Ask about this productRelated genes to: LONRF2 antibody
- Gene:
- LONRF2 NIH gene
- Name:
- LON peptidase N-terminal domain and ring finger 2
- Previous symbol:
- -
- Synonyms:
- FLJ45273, RNF192
- Chromosome:
- 2q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-08-19
- Date modifiied:
- 2014-11-18
Related products to: LONRF2 antibody
Related articles to: LONRF2 antibody
- The pathogenesis of endometrial cancer (EC) remains poorly understood. This study aimed to delineate the expression profile of LON peptidase N-terminal domain and ring finger 2 (LONRF2) in EC and to elucidate its mechanistic role in modulating the proliferative, metabolic, and invasive capacities of EC cells. LONRF2 expression was analyzed in EC tissues and cell lines. EC cells overexpressing LONRF2 were evaluated for malignant phenotypes. Aldolase A (ALDOA) was identified as a LONRF2-interacting protein via immunoprecipitation and nano-liquid chromatography-tandem mass spectrometry. Their regulatory relationship was examined by assessing ALDOA stability and ubiquitination. Functional exploration of the LONRF2/ALDOA axis involved combined LONRF2 knockdown, ALDOA knockdown, ALDOA knockout, or treatment with the ALDOA inhibitor itaconate in EC cells to assess malignant phenotypes, along with a xenograft model to evaluate tumor growth. LONRF2 was downregulated in clinical EC tissue and cell lines. LONRF2 overexpression inhibited the growth, glycolysis, migration, and invasion of KLE cells. LONRF2 interacted with ALDOA and induced its ubiquitination and degradation. In line with this mechanism, the enhanced malignant phenotypes caused by LONRF2 silencing were reversed by either knocking down ALDOA or administering itaconate. ALDOA-knockout cells confirmed that itaconate suppresses EC cell growth, glycolysis, migration, and invasion by targeting ALDOA. Consistently, itaconate abolished the tumor-promoting effect of LONRF2 silencing in a xenograft model. This study identifies the LONRF2/ALDOA axis as a key driver of EC progression, primarily by regulating glycolysis. Targeting this axis, particularly LONRF2, presents a promising therapeutic strategy for EC. - Source: PubMed
Publication date: 2026/07/13
Shao JuanJiang CuiDuan YingchunChen LiGu JiashiSun HuanmeiXu Congjian - - Source: PubMed
Wood Heather - Protein misfolding is a major factor of neurodegenerative diseases. Post-mitotic neurons are highly susceptible to protein aggregates that are not diluted by mitosis. Therefore, post-mitotic cells may have a specific protein quality control system. Here, we show that LONRF2 is a bona fide protein quality control ubiquitin ligase induced in post-mitotic senescent cells. Under unperturbed conditions, LONRF2 is predominantly expressed in neurons. LONRF2 binds and ubiquitylates abnormally structured TDP-43 and hnRNP M1 and artificially misfolded proteins. Lonrf2 mice exhibit age-dependent TDP-43-mediated motor neuron (MN) degeneration and cerebellar ataxia. Mouse induced pluripotent stem cell-derived MNs lacking LONRF2 showed reduced survival, shortening of neurites and accumulation of pTDP-43 and G3BP1 after long-term culture. The shortening of neurites in MNs from patients with amyotrophic lateral sclerosis is rescued by ectopic expression of LONRF2. Our findings reveal that LONRF2 is a protein quality control ligase whose loss may contribute to MN degeneration and motor deficits. - Source: PubMed
Publication date: 2023/07/20
Li DanJohmura YoshikazuMorimoto SatoruDoi MiyukiNakanishi KeikoOzawa ManabuTsunekawa YujiInoue-Yamauchi AkaneNaruse HiroyaMatsukawa TakashiTakeshita YukioSuzuki NaokiAoki MasashiNishiyama AyumiZeng XinKonishi ChiekoSuzuki NarumiNishiyama AtsuyaHarris Alexander StephenMorita MarikoYamaguchi KiyoshiFurukawa YoichiNakai KentaTsuji ShojiYamazaki SatoshiYamanashi YujiShimada ShoichiOkada TakashiOkano HideyukiToda TatsushiNakanishi Makoto - - Source: PubMed
Youssef Mohieldin M MPark Jeehye - This study was designed to identify the differentially expressed miRNAs (DEMs) and genes (DEGs) in metastatic cervical cancer using bioinformatic tools. In this study, fifty-seven DEMs (48 downregulated and 9 upregulated) were identified, among which miR-4459 and miR-3195 expression was negatively associated with overall survival of cervical cancer patients. Then, 476 target DEGs were determined, and protein-protein interaction (PPI) network was constructed. Seventeen hub genes (, , , , , , , , , , , , , , , , and ) were finally selected to construct the miRNA-hub gene network. Overall, our study discovered the key miRNAs and mRNAs related to lymph node metastasis (LNM) in cervical cancer, which helps discover candidate therapeutic targets for cervical cancer. - Source: PubMed
Publication date: 2023/05/11
Ding YishanWu XiaorongYang Xiaofeng