Ask about this productRelated genes to: FLAD1 antibody
- Gene:
- FLAD1 NIH gene
- Name:
- flavin adenine dinucleotide synthetase 1
- Previous symbol:
- -
- Synonyms:
- PP591, FAD1
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-29
- Date modifiied:
- 2016-10-05
Related products to: FLAD1 antibody
Related articles to: FLAD1 antibody
- Hepatocellular carcinoma (HCC) is a malignant tumor with high heterogeneity and immunotherapeutic resistance worldwide, presenting a severe challenge in clinical prevention and treatment. N6-methyladenosine (mA) is the most common reversible post-transcriptional modification on eukaryotic mRNA, whose dynamic balance is precisely regulated by "demethylases" (Erasers). Recent studies have confirmed that the two core mA Erasers (FTO and ALKBH5) exhibit significant expression imbalance in HCC, which strongly drives malignant tumor progression. Erasers enhance the ferroptosis resistance of HCC cells by regulating the stability of lipid metabolism-related RNAs such as GPNMB and FLAD1, helping them adapt to adverse metabolic microenvironments such as hypoxia and nutrient deprivation. Meanwhile, FTO can promote exosome release, inhibit the antigen-presenting function of dendritic cells (DCs), and further induce CD8⁺ T cells into an exhausted state. These processes synergistically construct an immunosuppressive tumor microenvironment (TIME), facilitating HCC to escape immune attack. Small-molecule inhibitors targeting core targets such as FTO and the emerging PROTAC technology have shown potential in preclinical models for reversing immunosuppression and enhancing the efficacy of systemic therapy. This review systematically synthesizes the regulatory mechanisms of Erasers in the HCC "metabolism-immunity" axis, comprehensively summarizes Eraser intervention strategies based on different etiological backgrounds for the first time, and concludes the clinical translation progress of related targeted drugs, providing new ideas and targets at the epitranscriptomic level for overcoming HCC immunotherapeutic resistance. - Source: PubMed
Publication date: 2026/07/18
Wen QinLiu ChenyangLi ChaofanYuan Xingxing - Hypoxia, a hallmark of solid tumors, drives malignant progression and represents a major therapeutic challenge. Metabolic reprogramming induced by hypoxia creates unique metabolic vulnerabilities that can be exploited therapeutically. Here, we systematically compared the metabolic network differences between hypoxic and normoxic cells, and developed DepFormer, a transformer-based deep learning model, to nominate hypoxia-dependent metabolic genes in tumor cells. Oxidative phosphorylation was identified as the most significantly hypoxia-dependent metabolic pathway, and FLAD1 was predicted to be one of the key hypoxia-dependent metabolic genes. FLAD1 locus is amplified, and FLAD1 expression is upregulated across various tumor types, especially in hypoxic tumors. FLAD1 depletion disrupts activity of mitochondrial complex II, causing succinate/fumarate imbalance, which in turn prevents cancer cells from adapting to hypoxia. We further identified a drug-like inhibitor of FLAD1, which selectively inhibits growth of hypoxic tumor cells. Our study establishes DepFormer as an effective framework for predicting state-specific metabolic dependencies and reveals FLAD1 as a metabolic vulnerability and an innovative therapeutic target for hypoxic tumors. - Source: PubMed
Publication date: 2026/07/17
Zhao XiangyuWu TaoWu SananChen YujinZhang YuChen JingDiao KaixuanHe ZaokeYan JiaweiLu TianzhuXu ChaoLiu LuFan GaofengXu DongliangLi XinxiangXiong XiaopengCheng JianjunBai FangLiu Xue-Song - Cytosolic DNA and RNA sensing is crucial for innate immunity, playing essential roles in pathogen defense and autoinflammation induction. We reported the endogenous metabolite flavin adenine dinucleotide (FAD) as a molecular brake restraining both cytosolic DNA and RNA sensing. It bound directly to cytosolic nucleic acid sensors cyclic GMP-AMP synthase (cGAS) and retinoic acid-inducible gene I (RIG-I), occupying catalytic pockets to suppress their activity and downstream immune responses. Physiologically, FAD prevented self-nucleic acid-induced sterile inflammation and maintained immune homeostasis. FAD deficiency due to FAD synthase (FLAD1) ablation exacerbated auto-inflammation and cellular senescence. Upon viral infection, reduced FLAD1 activity lowered FAD amounts, which removed its inhibitory control over DNA and RNA sensors, thus facilitating extensive interferon-I (IFN-I) signaling activation. Consequently, FLAD1 depletion strengthened the innate immune response and protected mice from viral infection. Our findings identify FAD as a natural suppressor of both cytosolic DNA and RNA sensing, offering therapeutic potential for inflammatory diseases. - Source: PubMed
