Ask about this productRelated genes to: FLAD1 Blocking Peptide
- 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 Blocking Peptide
Related articles to: FLAD1 Blocking Peptide
- 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 - Hepatocellular carcinoma (HCC) remains one of the leading causes of cancer-related mortality worldwide, characterized by increasing incidence rates and challenging prognoses. This study integrates single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics to unravel the complex molecular and structural landscape of HCC, focusing on the identification of mitochondrial-related genes (MitRGs) and their pivotal role in disease progression. Utilizing scRNA-seq and bulk RNA-seq data, we performed a comprehensive differential expression analysis to highlight MitRGs. A modeling approach using 92 combinations of nine machine learning algorithms was applied, producing a predictive model with good performance. Among the genes analyzed, FLAD1 emerged as significantly upregulated in HCC tissues, correlating with advanced disease stages and poorer patient outcomes, and exhibited exceptional diagnostic accuracy with an AUC of 0.962. Functional enrichment analyses revealed that high FLAD1 expression is involved in crucial biological processes like copper ion detoxification and heme complex assembly. Interaction networks further elucidated the connection between FLAD1 and critical HCC pathways, with its expression levels negatively correlated with key immune effector cells such as CD8+ T cells and DCs. Spatial transcriptomics analysis provided a structural basis for this immune exclusion, demonstrating that an intact tumor capsule can function as a physical barrier that fosters an immune-exempt microenvironment. This analysis also validated FLAD1 upregulation within the spatial context of the tumor. Additionally, DNA methylation analysis indicated a hypomethylation pattern in the FLAD1 promoter region, likely contributing to its overexpression in HCC. Validation of FLAD1 protein levels in an in-house cohort via Western blotting further confirmed these findings. Collectively, our integrative study highlights the utility of MitRGs as potential biomarkers and positions FLAD1 as a dual prognostic and therapeutic target linked to the structural and immune landscape of HCC. - Source: PubMed
Publication date: 2025/10/29
Zhu PengMou LishaLu YingPu ZuhuiGuo Changchun - The Eisenia nordenskioldi complex is known for its high karyotype diversity and morphological type, and there are many cryptic species present in this complex. The species is widely distributed in the Palearctic biogeographic region including Northeast China. However, the taxonomy of this species complex remains inadequately defined. In our study, we examined the morphological characters of the Eisenia nordenskioldi complex in Northeast China that have not been examined before and used mitochondrial marker COI and nuclear markers ITS2, AKAP17 and FLAD1 to analyze their genetic variation. We described three new subspecies namely, E. nordenskioldi shenzi ssp. nov. E. n. jilinensis ssp. nov. and E. n. chinensis ssp. nov., which show morphological distinction and supported with molecular data. Molecular phylogenetic analyses show that the Eisenia nordenskioldi species complex is not monophyletic, supporting previous works. - Source: PubMed
Publication date: 2025/05/29
Qin MingyanZhao HuifengZhang YufengHan Anne Charis NShekhovtsov Sergei VWu DonghuiAspe Nonillon M - This study investigates the molecular mechanism by which the FTO-YTHDF2 axis regulates FLAD1 expression through m6A modification to drive immune evasion and tumor progression in hepatocellular carcinoma (HCC). By bioinformatics analysis of TCGA-HCC data, FLAD1 was identified as a key oncogenic driver, with elevated expression in HCC tissues and cells. Functional experiments revealed that FLAD1 knockdown suppressed HCC proliferation, migration, invasion, and PD-L1 expression while enhancing CD8 + T cell cytotoxicity (evidenced by increased IFN-γ, TNF-α, and LDH release). Mechanistically, FTO, an m6A demethylase, upregulated FLAD1 by removing m6A marks to counteract YTHDF2-mediated mRNA degradation. In vivo, FTO silencing reduced tumor growth and PD-L1 levels while elevating pro-inflammatory cytokines, and the effects negated by YTHDF2 knockdown. These findings establish that the FTO-YTHDF2 axis promotes HCC immune evasion and tumor progression via m6A-dependent FLAD1 stabilization, highlighting the axis as a therapeutic target to disrupt tumorigenesis and restore anti-tumor immunity. - Source: PubMed
Publication date: 2025/08/19
Xu ChenJiang LiangjunLu XianzhouLi Wei