Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

42 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Unraveling cell type–specific and reprogrammable human replication origin signatures associated with G-quadruplex consensus motifs

ABSTRACT: Short nascent strands purification coupled to next-generation sequencing allowed us to identify replication origins on human genome in an extensive way, by mapping replication origins in 4 different cell types, IMR-90 fibroblasts, hESC H9 cells, iPSC Th Cl-4 cells and HeLa cells. We demonstrated the existence of a cell type-specific reprogrammable signature of the cell identity revealed by specific efficiencies of conserved origin positions and not by the selection of cell-type specific subsets of origins. 4 different cell types were analyzed. For each cell types, 2 different biological replicates of short nascent strands at replication origins were purified. Each SNS sample was sequencing at least one time.

ORGANISM(S): Homo sapiens

SUBMITTER: Emilie Besnard

PROVIDER: E-GEOD-37757 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Unraveling cell type-specific and reprogrammable human replication origin signatures associated with G-quadruplex consensus motifs.

Besnard Emilie E Babled Amélie A Lapasset Laure L Milhavet Ollivier O Parrinello Hugues H Dantec Christelle C Marin Jean-Michel JM Lemaitre Jean-Marc JM

Nature structural & molecular biology 20120701 8

DNA replication is highly regulated, ensuring faithful inheritance of genetic information through each cell cycle. In metazoans, this process is initiated at many thousands of DNA replication origins whose cell type-specific distribution and usage are poorly understood. We exhaustively mapped the genome-wide location of replication origins in human cells using deep sequencing of short nascent strands and identified ten times more origin positions than we expected; most of these positions were co ...[more]

PMID: 22751019

Similar Datasets

The target proteins phosphoglycerate kinase 2 (PGK2), glycerol-3-phosphate dehydrogenase (GPD2)GPD2 and glucose-6-phosphate isomerase (GPI) were screened by combining transcriptome, proteomics and reverse docking, then, we. We detected the binding constant of the active compound using microscale thermophoresis (MST). It was found that esculetin bound well with three potential target proteins.

Project description:The results of this study demonstrated that esculetin can affect the glucose metabolism by binding to glycolytic proteins, thus playing an anti-tumor role, and the pathway comprising these proteins which have direct interactions are a potential novel targets for tumor treatment by esculetin.

2020-01-20 | PXD017062 | Pride

Esculetin inhibits cancer cell glycolysis by binding tumor PGK2, GPD2, and GPI

Project description:Glycolysis can improve the tolerance of tissue cells to hypoxia, and its intermediates provide raw materials for the synthesis and metabolism of the tumor cells. If it can inhibit the activity of glycolysis-related enzymes and control the energy metabolism of tumor, it can be targeted for the treatment of malignant tumor. The target proteins phosphoglycerate kinase 2 (PGK2), glycerol-3-phosphate dehydrogenase (GPD2) and glucose-6-phosphate isomerase (GPI) were screened by combining transcriptome, proteomics and reverse docking. We detected the binding constant of the active compound using microscale thermophoresis (MST). It was found that esculetin bound well with three potential target proteins. Esculetin significantly inhibited the rate of glycolysis, manifested by differences of cellular lactate production and glucose consumption in HepG2 cells with or without esculetin. It was found that GPD2 bound strongly to GPI, revealing the direct interaction between the two glycolysis-related proteins. Animal tests have further demonstrated that esculetin may have anticancer effects by affecting the activity of PGK2, GPD2 and GPI. The results of this study demonstrated that esculetin can affect the glucose metabolism by binding to glycolytic proteins, thus playing an anti-tumor role, and these proteins which have direct interactions are potential novel targets for tumor treatment by esculetin.

2020-03-03 | PXD017819 | Pride

Cornu aspersum Comparative Mucomics LC-MSMS

Project description:Here we apply an omics-style workflow to characterize the adhesive, lubricating, and protective mucus from Cornu aspersum snails. Through a combined transcriptomic, proteomic, and glycomic approach alongside the characterization of physical and chemical properties, we explain the origins of the functional differences between each of these biological materials.

2023-10-24 | PXD035534 | Pride

Cell type-specific chromatin states differentially prime squamous cell carcinoma tumor-initiating cells for epithelial to mesenchymal transition [ATAC-seq]

Project description:Epithelial to mesenchymal transition (EMT) in cancer cells has been associated with metastasis, stemness and resistance to therapy. The reason why some tumors undergo EMT and other not might reflect intrinsic properties of their cell of origin, although this possibility is largely unexplored. By targeting the same oncogenic mutations to discrete skin compartments, we show cell type-specific chromatin and transcriptional states differentially prime tumors to EMT. Squamous cell carcinomas (SCCs) derived from intrafollicular epidermis (IFE) are generally well-differentiated, while hair follicle (HF) stem cell-derived SCCs frequently exhibit EMT, efficiently form secondary tumors, and possess increased metastatic potential. Transcriptional and epigenomic profiling revealed IFE and HF tumor-initiating cells possess distinct chromatin landscapes and gene regulatory networks associated with tumorigenesis and EMT that correlate with accessibility of key epithelial and EMT transcription factor binding sites. These findings highlight the importance of chromatin states and transcriptional priming in dictating tumor phenotypes and EMT. Accessible chromatin regions were profiled using ATAC-seq, enriched peak regions were used to infer transcription factor binding sites.