Publication date: 2026/07/13
Wang YaoShen YanyanLiu JiayuQi QiGuo YueWang YunyingXie BoyangYan ChunyanLiu YanhongJin ZhiWang RuiboCao AipingLi JunchengSong ZengqingChen JingHan QiuyingZhu YingjieZhang KunWang TaixiaLi TaoPan XinHe XinhuaZhou TaoLi AilingZhang XueminWang NaXia QingZhang Weina - The FLAD1 gene encodes the key enzyme in the biosynthesis of flavin adenine dinucleotide (FAD). As an essential cofactor of various enzymatic reactions, FAD is potentially involved in a series of crucial biological processes. Mutations in the FLAD1 gene are implicated in the pathogenesis of severe metabolic disorders, including lipid storage myopathy (LSM) and multiple acyl-CoA dehydrogenase deficiency (MADD). However, the in vivo pathophysiological consequences of systemic FLAD1 deficiency remain poorly understood. To address this, we generated a tamoxifen-inducible Flad1 knockout mouse model and characterized the phenotype of widespread FLAD1 ablation. Our results demonstrated that inducible Flad1 depletion in adult mice results in gradual lethality within approximately one month, accompanied by marked weight loss, severe spinal curvature, and muscle dysfunction. Mechanistically, Flad1 deficiency led to a significant reduction in FAD levels, resulting in decreased cellular ATP content and consequently a dysfunction of intracellular energy metabolism. Our study presents the first inducible Flad1 knockout mouse model and establishes the in vivo functional relevance of FLAD1 in maintaining metabolic homeostasis and organismal survival. Collectively, this model serves as a crucial tool not only for elucidating the molecular mechanisms underlying FLAD1 and FAD deficiency-related pathological changes, but also for evaluating potential therapeutic strategies for diseases related to FLAD1 dysfunction. - Source: PubMed
Publication date: 2026/02/12
Xie BoyangQi QiWang YaoLiu JiayuLiu YanhongShen YanyanGuo YueWang RuiboLi JunchengYan ChunyanJin ZhiZhou TaoXia QingZhang WeinaLi Ailing - The (Michaelsen, 1892) species complex is a cosmopolitan earthworm group that is widely distributed throughout Asia, and has a high degree of diversity. Nonetheless, the species composition of this species complex remains ambiguous due to limited taxonomic investigation. An integrative taxonomic approach, incorporating both morphological and molecular datasets, is herein applied to elucidate the species complex across East Asia, with the objective of delimiting putative new species. External and internal morphological characters were examined for taxonomic identification. For molecular phylogenetic analysis, one mitochondrial marker, the cytochrome c oxidase subunit I (COI), and three nuclear loci, namely 28S rRNA (28S), A-kinase anchor protein 17A (AKAP17), and flavin adenine dinucleotide synthetase 1 (FLAD1) were used. Species delimitation was performed using three complementary methodological frameworks: Assemble Species by Automatic Partitioning (ASAP), the Generalized Mixed Yule Coalescent (GMYC) phylogenetic approach, and Bayesian Phylogenetics and Phylogeography (BPP). Congruent species boundaries were recovered across all analyses, with the single exception of the GMYC model applied to the mitochondrial COI data set. Furthermore, the interspecific K2P genetic distance exceeded 15%. This study has delimited two new species, namely and The two new species represent the first additions to the species complex in the past decade, thereby significantly contributing to our understanding of earthworm diversity in Asia. - Source: PubMed
Publication date: 2025/12/19
Liu MinMiao PuLiu ZhengAspe Nonillon MZhang YufengZhao Huifeng