AATF
- Known as:
- AATF
- Catalog number:
- 000879A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AATF
Related genes to: AATF
- Gene:
- AATF NIH gene
- Name:
- apoptosis antagonizing transcription factor
- Previous symbol:
- -
- Synonyms:
- DED, CHE-1, CHE1, BFR2
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-13
- Date modifiied:
- 2015-01-29
Related products to: AATF
Related articles to: AATF
- [This corrects the article DOI: 10.1016/j.omton.2026.201259.]. - Source: PubMed
Publication date: 2026/08/21
Suresh DiwakarSrinivas Akshatha NGunaseelan BharathwaajBharadwaj S A AmithMoorthy ManjuRamaswamy GopalkrishnaSatish SuchithaVishwanath PrashantSanthekadur Prasanna KumarChidambaram Saravana BabuKumar Divya P - Obesity (OB) predisposed to psoriasis (PSO) and aggravation of existing PSO. It is a risk factor for PSO and metabolic syndrome. However, the biological link between PSO and OB remains to be studied. The study aimed to explore the relationship between PSO and OB, identify potential predictive biomarkers, and investigate their expression and function in PSO. Mendelian randomization (MR) was used to observe the causal effect between OB and PSO. Using a public database, we identified key shared genes in PSO and OB. Functional enrichment analysis of key shared genes was performed. Single-cell RNA sequencing (ScRNA-seq) analysis was used to further analyse the pivotal biomarkers at the skin cell level in PSO. Motif enrichment analysis was used to screen key transcription factors (TFs). The functional characteristics of PSO skin cell subtypes were evaluated from a metabolic perspective. Two machine learning algorithms were used to screen diagnostic characteristic biomarkers for PSO-OB. The diagnostic efficacy of biomarkers was evaluated by logistic regression analysis and subject's working characteristic curve. Construct a cell model of PSO, and screen the significantly upregulated or downregulated target genes. Knock down the overexpressed target genes using siRNA to investigate their effects on the proliferation and inflammatory response of PSO cells, and clarify their role in the pathogenesis of PSO. MR Analysis showed that OB was a high-risk factor for PSO vulgaris. Nineteen key differentially expressed genes (DEGs) were screened between PSO and OB. Functional enrichment analysis showed that these key DEGs were significantly related to lipid metabolism, thermogenesis and ras signalling pathways. According to ScRNA-seq analysis, psoriatic skin cells were mainly composed of keratinocytes (KC), dendritic cells (DC), macrophages, natural killer cells (NK-cells), T cells, Treg cells and melanoma. Among them, the key DEG of PSO-OB COX7C was significantly correlated and enriched in PSO skin cell development. We identified 24 active transcriptional regulators behind the cellular diversity of psoriatic skin subtypes. We evaluated the role of psoriatic skin cell subtypes in terpenoid backbone biosynthesis, steroid hormone biosynthesis, propanoate metabolism and N-glycan from the perspective of metabolism abundant functions in lipid metabolism such as biosynthesis. Six key genes (AATF, COX7C, GHRH, KCNA3, PCSK1 and PLIN1) obtained by least absolute shrinkage and selection operator (LASSO) regression and support vector machine recursive feature elimination (SVM-RFE) algorithm can be used as promising diagnostic biomarkers for PSO and OB. COX7C significantly upregulates and promotes the proliferation of psoriatic cells while also positively regulating the inflammatory response in PSO. Overall, our study provides a comprehensive assessment of the relationship of potentially key genes in PSO and OB to lipid metabolism, psoriatic skin subtype cells and TFs. COX7C is a diagnostic biomarker for PSO-OB and positively regulates the proliferation and inflammatory response of PSO cells. Which may pave the way for exploring possible associations in the development of these two diseases. - Source: PubMed
Liu FanghuaSu HangHan RuxueLiu ShougangChen Yongfeng - Hepatocellular carcinoma (HCC), a leading cause of cancer death, has a dynamic and heterogeneous tumor microenvironment (TME) that drives progression and therapeutic resistance. We previously elucidated that apoptosis-antagonizing transcription factor (AATF) drives angiogenesis in HCC. However, its role in TME remains unexplored. We employed an orthotopic xenograft mouse model, implanting human HCC cells into the liver and achieved liver-specific silencing via tail vein injection of adeno-associated virus 8 (AAV8) carrying mouse-specific siAATF or siControl. Histological, biochemical, and molecular analyses, combined with whole-genome transcriptomics mapped to mouse and human genomes, were used to study TME and tumor compartments separately. Silencing of AATF in the TME significantly reduced tumor growth compared with controls. Furthermore, AATF loss disrupted key processes in TME, including inflammation, immune response, angiogenesis, and extracellular matrix remodeling. Mechanistically, TGF-β signaling was significantly suppressed in the TME, thereby affecting tumor cell-cycle and metabolic activity, ultimately leading to tumor regression. The long non-coding RNA (lncRNA) analysis identified MIR100HG as a key downstream regulator of AATF in the TGF-β signaling pathway. These findings expand the oncogenic role of AATF to include regulation of the TME via the AATF-MIR100HG-TGF-β axis, highlighting its potential as a therapeutic target in HCC. - Source: PubMed
