Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparative analysis of the transcriptional response to bulky DNA damages

ABSTRACT: Comparative analysis of the transcriptional response to bulky DNA damages

PROVIDER: PRJNA986894 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR25010515.fastq.gz	Fastqsanger.gz
	SRR25010516.fastq.gz	Fastqsanger.gz
	SRR25010517.fastq.gz	Fastqsanger.gz
	SRR25010518.fastq.gz	Fastqsanger.gz
	SRR25010519.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Comparative analysis of the transcriptional response to bulky DNA damages

Project description:A systematic RNA-seq study comparing the transcriptional response to three independent bulky DNA damage inducing agents: UV, the chemotherapy cisplatin and benzo[a]pyrene, a component of cigarette smoke. It was performed in 2 different cell lines - GM12878 immortalized lymphoblast cell line and A549 lung cancer cell line.

2023-12-29 | GSE235681 | GEO

Comparative transcriptional analysis of the satellite glial cell injury response

Project description:Comparative transcriptional analysis of the satellite glial cell injury response

| PRJNA780916 | ENA

Gene architecture is a determinant of the transcriptional response to bulky DNA damages.

Project description:Bulky DNA damages block transcription and compromise genome integrity and function. The cellular response to these damages includes global transcription shutdown. Still, active transcription is necessary for transcription-coupled repair and for induction of damage-response genes. To uncover common features of a general bulky DNA damage response, and to identify response-related transcripts that are expressed despite damage, we performed a systematic RNA-seq study comparing the transcriptional response to three independent damage-inducing agents: UV, the chemotherapy cisplatin, and benzo[a]pyrene, a component of cigarette smoke. Reduction in gene expression after damage was associated with higher damage rates, longer gene length, and low GC content. We identified genes with relatively higher expression after all three damage treatments, including NR4A2, a potential novel damage-response transcription factor. Up-regulated genes exhibit higher exon content that is associated with preferential repair, which could enable rapid damage removal and transcription restoration. The attenuated response to BPDE highlights that not all bulky damages elicit the same response. These findings frame gene architecture as a major determinant of the transcriptional response that is hardwired into the human genome.

| S-EPMC10761554 | biostudies-literature

A tendon comparative transcriptional atlas

Project description:A tendon comparative transcriptional atlas

| PRJNA576271 | ENA

A study of temporal transcriptional changes induced by a low concentration BPDE in cultured human cells

Project description:The environmental carcinogen, (±)-anti-benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE), causes bulky-adduct DNA damages, triggers certain signaling pathways, and elicits gene expression changes. Here, we focused on the temporal gene expression changes induced by a low concentration (0.05 µM) BPDE in human amnion epithelial FL cells. Differential gene expression profiles at 1, 10 and 22 h post BPDE treatment were obtained using Affymetrix HG-U133 Plus 2.0 oligonucleotide microarrays. A cohort of gene expression changes related to cell cycle progression, cell growth or apoptosis, stress response, and post-transcriptional regulation was validated with quantitative real-time RT-PCR. The alteration of several cell cycle-related genes was correlated and possibly contributed to the cell cycle arrest phenotype. Paradoxical transcriptional regulations regarding cell growth or apoptosis emerged in response to BPDE treatment, which indicated that cell fate was determined by integrated signals. The temporal transcriptional changes would be of help to clarify the molecular mechanism of cellular response to BPDE. Keywords: time course

2009-01-01 | GSE10979 | GEO

Comparative physiology and transcriptional networks underlying the heat shock response in Populus trichocarpa, Arabidopsis thaliana and Glycine max

Project description:This SuperSeries is composed of the following subset Series: GSE26195: Comparative physiology and transcriptional networks underlying the heat shock response in Populus trichocarpa, Arabidopsis thaliana and Glycine max [Populus] GSE26197: Comparative physiology and transcriptional networks underlying the heat shock response in Populus trichocarpa, Arabidopsis thaliana and Glycine max [Arabidopsis] GSE26198: Comparative physiology and transcriptional networks underlying the heat shock response in Populus trichocarpa, Arabidopsis thaliana and Glycine max [Soy] Refer to individual Series

2011-04-01 | E-GEOD-26199 | biostudies-arrayexpress

Structure of TFIIH/Rad4-Rad23-Rad33 in damaged DNA opening in Nucleotide Excision Repair

Project description:TFIIH is a 10-protein complex that is conserved throughout eukaryotes. TFIIH has two primary cellular functions: transcription initiation and nucleotide excision repair (NER). NER in eukaryotes begins by recognition of a bulky lesion by the obligate dimer Rad4-Rad23. This is followed closely by the recruitment of TFIIH which is a structural scaffold, opens a bubble around damaged DNA and scans the damaged strand for bulky lesions. This facilitates the recruitment of two exonucleases which excise the damages strand before an undamaged complement is synthesize. In yeast (Saccharomyces cerevisiae), TFIIH is composed of the two helicases Ssl2 and Rad3, the scaffolding subunits Tfb1, Tfb2, Tfb4 and Ssl1 and the kinase subunits Kin28, Ccl1 and Tfb3, though these later 3 are dispensable for NER.

2021-07-07 | PXD021212 | Pride

Perturbation on DNA replication by cohesin dysfunction leads to gross genomic damages [END-seq]

Project description:Cohesin loss-of-function mutations are frequently observed in tumors, but the mechanism is unclear. Here, we found that depletion of RAD21, a core subunit of cohesin, leads to massive DNA breaks, up to five-fold, and 147 translocation hotspot genes that are co-mutated with cohesin in multiple cancers. DNA damages are independent of RAD21-loss-induced transcription alteration and loop anchor elimination. However, translocation junctions coincide with the asymmetrically distributed Okazaki fragments of DNA replication, suggesting that RAD21 depletion causes replication stresses evidenced by the slower replication speed and increased stalled forks. Mechanistically, approximately 30% of the human genome exhibits an earlier replication timing after RAD21 depletion, caused by the early initiation of >900 extra dormant origins. Correspondingly, most translocation hotspot genes lie in timing-altered regions. Therefore, we conclude that cohesin dysfunction causes severe replication stresses induced by extra DNA replication, resulting in gross DNA damages that may induce tumorigenesis.

2023-05-18 | GSE211343 | GEO

Comparative host transcriptome in response to pathogenic fungi identifies common and species-specific transcriptional antifungal host response pathways

Project description:Comparative host transcriptome in response to pathogenic fungi identifies common and species-specific transcriptional antifungal host response pathways

| PRJNA682949 | ENA

Perturbation on DNA replication by cohesin dysfunction leads to gross genomic damages [PEM-seq-mutant]

Project description:Cohesin mutations are frequently observed in tumors, but the mechanism is unclear. Here, we found that depletion of RAD21, a core subunit of cohesin, leads to gross DNA breaks and consequently elevates genome-wide chromosomal translocation levels up to five-fold in mammalian cells. These damages are independent of transcription alteration and loop anchor robustness. However, identified translocations occur asymmetrically on the chromatin Watson and Crick strands, coincident with Okazaki fragments of DNA replication. Moreover, early DNA replication initiates at about one thousand extra dormant origins after RAD21 depletion, which is independent of CTCF, resulting in earlier replicating timing at approximately 30% or 13% of the human or mouse genomic regions, respectively. And the translocation hotspot genes arising in RAD21-depleted cells are accompanied by dysregulated replication timing. Therefore, we conclude that cohesin dysfunction leads to perturbed DNA replication timing, which further results in gross DNA damages that may be involved in tumorigenesis.

2023-05-18 | GSE211347 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data