XuetongBai HaiyanRen NingningWang Yangang - Effective antiviral immunity requires a delicate balance between controlling infection and preventing excessive inflammation. NLRX1, an atypical member of the NOD-like receptor family, plays a crucial regulatory role in this process by modulating immune responses to both RNA and DNA viruses. Unlike other NLRs, NLRX1 does not directly activate inflammatory pathways, but rather fine tunes immune responses through interactions with key signaling initiators like MAVS, FAF1, viral RNA, and FBXO6. These interactions allow NLRX1 to influence antiviral pathways in a highly context-dependent manner. In RNA virus infections, NLRX1 can either enhance immune signaling to restrict viral replication or suppress type 1 IFN responses to promote viral persistence. Similarly, in DNA viral infections, NLRX1 exerts either protective or pathogenic effects, though the precise mechanisms remain unclear. Emerging evidence suggests that NLRX1 may also serve as a key regulator of inflammation and metabolic processes during infection, further contributing to its complex role in immunity. By synthesizing current research, this review provides insight into how NLRX1 regulates immune signaling in RNA and DNA viral infections, highlighting its dynamic role in antiviral immunity and the remaining gaps in our understanding. - Source: PubMed
Publication date: 2025/04/28
Woolls Mackenzie KElliott Carley MIvester Hannah MAllen Irving Coy