ATAD2
- Known as:
- ATAD2
- Catalog number:
- 002107A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATAD2
Related genes to: ATAD2
- Gene:
- ATAD2 NIH gene
- Name:
- ATPase family AAA domain containing 2
- Previous symbol:
- -
- Synonyms:
- PRO2000, DKFZp667N1320, MGC5254, MGC29843, CT137, ANCCA
- Chromosome:
- 8q24.13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-24
- Date modifiied:
- 2019-01-18
Related products to: ATAD2
Related articles to: ATAD2
- Gastric cancer is the fifth most common cancer and the third leading cause of cancer-related deaths worldwide. Currently, research on the tumor microenvironment of gastric cancer remains to be developed. In this study, we obtained scRNA-seq data of gastric cancer from the GEO database, and used the Seurat package for clustering. We used the Bayesian cell Proportion Reconstruction algorithm to calculate the cell subpopulation content in TCGA samples, and combined it with TCGA survival data to perform Kaplan-Meier and univariable Cox analyses. We further performed multivariable Cox regression analysis incorporating age, sex, TNM stage, and histological type to evaluate the independent prognostic value of PIA T-cells. We found that a prognostic improvement associated T cells (PIA T-cells) had a better prognosis in gastric adenocarcinoma tissues with higher levels of PIA T-cells. To further characterize the biological identity of this population, we analyzed canonical T-cell functional markers and found that PIA T-cells exhibited a distinct phenotypic profile (CD4(low/negative), CD8A(moderate), GZMB(moderate), IFNG(low)), distinguishing them from other T-cell subsets. Unlike other T cell subpopulations, PIA T-cells expressed significantly higher levels of eight genes (ASPM, ATAD2, CENPF, DUT, MKI67, NUSAP1, TOP2A, and TYMS). The study of PIA T-cells may provide insights into gastric cancer tumor microenvironment-related treatments and inform future therapeutic strategies. - Source: PubMed
Publication date: 2026/09/22
Wu TongLi ZengningTian JuanNong MinyuChen XuanhuaLi YongleRao YingLiu YixinWang ShuhanJiang Lihe - Triple-negative breast cancer (TNBC) exhibits marked molecular heterogeneity, posing ongoing therapeutic challenges. Metabolic reprogramming, particularly through the Warburg effect, offers a promising therapeutic target for TNBC treatment. Data mining and machine learning identified (+)-miliusol as a promising candidate. Its direct target, eukaryotic initiation factor 3D (EIF3D), was validated through mass spectrometry-coupled cellular thermal shift assay (MS-CETSA), a biotinylated probe, and a proteolysis-targeting chimera (PROTAC) approach. EIF3D, an emerging oncoprotein and atypical translation initiation regulator, promotes tumor survival by selectively modulating protein synthesis. (+)-Miliusol demonstrates potent anti-proliferative and anti-migratory activity against TNBC in both and . Integrated proteomic and transcriptomic analyses revealed that (+)-miliusol suppresses TNBC progression through EIF3D-mediated translational regulation. Mechanistically, it disrupts the EIF3D-AlkB homolog 5 (ALKBH5)-glucose transporter type 4 (GLUT4) axis, EIF3D-HIF1 signaling, and the EIF3D-RuvB like AAA ATPase 1 (RUVBL1)--catenin pathway, thereby inhibiting glycolysis and metastasis while inducing ER stress-dependent apoptosis caspase-12 and JNK activation. Additionally, (+)-miliusol blocks EIF3D-HIF1 and EIF3D-ALKBH3 interactions, impairing ATAD2/PAK1-regulated Warburg-effect networks and triggering autophagy-associated cell death. (+)-Miliusol induces TNBC cell death by selectively suppressing translation of critical glycolytic and metastatic regulators. These findings establish EIF3D-mediated translational control as a promising therapeutic avenue for TNBC treatment. - Source: PubMed
Publication date: 2026/03/16
Zhang JinJia LinChen XiyaWu YanSun XiaohanZou LingCheng XiaolingHuang JingnanZhou HongchaoDai LingyunZhou LeHe ZhendanLiu BoHao YueYao Dahong - Endometrial cancer is one of the gynecological malignancies, currently ranking first in mortality among the three major gynecological cancers. Effective treatment options remain scarce. ATAD2, a chromatin remodeler, is implicated in solid tumor progression, but its role in endometrial cancer (EC) and tumor microenvironment (TME) remodeling remains unclear. This study investigated the functional impact and mechanisms of ATAD2 in EC pathogenesis. - Source: PubMed
