ANKZF1
- Known as:
- ANKZF1
- Catalog number:
- 001665A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ANKZF1
Related genes to: ANKZF1
- Gene:
- ANKZF1 NIH gene
- Name:
- ankyrin repeat and zinc finger domain containing 1
- Previous symbol:
- -
- Synonyms:
- FLJ10415, ZNF744, Vms1
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-22
- Date modifiied:
- 2019-04-09
Related products to: ANKZF1
Related articles to: ANKZF1
- ANKZF1, the mammalian ortholog of yeast Vms1, is a multidomain cytosolic protein. Occasionally, the protein is also found in mitochondria, although the reason for its mitochondrial localization and the mechanism of its mitochondrial targeting remain unclear. Despite the absence of any predicted mitochondrial targeting sequence or domain (MTS/MTD) in the protein, ANKZF1 possesses multiple internal matrix-targeting sequence-like sequences (iMTS-Ls). In this study, we demonstrate that the N-terminal 73 residues of ANKZF1 negatively regulate its mitochondrial targeting, and this portion of the protein is sufficient to hinder mitochondrial targeting of Δ73-ANKZF1 upon co-expression. Using a series of truncation mutants of ANKZF1, we further demonstrate that the iMTS-Ls comprised of residues 231-240 of ANKZF1 are essential for its mitochondrial localization. Furthermore, the sequence of this region is well conserved across different organisms, indicating the structural and functional importance and role in maintaining the mitochondrial targeting of the protein. Importantly, residues 231-324 of ANKZF1 form two consecutive predicted iMTS-Ls, which together constitute an independent mitochondrial signal sequence that can target green fluorescent protein (GFP) to the mitochondria when fused to the N terminus. Furthermore, by molecular dynamics simulation, we show that the deletion of the N-terminal 74 amino acids of ANKZF1 leads to a massive structural rearrangement within the protein, causing the opening of its C-terminal part and solvent exposure of the 231-240 residues. We postulate that these structural rearrangements and exposure of the internal MTS in the absence of the N-terminal segment of ANKZF1 lead to its mitochondrial translocation. - Source: PubMed
Publication date: 2026/04/01
Ali MudassarMaheswaran BhoopeshSahu DevidMalhotra NidhiMapa Koyeli - Linking genetic data with electronic health records in hospital biobanks promises to advance precision medicine, but limited ancestral diversity constrains discovery and generalizability. We analyzed 93,936 participants from the UCLA ATLAS Community Health Initiative to inform disease prevalence and genetic risk across five continental and 36 fine-scale ancestry groups. We discovered numerous unreported gene-phenotype associations, including FN3K with intestinal disaccharidase deficiency in Europeans and admixed Americans. Polygenic scores (PGS) robustly predicted common diseases, with effects markedly diminished in non-Europeans. Furthermore, we reduced the pronounced European bias in curated clinical variants using computational predictors, uncovering unreported disease-gene associations, including ANKZF1 and peripheral vascular disease in African Americans. Longitudinal data revealed that semaglutide efficacy varies across ancestries, is associated with PGS for type 2 diabetes, and is modulated by genetic variation in PTPRU. These findings illustrate how ancestrally diverse biobanks from a single health system yield robust disease associations and pharmacogenomic insights. - Source: PubMed
Publication date: 2026/03/27
Haas RoniMargolis Michael PWei AngelaYamaguchi Takafumi NFeng JeffreyTran ThaiTozzo VeronicaQueen Katelyn JMootor Mohammed Faizal EemanPatil VishakhaBroudy Michael ETung PaulAlam ShafiulMartinez Danielle BPatel YashCaggiano ChristaZeltser NicoleHugh-White RupertArbet JaronShemirani RuhollahTian MaoThapaliya PraptiEloyan LoraChen Lawrence OLapinska SandraAriannejad MaryamLajonchere Clara Kenny Eimear EPasaniuc BogdanBui Alex A TArboleda Valerie AChang Timothy SZaitlen NoahSpellman Paul TBoutros Paul CGeschwind Daniel H - BACKGROUND: Prostate cancer (PCa) is characterized not merely as a malignant tumor, but also as a metabolic disorder encompassing dysregulation of glycolysis. This study was purposed to develop a new effective prognostic model correlated with glycolysis-related genes (GRGs) and investigate its potential mechanisms in PCa. METHODS: We compared the expression differences of GRGs. A glycolysis-associated prognostic model was then developed to categorize PCa patients into different risk subgroups. The diagnostic accuracy and predictive efficacy of the models were assessed. Furthermore, a comprehensive nomogram was developed, incorporating the risk score feature, T and N stage, Gleason score, and age, which was further calibrated for