Evaluation of ATAD2 as a potential target in hepatocellular carcinoma
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ABSTRACT:
PROVIDER: PRJNA737831 | ENA |
REPOSITORIES: ENA
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Project description:We evaluated differentially expressed genes (DEGs) between hepatocellular carcinoma cell lines (Hep3B, SNU449, and PLC/PRF/5) treated with ATAD2 siRNA or control using Affymetrix array data whether ATAD2 could be potential target in hepatocellular carcinoma.
2022-06-15 | GSE178243 | GEO
Project description:Custom gene expression panel for evaluation of potential molecular markers in hepatocellular carcinoma
| PRJNA790925 | ENA
Project description:ATAD2, expressed predominantly in embryonic stem cells as well as in spermatogenic cells emerges as a pivotal regulator of chromatin dynamics by mediating chromatin-bound histone chaperone turnover. Here, investigating the role of ATAD2 in spermatogenesis, we show that through its preponderant expression in haploid male germ cells, ATAD2 modulates the HIRA-dependent H3.3 genome localization and H3.3-dependent gene transcriptional regulation. Furthermore, by influencing histone eviction and the assembly of protamines, it ensures proper chromatin condensation and genome packaging in mature spermatozoa. The disruption of Atad2 results in aberrant mature spermatozoa genome organization, impacting male fertility. Collectively, these findings confirm the occurrence of an overlooked chromatin dynamic regulatory level controlling histone deposition-removal balance, depending on an ATAD2-controlled histone chaperone-chromatin interaction.
2026-01-05 | GSE277943 | GEO
Project description:ATAD2, expressed predominantly in embryonic stem cells as well as in spermatogenic cells emerges as a pivotal regulator of chromatin dynamics by mediating chromatin-bound histone chaperone turnover. Here, investigating the role of ATAD2 in spermatogenesis, we show that through its preponderant expression in haploid male germ cells, ATAD2 modulates the HIRA-dependent H3.3 genome localization and H3.3-dependent gene transcriptional regulation. Furthermore, by influencing histone eviction and the assembly of protamines, it ensures proper chromatin condensation and genome packaging in mature spermatozoa. The disruption of Atad2 results in aberrant mature spermatozoa genome organization, impacting male fertility. Collectively, these findings confirm the occurrence of an overlooked chromatin dynamic regulatory level controlling histone deposition-removal balance, depending on an ATAD2-controlled histone chaperone-chromatin interaction.
2026-01-05 | GSE283879 | GEO
Project description:ATPase Family AAA domain containing 2 (ATAD2) expression is elevated in many cancer types including ovarian cancer. Therefore, we analyzed the role of ATAD2 in ovarian cancer. Pharmacological inhibition of ATAD2 expression in ovarian cancer cell lines resulted in decreased proliferation, and increased cell death.
2024-12-01 | GSE192673 | GEO
Project description:Although the conserved AAA ATPase â bromodomain factor, ATAD2, has been described as a transcriptional co-activator upregulated in many cancers, its function remains poorly understood. Here, using a combination of ChIP-seq, ChIP-proteomics and RNA-seq experiments in embryonic stem cells, we found that Atad2 is an abundant nucleosome-bound protein present on active genes, associated with chromatin remodelling, DNA replication and DNA repair factors. A structural analysis of its bromodomain and subsequent investigations demonstrate that histone acetylation guides ATAD2 to chromatin, resulting in an overall increase of chromatin accessibility and histone dynamics, which is required for the proper activity of the highly expressed gene fraction of the genome. While in exponentially growing cells Atad2 appears dispensable for cell growth, in differentiating ES cells, Atad2 becomes critical in sustaining specific gene expression programs, controlling proliferation and differentiation. Altogether, this work defines Atad2âs function as a facilitator of general chromatin-templated activities such as transcription. Transcriptomic analyses comparing ES cells stably expressing anti-Atad2 shRNA versus cells expressing control shRNA, in day 3 LIF (-) differentiating ES cells (3 replicates for each condition) were performed using the Illumina MouseWG-6 v2.0 expression beadchip technology
2016-03-24 | E-GEOD-69899 | biostudies-arrayexpress
Project description:Although the conserved AAA ATPase – bromodomain factor, ATAD2, has been described as a transcriptional co-activator upregulated in many cancers, its function remains poorly understood. Here, using a combination of ChIP-seq, ChIP-proteomics and RNA-seq experiments in embryonic stem cells, we found that Atad2 is an abundant nucleosome-bound protein present on active genes, associated with chromatin remodelling, DNA replication and DNA repair factors. A structural analysis of its bromodomain and subsequent investigations demonstrate that histone acetylation guides ATAD2 to chromatin, resulting in an overall increase of chromatin accessibility and histone dynamics, which is required for the proper activity of the highly expressed gene fraction of the genome. While in exponentially growing cells Atad2 appears dispensable for cell growth, in differentiating ES cells, Atad2 becomes critical in sustaining specific gene expression programs, controlling proliferation and differentiation. Altogether, this work defines Atad2’s function as a facilitator of general chromatin-templated activities such as transcription.
2016-03-24 | GSE70314 | GEO
Project description:Although the conserved AAA ATPase – bromodomain factor, ATAD2, has been described as a transcriptional co-activator upregulated in many cancers, its function remains poorly understood. Here, using a combination of ChIP-seq, ChIP-proteomics and RNA-seq experiments in embryonic stem cells, we found that Atad2 is an abundant nucleosome-bound protein present on active genes, associated with chromatin remodelling, DNA replication and DNA repair factors. A structural analysis of its bromodomain and subsequent investigations demonstrate that histone acetylation guides ATAD2 to chromatin, resulting in an overall increase of chromatin accessibility and histone dynamics, which is required for the proper activity of the highly expressed gene fraction of the genome. While in exponentially growing cells Atad2 appears dispensable for cell growth, in differentiating ES cells, Atad2 becomes critical in sustaining specific gene expression programs, controlling proliferation and differentiation. Altogether, this work defines Atad2’s function as a facilitator of general chromatin-templated activities such as transcription.
2016-03-24 | GSE70312 | GEO
Project description:Although the conserved AAA ATPase – bromodomain factor, ATAD2, has been described as a transcriptional co-activator upregulated in many cancers, its function remains poorly understood. Here, using a combination of ChIP-seq, ChIP-proteomics and RNA-seq experiments in embryonic stem cells, we found that Atad2 is an abundant nucleosome-bound protein present on active genes, associated with chromatin remodelling, DNA replication and DNA repair factors. A structural analysis of its bromodomain and subsequent investigations demonstrate that histone acetylation guides ATAD2 to chromatin, resulting in an overall increase of chromatin accessibility and histone dynamics, which is required for the proper activity of the highly expressed gene fraction of the genome. While in exponentially growing cells Atad2 appears dispensable for cell growth, in differentiating ES cells, Atad2 becomes critical in sustaining specific gene expression programs, controlling proliferation and differentiation. Altogether, this work defines Atad2’s function as a facilitator of general chromatin-templated activities such as transcription.
2016-03-24 | GSE70313 | GEO
Project description:Epigenetic deregulation is a critical event in human malignancies. A number of DNA methylation markers are currently under evaluation as diagnostic and prognostic biomarkers for many cancers. However, its potential role in hepatocellular carcinoma (HCC) is under-explored. Aims: To develop a DNA methylation-based prognostic signature in surgically resected HCC
2015-02-13 | GSE56588 | GEO