Publication date: 2026/06/21
Wang CanOsipova AnastasiiaWang YuanyuanLi FeiWang HengyuHu JingshuChen Xiuwei - Thyroid cancer (THCA) is the 9th most common endocrine tumor worldwide. However, its etiology and pathogenesis are not fully understood. Therefore, this study aimed to identify the biomarkers associated with chromatin remodeling in patients with THCA. THCA-related datasets and chromatin remodeling related genes were included in this study. Differential expression analysis and 2 machine learning algorithms were employed to identify candidate genes. Biomarkers were identified by receiver operating characteristic curve analysis. The prognostic potential of the biomarkers was explored using Kaplan-Meier (KM) survival analysis. Key genes linked to biomarkers were identified using weighted gene co-expression network analysis. Immune infiltration analysis was performed to explore differences in immune infiltration between THCA and control groups. Finally, the expression for biomarker was validated in clinical samples using reverse transcription quantitative polymerase chain reaction. Five biomarkers (CHD4, SMARCA2, CHD3, ATAD2, and SMARCA4) were screened. KM survival analysis revealed that patients with higher expression of SMARCA4, CHD4, and ATAD2 had a higher survival rate, whereas in the lower expression groups of CHD3 and SMARCA2, the survival rate of THCA patients was lower. A total of 98 genes related to biomarkers were identified using weighted gene co-expression network analysis. In addition, a total of 20 immune cells infiltrated differentially in THCA and controls, with the largest positive correlation between immature dendritic cells and ATAD2, with a correlation coefficient of 0.54, and a large positive correlation between CD56dim natural killer cells and SMARCA4, which was 0.5. Reverse transcription quantitative polymerase chain reaction revealed that the expression of biomarkers was consistent with the results of the bioinformatics analysis. In summary, SMARCA4, CHD4, and ATAD2 were overexpressed, whereas CHD3 and SMARCA2 were downregulated in THCA samples. This study identified 5 biomarkers (CHD4, SMARCA2, CHD3, ATAD2, and SMARCA4) associated with chromatin remodeling in THCA. Current reference points for the prevention and treatment. - Source: PubMed
Wang ShiguiSun ShuangshuangWang XiangzhongChen Xiang - Glioblastoma (GBM) cancer stem cells (CSCs) contribute to tumor recurrence, treatment resistance, and dismal clinical outcomes. Genetic and pharmacological evidence suggests that the nuclear scaffolding protein WD-repeat containing protein 5 (WDR5) is a therapeutic vulnerability of the CSC population. However, previously reported WDR5 inhibitors display low permeability and are unable to penetrate the blood-brain barrier (BBB), limiting their utility in GBM. Herein, we report the structure-guided development of a series of triazole-based WDR5 WIN-site inhibitors designed to increase passive brain penetration. We identified triazole-based WDR5 inhibitors that are potent, passively permeable, and in some cases more brain penetrant than other scaffolds. We phenotypically assessed our WDR5 inhibitors in a panel of patient-derived CSC models and uncovered unique WDR5-regulated metabolic genes in GBM. We also evaluated their antiproliferative activity against CSCs both in vitro and in vivo. Finally, to identify potential combination opportunities, we screened a 2,100-compound chemical probe library and identified that the ATAD2 inhibitor BAY-850 synergizes with WDR5 inhibitors to enhance CSC killing. Our work diversifies the chemical matter targeting WDR5, clarifies the in vitro consequences of WIN-site inhibition in CSCs, and encourages the future development of next-generation WDR5 inhibitors with the potential to achieve in vivo efficacy in the brain. - Source: PubMed
Publication date: 2026/05/05
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