FBXL11 antibody - N-terminal region (ARP31697_P050)
- Known as:
- FBXL11 (anti-) - N-terminal region (ARP31697_P050)
- Catalog number:
- arp31697_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FBXL11 antibody - N-terminal region (ARP31697_P050)
Related genes to: FBXL11 antibody - N-terminal region (ARP31697_P050)
- Gene:
- KDM2A NIH gene
- Name:
- lysine demethylase 2A
- Previous symbol:
- FBXL11
- Synonyms:
- KIAA1004, FBL11, LILINA, DKFZP434M1735, FBL7, FLJ00115, CXXC8, JHDM1A
- Chromosome:
- 11q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-27
- Date modifiied:
- 2016-10-05
Related products to: FBXL11 antibody - N-terminal region (ARP31697_P050)
Related articles to: FBXL11 antibody - N-terminal region (ARP31697_P050)
- Identifying key candidate genes regulation on content and composition of intramuscular fat (IMF) deposition is critical for enhancing meat quality traits. As a specific demethylase for histone H3 lysine 36 dimethylation (H3K36me2), lysine demethylase 2 A (KDM2A) epigenetically modulates cellular processes including proliferation and differentiation by modifying chromatin architecture. Nevertheless, the regulatory role and precise molecular mechanism of this macromolecular interaction during intramuscular adipogenesis requires further investigation. In vitro goat intramuscular adipogenesis assays indicated that KDM2A ablation promotes IMF deposition and polyunsaturated fatty acid (PUFA) synthesis, whereas KDM2A overexpression has the opposite effect. Consistently, adipocyte-specific KDM2A knockout mice models under high-fat diet/glycerol induction all revealed its genetically deletion specifically increased IMF accumulation and PUFA content in vivo. Furthermore, we mechanistically demonstrated that disruption of KDM2A promotes intramuscular adipogenesis through structural modification of the chromatin landscape, specifically via the elevation of H3K36me2 at the peroxisome proliferator-activated receptor gamma (PPARγ) locus and subsequently activating its transcription. Collectively, our work uncovers KDM2A as an epigenetic modulator of IMF deposition, offering novel insights for meat quality enhancement via heritable epigenetic regulation. The demonstrable efficacy of targeting this pathway underscores its epigenetic potential in livestock improvement programs. - Source: PubMed
Publication date: 2026/04/16
Yue BinglinHu HanzhuoSha PeiranLi XinmiaoWang PengZhou ZiliXiong XianrongLi JianLin YaqiuXiong Yan - Previous clinical studies have reported that not all depressed patients respond to antidepressants. Therefore, finding potential predictive molecular biomarkers is crucial for providing important guidelines in the diagnosis and treatment of depression. In recent years, some studies have identified potential signature molecules using machine learning analysis of transcriptomic data. In this study, we analyzed transcriptomic data from duloxetine-treated depressed patients and used a random forest algorithm to identify a set of characteristic microRNAs and mRNAs. For the mRNA expression dataset, we identified a gene set having 30 transcripts, including TNK2 (Gini index =2.11) and KDM2A (Gini index =1.81), with an AUC value 10-fold and cross-validation equal to 0.907. We also identified the feature microRNA sets (n = 20) with an AUC value of 0.711. Gene annotation function analysis suggests that those feature mRNAs mainly mediate myosin complex and EGFR-related activities. When we explored the relationship between microRNAs and mRNAs, 151 microRNA-mRNA pairs showed negative correlations, while 129 pairs showed positive correlations. Meanwhile, 58 microRNA-mRNA pairs showed potential functional regulatory relationships based on seed-region sequence complementarity. We also confirmed direct regulation between several characteristic microRNAs and mRNAs using luciferase reporter assays. Subsequently, we found that the expression levels of TNK2 (P = 0.0044) and KDM2A (P = 0.0080) were significantly up-regulated after duloxetine treatment of SYSH cells. In a depressive animal model, mice administered with duloxetine showed altered mRNA and protein expression of those feature genes in the prefrontal cortex. Altogether, we identified the signature microRNAs and mRNAs that can distinguish duloxetine-effective and duloxetine-ineffective phenotypes and a close regulatory relationship between signature microRNAs and mRNAs. These characteristic molecular signatures may serve as predictive biomarkers for duloxetine efficacy, enabling patient stratification before and during treatment and providing a theoretical foundation for individualized antidepressant therapy and informed clinical decision-making. - Source: PubMed
Publication date: 2026/04/16
