Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

UVDE-seq mapping of UV-induced 6-4PPs and atypical TA photoproducts

ABSTRACT: UVDE-seq mapping of UV-induced 6-4PPs and atypical TA photoproducts

PROVIDER: PRJNA787240 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17169413.fastq.gz	Fastqsanger.gz
	SRR17169414.fastq.gz	Fastqsanger.gz
	SRR17169415.fastq.gz	Fastqsanger.gz
	SRR17169416.fastq.gz	Fastqsanger.gz
	SRR17169417.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 10

Similar Datasets

UVDE-seq mapping of UV-induced 6-4PPs and atypical TA photoproducts

Project description:We used a novel high-throughput sequencing method known as UVDE-seq to map the formation of UV-induced 6-4 photoproducts (6-4PP) and atypical thymidine-adenine (TA) photoproducts at single nucleotide resolution across the yeast genome in wild-type and rad16 mutant cells, which are deficient in GG-NER. We also analyzed 6-4PP and TA photoproducts in UV-irradiated yeast genomic DNA (i.e., naked DNA).

2023-02-28 | GSE190471 | GEO

UVDE-HS-seq mapping of UV-induced 6-4PPs and atypical TA photoproducts

Project description:We used a novel high-throughput sequencing method known as UVDE-HS-seq to map the formation of UV-induced 6-4 photoproducts (6-4PP) and atypical thymidine-adenine (TA) photoproducts at single nucleotide resolution across the yeast genome in wild-type cells. We also analyzed 6-4PP and TA photoproducts in UV-irradiated yeast genomic DNA (i.e., naked DNA).

2023-02-28 | GSE214217 | GEO

UVDE-HS-seq mapping of UV-induced 6-4PPs and atypical TA photoproducts

Project description:UVDE-HS-seq mapping of UV-induced 6-4PPs and atypical TA photoproducts

| PRJNA884390 | ENA

UVDE-seq mapping of UV-induced non-CPD lesions

Project description:UVDE-seq mapping of UV-induced non-CPD lesions

| PRJNA604574 | ENA

CPD-seq mapping of UV damage formation and repair in yeast

Project description:UV-induced DNA lesions are an important contributor to mutagenesis and cancer, but it is not fully understood how the chromosomal landscape influences UV lesion formation and repair. We have used a novel high-throughput sequencing method to precisely map UV-induced cyclobutane pyrimidine dimers (CPDs) at nucleotide resolution throughout the yeast genome. Analysis of CPD formation reveals that nucleosomal DNA having an inward rotational setting is protected from CPD lesions. In strongly positioned nucleosomes, this nucleosome 'photofootprint' overrides intrinsic dipyrimidine sequence preferences for CPD formation. CPD formation is also inhibited by DNA-bound transcription factors, in effect protecting important DNA elements from UV damage. Analysis of CPD repair revealed a clear signature of efficient transcription-coupled nucleotide excision repair. Repair was less efficient at translational positions near a nucleosome dyad and at heterochromatic regions in the yeast genome. These findings define the roles of nucleosomes and transcription factors in UV damage formation and repair. UV mapping data was analyzed for yeast cells irradiated with 125J/m2 and allowed to repair for 0hr (2 samples), 20 minutes, 1 hour, or 2 hours. Data is also included for naked DNA irradiated with UV 60 or 90 J/m2

2016-08-19 | E-GEOD-79977 | biostudies-arrayexpress

UV-induced DNA lesion mapping in retinoblastoma 1 (RB1) knock out cells

Project description:UV-induced DNA lesion mapping in retinoblastoma 1 (RB1) knock out cells

| PRJNA723855 | ENA

Epigenetic and genetic dissections of UV-induced global gene dysregulation in skin cells through multi-omics analyses

Project description:In this study, we performed integrative multi-omics studies to understand the complex mechanisms underlying UV photobiological effects. While H3K27ac and genetic mutations can both contribute to UV-induced transcriptomic changes, additional omics-based studies on other histone modifications, DNA methylation, and whole genome mapping of genetic mutations will provide a thorough understanding of UV-gene interactions in skin disease pathogenesis. The new UV target genes that we identified have important clinical implications in skin carcinogenesis..

2017-04-11 | GSE97577 | GEO

CPD-seq mapping of UV damage formation and repair in yeast

2016-08-19 | GSE79977 | GEO

Using pooled earthworm RNA to test 244K probes on TA-1, TA-2, TA-3, TA-4 test arrays

Project description:This SuperSeries is composed of the following subset Series: GSE16536: Using pooled earthworm RNA to test 244K probes on TA-1 test array design 2520022 sense 1 GSE16548: Using pooled earthworm RNA to test 244K probes on TA-2 test array design 2520023 antisense 1 GSE16549: Using pooled earthworm RNA to test 244K probes on TA-3 test array design 2520024 sense 2 GSE16550: Using pooled earthworm RNA to test 244K probes on TA-4 test array design 2520025 antisense 2 Refer to individual Series

2010-05-18 | E-GEOD-16551 | biostudies-arrayexpress

Excision repair hotspots of UV-induced DNA damage in the human genome

Project description:We recently developed high-throughput sequencing approaches, eXcision Repair sequencing (XR-seq) and Damage-seq, to generate genome-wide mapping of DNA damage formation and excision repair, respectively, with single-nucleotide resolution. Here, we adopted time-course XR-seq data to profile UV-induced excision repair dynamics, paired with Damage-seq data to quantify the overall induced DNA damage. We identified genome-wide repair hotspots that are subject to exemplified amount of repair very soon after UV irradiation. We show that such repair hotspots do not result from hypersensitivity to DNA damage and are thus not damage hotspots. We find that the earliest repair occur preferentially in promoters and enhancers from open-chromatin regions. The repair hotspots are also significantly enriched for frequently interacting regions and super-enhancers, both of which are hotspots for local chromatin interactions. We further extend the interrogation of chromatin organization to DNA replication timing and conclude that early-repair hotspots are enriched for early-replication domains. Collectively, we report genome-wide early-repair hotspots of UV-induced damage, in association with chromatin states and epigenetic compartmentalization of the human genome.

2020-04-09 | GSE148303 | 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