accuracy. Risk groups were analyzed for correlation with tumor-infiltrating immune cells (TIICs), immune function, and immunotherapy. In addition, we performed functional enrichment analyses. RESULTS: Through constructing Cytoscape regulatory networks, 10 hub genes were identified, and their significance was evaluated and validated. As a result, we confirmed 12 genes (B3GALT6, ANKZF1, IDUA, ENO2, ALDH1A3, GUSB, AURKA, CDK1, LDHB, ALDH3B2, GALM, and ADH1C) for prognostic modeling and calculation of risk scores. Mutations, TIICs, and drug sensitivity were also analyzed. Furthermore, the PTTG1, associated with glycolysis and tumor immunity, was confirmed in vivo. CONCLUSIONS: Overall, these findings underscore the prognostic relevance of glycolysis-related genes in prostate cancer and provide novel insights into their association with disease progression and the tumor immune microenvironment. - Source: PubMed
Publication date: 2026/02/23
Wang JinhuaChen XiongYang GuoWang Xiaorong - : Patients with "driver gene-negative" LUAD lack effective targeted therapies. This study aimed to elucidate the role of the glycolysis pathway in driver gene-negative LUAD to identify key genes and potential therapeutic targets. : Bulk RNA sequencing data from 49 patients with driver gene-negative LUAD were analyzed. The driver gene-negative status of patients was confirmed by immunoblotting. Gene set enrichment analysis (GSEA) was conducted on six hallmark pathways related to glycolysis. Additionally, key genes were identified and a risk score model was constructed. Finally, single-cell RNA sequencing data were processed using the Seurat package for data cleaning, dimensionality reduction clustering, and cell type identification. : GSEA analysis revealed significant enrichment of the glycolysis pathway in driver gene-negative LUAD. Differential expression analysis identified 144 genes associated with the glycolysis pathway. Six glycolysis-related genes (ANKZF1, GPR87, KIF2A, LCT, MIF, SDHC) were identified associated with poor prognosis. Single-cell sequencing analysis validated the key role of MIF in the glycolysis process and revealed a positive feedback regulatory axis between MIF and HIF-1α, which may promoting glycolysis and malignant transformation. : This study elucidated glucose metabolic reprogramming mechanisms and highlighted the MIF-HIF-1α axis as a promising therapeutic target in "driver gene-negative" LUAD, which may offer new avenues for improving outcomes, particularly those lacking conventional targeted therapy options. - Source: PubMed
Publication date: 2025/10/10
Yang Hao-ShuaiLi Yuan-HaoChen QiLuo Hong-HeYu Qi-DuoHan YuZhu WeijieZhang JinLiang Chao-Yang - Mitochondria, the double membrane-bound organelles of endosymbiotic origin, are crucial centers for cellular energy production and several essential metabolic pathways. Recent studies reveal that mitochondria become dysfunctional following numerous cellular stresses, and during pathologies, demanding an extensive investigation of mitochondrial turnover mechanisms. Apart from the specific response pathways to tackle different stresses, mitophagy, or degradation of mitochondria by autophagy, is a critical quality control mechanism that clears irreversibly damaged mitochondria. Mitophagy is majorly executed either by receptor-mediated or PINK1-Parkin-dependent pathways. Here, we show that the human orthologue of yeast Vms1, ANKZF1, participates in PINK1-Parkin-mediated mitophagy. We show that ANKZF1 is extensively recruited to damaged mitochondria along with Parkin during mitochondrial proteotoxic stress induced by the expression of a single misfolded/aggregated protein or during uncoupler-induced membrane depolarization. Importantly, ANKZF1 recruitment to damaged mitochondria is significantly enhanced in the presence of Parkin, and ANKZF1 physically interacts with Parkin and LC3 during mitochondrial proteotoxic or depolarization stress. ANKZF1 harbors six putative LC3-interacting regions (LIRs), LIR4 present at residues 333-336, is particularly important for ANKZF1-LC3 interaction. Furthermore, we show that ANKZF1 knockout cells are compromised in clearing stress-damaged mitochondria by mitophagy, indicating an important role of ANKZF1 in mitochondrial turnover during stress. In summary, we show a new role of ANKZF1 in eliminating the stress-damaged mitochondria, reiterating the mito-protective role of Vms1/ANKZF1 during mitochondrial stresses. PINK1/Parkin signaling leads to polyubiquitination of outer mitochondrial membrane (OMM) proteins on stressed mitochondria. ANKZF1 functions as an adaptor protein, binding to polyubiquitinated OMM proteins via UBA domain and autophagosome receptor LC3 via LIR motif. - Source: PubMed
Publication date: 2025/07/29
Ali MudassarAnjali Mapa Koyeli