Similar Datasets
Project description:Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for Pol κ in HEK293T cells.
2022-12-16 | GSE220603 | GEO
Project description:Efficient eukaryotic DNA replication relies on the coordinated actions of replicative and error-prone polymerases, with the latter providing flexibility at the cost of mutagenesis. DNA polymerase η (Pol η) is most recognised for tolerating UV-induced DNA damage via translesion synthesis (TLS). However, emerging evidence suggests a broader contribution of error-prone polymerases to DNA synthesis. To elucidate the roles of Pol η during unperturbed replication, we applied polymerase usage sequencing (Pu-seq) to map its activity genome-wide. Our findings demonstrate that Pol η preferentially participates in lagging-strand replication, consistent with observations in budding yeast. Furthermore, Pol η usage varied throughout S phase, with a pronounced enrichment in late-replicating domains, dependent on PCNA ubiquitylation. Under moderate doses of UV, Pol η usage retained its replicative strand bias, which contrasted with the prominent strand bias observed in transcribed regions resulting from asymmetric repair processes. These results reveal that Pol η′s flexibility and intrinsic coupling with replication forks extend beyond TLS in human cells. In cancer genomes, characteristic Pol η mutations are enriched in late-replicating regions and correlate with RAD18 expression, implicating PCNA-mediated Pol η activation in mutagenesis. Together, these findings reveal an unexpected bias in Pol η usage during unperturbed replication which may represent a key contribution to the mutational burden in the human genome.
2026-08-27 | GSE308762 | GEO
Project description:POLH ChIP-seq data in HEK293T cells
| PRJNA838014 | ENA
Project description:DNA polymerase eta (pol eta) is best known for its ability to bypass UV-induced thymine-thymine (T-T) dimers and other bulky DNA lesions, but pol eta also has other cellular roles. Here, we present evidence that pol eta competes with DNA polymerases alpha and delta for the synthesis of the lagging strand genome-wide, where it also shows a preference for T-T in the DNA template. Moreover, we found that the C-terminus of pol eta which contains a PCNA-Interacting Protein motif is required for pol eta to function in lagging strand synthesis. Finally, we provide evidence that a pol η dependent signature is also found to be lagging strand specific in patients with skin cancer. Taken together, these findings provide insight into the physiological role of DNA synthesis by pol eta and have implications for our understanding of how our genome is replicated to avoid mutagenesis, genome instability and cancer.
2018-12-14 | GSE110241 | GEO
Project description:Efficient eukaryotic DNA replication relies on the coordinated actions of replicative and error-prone polymerases, with the latter providing flexibility at the cost of mutagenesis. DNA polymerase η (Pol η) is most recognised for tolerating UV-induced DNA damage via translesion synthesis (TLS). However, emerging evidence suggests a broader contribution of error-prone polymerases to DNA synthesis. To elucidate the roles of Pol η during unperturbed replication, we applied polymerase usage sequencing (Pu-seq) to map its activity genome-wide in human cells. Our findings demonstrate that Pol η preferentially participates in lagging-strand replication, consistent with observations in budding yeast. Under moderate doses of UV, Pol η usage retains its replicative strand bias, which contrasts with the prominent strand bias observed in transcribed regions resulting from asymmetric repair processes. In addition to strand bias, Pol η usage varies throughout S phase, with a pronounced enrichment in late-replicating domains, dependent on PCNA ubiquitylation. These results reveal that Pol η’s flexibility and intrinsic coupling with replication forks extend beyond TLS in human cells. In cancer genomes, characteristic Pol η mutations are enriched in late-replicating regions and correlate with RAD18 expression, consistent with a link between PCNA ubiquitylation and Pol η-mediated mutagenesis in these regions. Together, these findings reveal an unexpected bias in Pol η usage during unperturbed replication which may represent a key contribution to the mutational burden in the human genome.
2026-08-27 | GSE308763 | GEO
Project description:JMJD2A was chromatin immunoprecipitated from HEK293T cells overexpressing GFP-JMJD2A. From Van Rechem et al. 2011 JBC Determination of JMJD2A binding sites by MA2C analysis
2013-08-01 | E-GEOD-48765 | biostudies-arrayexpress
Project description:ZNF728 ChIP-seq in HEK293T cells
| PRJNA686653 | ENA
Project description:JMJD2A was chromatin immunoprecipitated from HEK293T cells overexpressing GFP-JMJD2A. From Van Rechem et al. 2011 JBC
2013-08-01 | GSE48765 | GEO
Project description:We performed a set of microarray and chromatin-immunoprecipitation (ChIP)-chip experiments using siRNA against the (pro)renin receptor ((P)RR), stable overexpression of PLZF, the PLZF translocation inhibitor genistein and the specific V-ATPase inhibitor bafilomycin to dissect transcriptional pathways downstream of the (P)RR. In this dataset, we include the ChIP-chip data obtained from PLZF overexpressing KELLY cells, from PLZF overexpressing HEK293T cells and from KELLY as well as HEK293T cells both stably transfected with an insertless control vector.
2013-07-05 | E-GEOD-39960 | biostudies-arrayexpress
Project description:Chromatin immunoprecipitation (ChIP) has been a cornerstone for epigenetic analyses over the last decades, but even coupled to sequencing approaches (ChIP-seq), it is ultimately limited to one protein at a time. In a complementary effort, we here combined ChIP with label-free quantitative (LFQ) mass spectrometry (ChIP-MS) to interrogate local chromatin compositions. We demonstrate the versality of our approach at telomeres, with transcription factors, in tissue and by dCas9-driven locus-specific enrichment.
2024-03-05 | PXD039701 | Pride