Publication date: 2026/06/06
Suresh DiwakarSrinivas Akshatha NGunaseelan BharathwaajBharadwaj S A AmithMoorthy ManjuRamaswamy GopalkrishnaSatish SuchithaVishwanath PrashantSanthekadur Prasanna KumarChidambaram Saravana BabuKumar Divya P - To clarify the therapeutic targets and signaling pathways of total flavone (AATF) in gout treatment, we integrated network pharmacology and experiments. Network pharmacology was applied to screen AATF's anti-gout targets, construct protein-protein interaction (PPI) and drug-component-disease-target-pathway networks, and conduct gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. A dual gout rat model was established using potassium oxonate, adenine, and monosodium urate (MSU) crystals, followed by assessments including toe swelling measurement, hematoxylin-eosin (HE) staining of kidney and joint tissues, digital radiography (DR) imaging, detection of serum uric acid and xanthine oxidase (XOD) activity, enzyme-linked immunosorbent assay (ELISA) of inflammatory factors, and Western blot validation of key targets. Network pharmacology revealed that AATF modulates inflammatory responses and the tumor necrosis factor (TNF) pathway via core targets including albumin (ALB), TNF, interleukin-6 (IL-6), and tumor protein 53 (TP53). experiments showed that AATF significantly ameliorated renal and joint pathological damage, reduced serum uric acid/XOD activity, downregulated serum interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), IL-6, cyclooxygenase-2 (COX-2) levels, and inhibited joint nuclear factor kappa B (NF-κB), extracellular signal-regulated kinase 1 (ERK1), matrix metalloproteinase 9 (MMP9) expression. Collectively, AATF exerts anti-gout effects through multi-target and multi-pathway mechanisms linked to the TNF signaling pathway, providing critical preliminary evidence for its preclinical development. - Source: PubMed
Publication date: 2026/06/18
Wang YilinWang ShuangLi ZhaoxiaChen XiZhang ChengyiHan XiaoxueWan LimeiFan SuiqiangLiu YitingGuo ZiyanHuang XiaoqiangXu XiaozeZhou XinXing Bingfeng - A recent study delves into intricate relationship between microRNAs (miRNAs), specifically focusing on their role in cancer development. miRNAs are highlighted for their capacity to modify genetic profile and modulate epigenetic architecture, establishing regulatory circuit between epigenetic modulation and miRNAs. Notably, antipsychotic drugs, particularly pimozide, is reported to influence miRNA expression, impacting essential processes in cancer development such as cell proliferation and apoptosis. Anti-cancer properties of pimozide have sparked interest in its potential role in cancer treatment, although precise mechanism of its antitumor function remains elusive. The study focuses on a newly discovered miRNA, miR-2909, encoded by the apoptosis antagonizing transcription factor (AATF) gene, which has been implicated in oncogenesis. This research aims to unravel the interplay between pimozide and miR-2909, investigating their influence on epigenetic modulations and their functional relevance to cellular proliferation and apoptosis in cancer cells. Utilizing bioinformatic tools for structural prediction, pharmacokinetic property assessment, and molecular docking interactions, the study reveals a strong binding affinity between pimozide and miR-2909.Validation through various experimental methods, including qRT-PCR, western blotting, immunofluorescence, transient transfection, CHIP assay, and flow cytometry confirms the interplay between pimozide and miR-2909. The results demonstrate a pivotal role in the regulation of genes responsible for cellular proliferation and apoptosis. Additionally, the study uncovers that pimozide's pharmaco-epigenomic response is mediated through miR-2909, promoting DNA methylation and leading to decreased cellular proliferation, increased apoptosis, ROS generation, and altered cell-cycle dynamics. In conclusion, the findings identify pimozide as a potential chemotherapeutic agent acting through the regulation of the oncomiR-2909. Insight Box This study uncovers a novel pharmaco-epigenomic mechanism by which the antipsychotic drug pimozide exerts anti-cancer effects in breast and lung cancer cells. We demonstrate that pimozide downregulates oncogenic miR-2909, leading to the upregulation of DNMT3B, which mediates epigenetic silencing of key proliferation genes and promotes apoptosis. This integrative approach-combining molecular biology, gene expression profiling, and epigenetic analysis-provides new biological insight into the repurposing of psychiatric drugs for cancer therapy. Our findings highlight the therapeutic potential of targeting microRNA-epigenetic interactions and suggest a broader applicability of integrating pharmacology with systems biology to uncover unconventional roles of known drugs in cancer treatment. - Source: PubMed
Malik DeeptiRaina AshvinderSingh JitenderKaushik HitaishiKaur GurjeetBansal SeemaSarma PhulenJain AshishMedhi Bikash