Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RecB DNA degradation

ABSTRACT: DNA degradation in E. coli recB cells

PROVIDER: PRJEB27616 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR2682530.fastq.gz	Fastqsanger.gz
	ERR2683090.fastq.gz	Fastqsanger.gz
	ERR2683100.fastq.gz	Fastqsanger.gz
	ERR2683110.fastq.gz	Fastqsanger.gz
	ERR2682531.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 38

Similar Datasets

Tissue-specific cell-free DNA degradation quantifies circulating tumor DNA burden

Project description:Profiling of circulating tumor DNA (ctDNA) may offer a non-invasive approach to monitor disease progression. Here, we developed a quantitative method, exploiting local tissue-specific cell-free DNA (cfDNA) degradation patterns, that accurately estimates ctDNA burden independent of genomic aberrations. Nucleosome-dependent cfDNA degradation at promoters and first exon-intron junctions was strongly associated with differential transcriptional activity in tumors and blood. A quantitative model, based on just 6 regulatory regions, could accurately predict ctDNA levels in colorectal cancer patients. Strikingly, a model restricted to blood-specific regulatory regions could predict ctDNA levels across both colorectal and breast cancer patients.

| EGAS00001004657 | EGA

SUMO-chain-regulated proteasomal degradation timing exemplified in DNA replication initiation

Project description:Similar to ubiquitin, SUMO forms chains, but the identity of SUMO-chain-modified factors and the purpose of this modification remain largely unknown. Here, we identify budding yeast SUMO protease Ulp2, able to disassemble SUMO chains, as a DDK interactor enriched at replication origins that promotes DNA replication initiation. Replication-engaged DDK is SUMOylated on chromatin, becoming a degradation-prone substrate when Ulp2 no longer protects it against SUMO-chain assembly. Specifically, SUMO chains channel DDK for SUMO-targeted ubiquitin ligase Slx5/Slx8-mediated and Cdc48 segregase-assisted proteasomal degradation. Importantly, the SUMOylation-defective ddk-KR mutant rescues inefficient replication onset and MCM activation in cells lacking Ulp2, suggesting that SUMO chains time DDK degradation. Using two unbiased proteomic approaches, we further identify subunits of the MCM helicase and other factors as SUMO-chain-modified degradation-prone substrates of Ulp2 and Slx5/Slx8. We thus propose SUMO-chain-/Ulp2-protease-regulated proteasomal degradation as a mechanism that times the availability of functionally-engaged SUMO-modified protein pools during replication and beyond.

2019-09-10 | GSE113835 | GEO

ER-associated degradation ligase HRD1 links ER stress to DNA damage repair by modulating the activity of DNA-PKcs

Project description:ER-associated degradation ligase HRD1 links ER stress to DNA damage repair by modulating the activity of DNA-PKcs

2024-08-20 | PXD055020 |

DNA damage-induced transcription stress triggers the genome-wide degradation of promoter-paused Pol II

Project description:The precise regulation of RNA Polymerase II (Pol II) transcription after genotoxic stress is crucial for proper execution of the DNA damage-induced stress response. While stalling of Pol II on transcription-blocking lesions (TBLs) blocks transcript elongation and initiates DNA repair in cis, TBLs additionally elicit a response in trans that regulates transcription genome-wide. Here we uncover that after an initial elongation block in cis, TBLs trigger the genome-wide VCP-mediated proteasomal degradation of promoter-paused Pol II in trans. This degradation is mechanistically distinct from processing of TBL-stalled Pol II, is signaled via GSK3, and contributes to the TBL-induced transcription block, even in transcription-coupled repair-deficient cells. Thus, our data reveal the targeted degradation of promoter-bound Pol II as an important new component of the transcription stress response that enables the genome-wide adaptation of transcription to genotoxic stress.

2022-06-27 | GSE169480 | GEO

Nucleoptosis: Nucleolar ISG20L2 mediates cell death through genomic DNA degradation

Project description:Nucleoptosis: Nucleolar ISG20L2 mediates cell death through genomic DNA degradation

| PRJNA1078328 | ENA

EBF1 degradation in B Cells

Project description:EBF1 degradation in B Cells

| PRJNA828547 | ENA

SUMO-chain-regulated proteasomal degradation timing exemplified in DNA replication initiation

Project description:SUMO-chain-regulated proteasomal degradation timing exemplified in DNA replication initiation

| PRJNA454214 | ENA

degradation glassland

Project description:degradation glassland Metagenome

| PRJNA1105764 | ENA

Protein interaction network analysis reveals growth conditions-specific crosstalk between chromosomal DNA replication and other cellular processes in E. coli

Project description:E. coli and many other bacterial species can alternate their cell cycle according to nutrient availability. As a result, they grow and divide very fast under optimal conditions or slow down the cell cycle when conditions deteriorate. This adaptability is underlined by mechanisms coordinating cell growth with duplication of genetic material and cell division. Several mechanisms regulating DNA replication process in E. coli have been described so far with biochemical details, nevertheless we still don’t fully understand the source of remarkable precision that bacterial cells coordinate their growth and chromosome replication with. To shed light on regulation of E. coli DNA replication at systemic level, we used affinity purification coupled with mass spectrometry (AP-MS) to characterize protein-protein interactions (PPIs) formed by key E. coli replication proteins, under disparate bacterial growth conditions and phases. We present the resulting dynamic replication protein interaction network (PIN) and highlight links between DNA replication and several cellular processes, like outer membrane synthesis, RNA degradation and modification or starvation response.

2022-03-03 | PXD030113 | Pride

Lurbinectedin specifically triggers the degradation of phosphorylated RNA Polymerase II and the formation of DNA breaks in cancer cells

Project description:We have defined the mechanism of action of lurbinectedin, a marine-derived drug exhibiting a potent anti-tumorigenic activity across several cancer cell lines and tumor xenografts. This drug currently undergoing clinical evaluation in ovarian, breast and small-cell lung cancer patients inhibits the transcription process through (1) its binding to CG rich sequences, mainly located around the promoter of protein coding genes; (2) the irreversible stalling of elongating RNA polymerase II (Pol II) on the DNA template and its specific degradation by the ubiquitin/proteasome machinery and (3) the generation of DNA breaks. The finding that inhibition of Pol II phosphorylation prevents its degradation and the formation of DNA breaks after drug treatment underscores the connection between transcription elongation and DNA repair. Our results not only help to better understand the high specificity of this drug in cancer therapy but also improve our understanding of an important transcription regulation mechanism.

2017-01-13 | GSE77071 | 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