2016-09-01 | E-GEOD-70474 | biostudies-arrayexpress

Transcriptomic analyses of primary uveal melanomas

Project description:SF3B1 is coding an essential splicing factor. This gene was found recurrently mutated in uveal melanoma. To understand the consequences of these hotspot SF3B1 mutations, we performed high coverage RNA-seq on 74 primary uveal melanomas, which were treated by primary enucleation. We analyzed data for aberrant splicing in relation with SF3B1 status.

2016-07-03 | E-MTAB-4097 | biostudies-arrayexpress

Ligand-Dependent Enhancer Activation Regulated by Topoisomerase-I Activity

Project description:The discovery that enhancers are regulated transcription units, encoding eRNAs, has raised new questions about the mechanisms of their activation. Here, we report an unexpected molecular mechanism that underlies ligand-dependent enhancer activation, based on DNA nicking to relieve torsional stress from eRNA synthesis. Using dihydrotestosterone (DHT)-induced binding of androgen receptor (AR) to prostate cancer cell enhancers as a model, we show rapid recruitment, within minutes, of DNA topoisomerase I (TOP1) to a large cohort of AR-regulated enhancers. Furthermore, we show that the DNA nicking activity of TOP1 is a prerequisite for robust eRNA synthesis and enhancer activation and is kinetically accompanied by the recruitment of ATR and the MRN complex, followed by additional components of DNA damage repair machinery to the AR-regulated enhancers. Together, our studies reveal a linkage between eRNA synthesis and ligand-dependent TOP1-mediated nicking - a strategy exerting quantitative effects on eRNA expression in regulating AR-bound enhancer-dependent transcriptional programs. Genome-wide binding analysis of AR, TOP1, MRE11 in prostate cancer cell line LNCaP with or without 5alpha-dihydrotestosterone (DHT) treatment. Nascent RNA analysis by global nuclear run-on (GRO-seq) in LNCaP cells transfected with siRNA with or without DHT treatment. Distribution of transcriptionally engaged RNA Pol II in LNCaP cells with or without DHT treatment by precision nuclear run-on and sequencing (PRO-seq).

2015-01-22 | E-GEOD-63202 | biostudies-arrayexpress

TSSdelta rppH vsdelta rppHdelta hns double mutant

Project description:Transcription start site mapping in Escherichia coli delta rppH vs delta rppH delta hns at 30C

2013-12-15 | E-MTAB-2150 | biostudies-arrayexpress

Histone Demethylase Lsd1 is Required to Repress Hematopoietic Stem and Progenitor Cell Signatures During Blood Cell Maturation

Project description:Here we describe that lysine-specific demethylase 1 (Lsd1/KDM1a), which demethylates histone H3 on LysM-bM-^@M-^I4 or LysM-bM-^@M-^I9 (H3K4/K9), is an indispensible epigenetic governor of hematopoietic differentiation. Integrative genomic analysis in primary hematopoietic cells, combining global occupancy of Lsd1, genome-wide analysis of its histone substrates H3K4 mono- and di-methylation and gene expression profiling, reveals that Lsd1 represses hematopoietic stem and progenitor cell (HSPC) gene expression programs during hematopoietic differentiation. We found that Lsd1 function was not restricted to transcription start sites, but is also critical at enhancers. Loss of Lsd1 at these sites was associated with increased H3K4me1 and H3K4me2 methylation levels on HSPC genes and their derepression. Failure to fully silence HSPC genes compromised differentiation of hematopoietic stem cells and mature blood cell lineages. Our data indicate that Lsd1-mediated concurrent repression of enhancer and promoter activity of stem and progenitor cell genes is a pivotal epigenetic mechanism required for proper hematopoietic maturation. To identify direct target genes of Lsd1 in myeloid cells we mapped global occupancy of Lsd1 in 32D granuolocytic progenitor cells and compared H3K4me1/me2/me3 and H3K27ac histone modifications in Lsd1fl/fl (wild type) vs. Lsd1fl/f Mx1Cre (knockout) Gr1dim Mac1 granuolocytic progenitor cells.

2013-06-25 | E-GEOD-40440 | biostudies-arrayexpress

Assembly of methylated LSD1 and CHD1 drives AR-dependent transcription and translocation [ChIP-Seq]

Project description:The aim of the study is to identify AR target gens in LNCaP cells 5 samples corresponding to LSD1 K114me2 or CHD1 genome-binding in DHT-treated and control LNCaP cells. 6 samples corresponding to LSD1 K114me2 or CHD1 genome-binding in LNCaP cells knocked-down for LSD1 or CHD1 and treated with DHT.

2015-12-07 | E-GEOD-64528 | biostudies-arrayexpress

Genome-wide distribution of Pbx1/2/3 in mouse cortex at embryonic day 12.5 [ChIP-seq]

Project description:We demonstrate using conditional mutagenesis that Pbx1, with and without Pbx2+/ sensitization, regulates regional identity and laminar patterning of the developing mouse neocortex in cortical progenitors (Emx1-Cre) and in newly generated neurons (Nex1-Cre). Pbx1/2 mutants have three salient molecular phenotypes of cortical regional and laminar organization: hypoplasia of the frontal cortex, ventral expansion of the dorsomedial cortex, and ventral expansion of Reelin expression in the cortical plate of the frontal cortex, concomitant with an inversion of cortical layering in the rostral cortex. Molecular analyses, including PBX ChIP-seq, provide evidence that PBX promotes frontal cortex identity by repressing genes that promote dorsocaudal fate. Chromatin immunoprecipitation was performed using antibody against Pbx1/2/3/ (sc-888, Santa Cruz). Wild type E12.5 mouse whole cortex was used for the analysis.

2016-02-27 | E-GEOD-78720 | biostudies-arrayexpress

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