Zhao YanLei ChunguangTao YanlinXiong LanDwivedi YogeshWang Qingzhong - NLRP14 is an essential maternal factor for mammalian embryonic development. Maternal ablation of NLRP14 in mice impairs DNA demethylation and calcium homeostasis in zygotes, causing early embryonic arrest. However, the underlying biochemical events remain largely unknown. Here, we identified two binding partners (KDM2A and UHRF1) of NLRP14 and further solved structures of NLRP14-KDM2A-SKP1 and NLRP14-UHRF1. Structural analysis revealed that NLRP14 modulates the SKP1-CUL1-F-box (SCF) E3 ubiquitin ligase and the RING-type E3 ubiquitin ligase UHRF1 through two distinct mechanisms. Mechanistically, NLRP14 competitively inhibits KDM2A-mediated SCF assembly or allosterically inhibits the activity of UHRF1 by occupying the E2 ubiquitin-conjugating enzyme (UBE2D) binding site of the ubiquitin-like (UBL) domain. Deletion of NLRP14 in mice increases ubiquitination levels in oocytes during maturation and after fertilization. Collectively, our findings identify NLRP14 as a dual regulator that restrains E3 ubiquitin ligase-driven ubiquitination by limiting SCF complex assembly and attenuating UHRF1 activity. This regulatory role is required to prevent excessive protein ubiquitination and maintain proteostasis during the oocyte-to-embryo transition, thereby supporting early embryonic development. Our study uncovers maternal regulation of proteostasis in oocytes and suggests that dysregulating proteostasis is an important factor in the pathogenesis of reproductive disorders. - Source: PubMed
Publication date: 2026/04/08
Liu SibeiQi QianqianChi PengliangJiao HaizhanYan LiLu YuechaoZhang RongrongLi JinhongJu SichengHan ZhuoZhang ZihanLiu QingtingOu GuojinLi JialuChen JingWang XiangLi LeiGuo LiJiao XueHu HongliJiang YongmeiDeng Dong - High myopia (HM) poses a growing public health challenge due to its increasing prevalence and the associated risks of blinding complications and psychological comorbidities. While traditionally considered an isolated ocular condition, emerging evidence implicates systemic mechanisms, notably through the gut-eye axis and immune factors, play important part in the pathogenesis of HM. Histone demethylase Kdm2a, the key H3K36me2 modification eraser, is critically involved in various inflammatory diseases, yet its specific role in the gut-eye axis and HM remains elusive. To address this, the HM model was successfully established. HM mice exhibited significant scleral thinning, reduced collagen protein, and prominent anxiety-like behaviors. Crucially, they were suffering from gut microbial dysbiosis and intestinal barrier impairment. Intriguingly, upregulated Kdm2a and correspondingly decreased H3K36me2 levels were observed in the intestinal epithelial cells (IECs) of HM mice. Treatment with Daminozide (DA), the selective inhibitor of Kdm2a, effectively suppressed myopia progression and ameliorated psychological comorbidities. Mechanistically, DA restored gut microbiota homeostasis, colonic morphology, and barrier integrity. The transcriptomic profiling further revealed the protective effects of Kdm2a inhibition on modulating key pathways involved in intestinal inflammation and tissue remodeling. Collectively, this work elucidates a novel gut-eye pathway in HM pathogenesis and identifies Kdm2a in IECs as a promising therapeutic target for HM and its associated psychological comorbidities. - Source: PubMed
Publication date: 2026/02/14
Li ZixuanLi HaoZhang ShiboWang XixiJi XinpeiZhang JianpingHou DengyongFan MengyaLiu RuisangXiang YanJiang YuyuDing YingyingZhan YanbinFang LibenSun BinLi HuafeiLiu XingguangZhang YunkaiRen Xiaomeng - Disseminated tumor cells can form clusters via cell-cell adhesion, which increases their capacity to initiate metastasis. Metastatic clusters are characterized by distinct changes in transcription, suggesting that epigenetic mechanisms underlie their unique phenotypic state. By performing functional epigenomic studies in models of non-small cell lung cancer, we identified the histone H3 lysine 36 (H3K36) demethylase KDM2A as being differentially required for the fitness of metastatic cell clusters. This contextual dependency on KDM2A is predicated by tumor cell-cell aggregation, which specifically induces KDM2A binding to CpG island enriched promoters. At these defined genomic loci, KDM2A maintains H3K36 monomethylation, which preferentially correlates with transcriptional activation. KDM2A directly targets oxidative phosphorylation genes and KDM2A activity is required for optimal mitochondrial respiration and apical cell junction integrity in cell clusters. Consequently, suppressing KDM2A reduces metastatic seeding and colonization in multiple organs, including in the brain. These findings reveal a chromatin regulatory mechanism by which homotypic cell communication instructs the epigenome of disseminated tumor cells to potentiate their metastatic competence. - Source: PubMed
Publication date: 2026/01/23
Kravitz Carolyn JPatel KiranWingrove EmilyZhao DejianTang TangChande SampadaZhao MinghuiHuo YuchenWestbrook Thomas FYan QinNguyen Don X