ATAD3A
- Known as:
- ATAD3A
- Catalog number:
- 002109A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATAD3A
Related genes to: ATAD3A
- Gene:
- ATAD3A NIH gene
- Name:
- ATPase family AAA domain containing 3A
- Previous symbol:
- -
- Synonyms:
- FLJ10709
- Chromosome:
- 1p36.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-24
- Date modifiied:
- 2019-01-18
Related products to: ATAD3A
Related articles to: ATAD3A
- Triple-negative breast cancer (TNBC) represents the most aggressive form of breast cancer and is associated with the worst prognosis. Ferroptosis holds great promise as an emerging therapeutic strategy; however, TNBC cells demonstrate reduced sensitivity to ferroptosis as a result of elevated mitochondrial membrane potential (MMP), inadequate production of reactive oxygen species (ROS), and the presence of activated antioxidant defencses, making it difficult for lipid peroxidation to accumulate to a lethal threshold. As an emerging therapeutic strategy, sonodynamic therapy (SDT) is particularly suitable for deep-seated tumors due to the excellent tissue penetration capabilities of ultrasound (US). Nevertheless, current sonosensitizer typically experience limited sonodynamic efficacy and inadequate targeting of tumors, whereas small interfering RNA (siRNA) presents a highly promising option for gene therapy, its efficacy is heavily dependent on efficient and safe cellular delivery vectors. Therefore, we designed and synthesized a folate-modified Fe-TCPP metal-organic framework (FTFA) nanoplatform that serves both as a siATAD3A gene therapy carrier and as a sonosensitizer to generate ROS upon ultrasound (US) irradiation. ATAD3A displays high expression levels in TNBC and is linked to a negative prognosis; it's silencing reduces MMPs and increases ROS-induced apoptosis. siATAD3A was loaded onto FTFA to prepare FTFA@siATAD3A, which was delivered to TNBC cells via folate receptor-mediated targeting. Under US irradiation, the Fe3+ loaded within this platform synergistically triggers a ferroptosis cascade involving the Fenton reaction, lipid peroxidation, and GPX4 downregulation, effectively inducing ferroptosis. This method greatly reduces the proliferation of cells, as well as their migration and tumor growth when tested in living organisms, and it also shows excellent compatibility with biological tissues. In summary, FTFA@siATAD3A provides a novel strategy for the synergistic gene-ferroptosis therapy of TNBC using sonodynamic effects. - Source: PubMed
Du YangYang JiangnanChen ShuaiYang XiaoxinWang YianYang YiyuanFu Deyuan - Acute kidney injury (AKI) is a clinical syndrome associated with severe morbidity and high mortality, for which there are no currently effective therapies. Aging, a state associated with Klotho protein decline, is an independent risk factor for AKI development and progression. Here, we report that Klotho-derived peptide 1 (KP1), a small peptide that recapitulates the renoprotective potential of Klotho, effectively protects against AKI in mouse models induced by either cisplatin or ischemia-reperfusion injury. KP1 treatment improved kidney function, ameliorated structural damage, inhibited tubular cell apoptosis, and preserved mitochondrial integrity in both models. Mechanistically, KP1 entered kidney proximal tubular epithelial cells via endocytosis, directly targeted the mitochondrial protein ATPase family AAA domain-containing protein 3A (ATAD3A), and prevented its degradation, and preserved its function. By interacting with the hypoxia inducible gene 1 (HIG1) domain family member 2A (HIGD2A) and maintaining its expression and function within the mitochondria, ATAD3A prevented cytochrome c release and inhibited caspase activation following injury, thereby alleviating renal tubular cell apoptosis. Collectively, these studies demonstrate that KP1 is a promising therapeutic agent for AKI by directly targeting and preserving mitochondrial integrity. Our findings also lay the groundwork for developing novel therapeutic strategies to treat diseases associated with mitochondrial dysfunction. - Source: PubMed
Publication date: 2026/08/25
Zhang XiaoyaoLin ShihuiWu TianyuZhang ZhixinZhou HongHong XueLiu Youhua - Host genetic susceptibility to urogenital () reinfection remains poorly understood. Coding variants identified in prior genome-wide association studies (GWAS) explained only a small fraction of the risk of reinfection. Our goal in this study was to characterize whether more risk would be captured by sequence variation that traditional GWAS insufficiently captures. Specifically, we evaluated the risk attributable to SNPs present in regulatory, non-coding regions; post-transcriptional regulation by microRNAs (miRNAs) that may depend on sequence variation in either the miRNA or the target mRNA; and copy number variants (CNVs). We analyzed GWAS data from African American women with or without documented urogenital reinfection. Fine mapping and independent association analyses identified 30 unique index single-nucleotide polymorphisms (iSNPs), which were expanded to variants in linkage disequilibrium. Regulatory annotation was performed using HaploReg, RegulomeDB, FORGEdb, rSNPBase, and GTEx. We examined whether genes identified in the reinfection GWAS are targeted by known infection-associated microRNAs using curated databases. Genome-wide CNV calling was conducted using SNP intensity data, followed by stringent quality control and gene-level association testing. Functional annotation prioritized 7 SNPs with strong regulatory evidence, with stringent criteria for regulatory relevance, using HaploReg, RegulomeDB, FORGEdb, and rSNPBase. The strongest signals were observed at the locus, where multiple intronic variants (including rs2486963 and rs2244385) overlapped regulatory chromatin, altered transcription factor binding motifs, and acted as -expression quantitative trait loci for in whole blood. Additional regulatory variants were identified near , , and , showing tissue-specific regulatory effects. MicroRNA analysis revealed extensive post-transcriptional targeting of and , while showed no curated -associated miRNA interactions. CNV analysis identified 5775 high-confidence events, with nominal gene-level associations observed for , , , and . These results indicate that a greater fraction of the susceptibility to urogenital reinfection may be driven by genetic variation affecting immune and epithelial pathways rather than protein-coding changes. - Source: PubMed
Publication date: 2026/06/16
Tiwari Hemant KVejandla Sandeep ChowdaryBuker IhsanDing MengchenSrinivasasainagendra VinodhPatki AmitGupta KanupriyaWeinhouse CarenGeisler William M - Pathogenic variants in cause a spectrum of multisystem disorders, with a recurrent dominant-negative variant (c.1582C>T; p.Arg528Trp) associated with neurodevelopmental disease. Given the tolerance of to heterozygous loss of function variants, allele-specific transcript reduction represents a promising therapeutic strategy. We designed and optimized allele-specific antisense oligonucleotides (ASOs) targeting the c.1582C>T transcript and evaluated their efficacy and specificity in affected fibroblasts using allele-specific primers and amplicon-based next generation sequencing. Therapeutic potential was further assessed in vivo in zebrafish embryos expressing human wild-type or mutant transcripts. An optimized gapmer ASO selectively reduced mutant transcripts while relatively sparing the wild-type allele. In addition to RNase H-mediated degradation, the ASO induced exon skipping, leading to degradation of the aberrant transcript without production of a truncated protein. In zebrafish, expression of mutant human in embryos caused developmental abnormalities including reduced eye size, which were robustly rescued by co-injection of the optimized ASO. Our findings provide proof of concept for allele-targeted ASO therapy for dominant-negative variants. This work highlights the therapeutic potential of ASOs for rare dominant disorders involving genes tolerant to heterozygous loss-of-function, and establishes zebrafish as a versatile platform for in vivo ASO optimization. - Source: PubMed
Publication date: 2026/05/23
Ezer ShlomitYanovsky-Dagan ShiraGranit AmitMcDougal MatthewHwang TaeyoungAntman IsraelKarni RotemYoon Wan HeeSaada AnnInbal AdiHarel Tamar - Aortic aneurysm and dissection (AAD) is a fatal vascular emergency with limited mechanism-based therapies. ATAD3A (ATPase family AAA [ATPases associated with diverse cellular activities] domain-containing protein 3A), a mitochondrial AAA ATPase enriched at organelle contact sites, has been implicated in mitochondrial signaling, but its role in AAD remains unclear. - Source: PubMed
Publication date: 2026/06/04
Lin JieXiong ShengjunAn YingWu LinDu YuxinLi Yiran EWu YujieDu ZunhuiYu WenjunGe JunboZhang YingmeiRen Jun