Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

EMseq of hiPSC, iMeLC, hPGCLC and hEGCLC of CTL08A genotype

ABSTRACT: In this work, hEGCLC have been obtained for the first time from hPGCLC in defined and feeder-free conditions. To study epigenetic changes (in terms of DNA methylation) during the transition from a pluripotent stem cell state to a germ cell identity and back again, we profiled hiPSC, iMeLC, day 6 hPGCLC and hEGCLC by EMseq.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Homo sapiens

SUBMITTER: Gaja Matassa

PROVIDER: E-MTAB-15142 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Large-scale discovery, analysis, and design of protein energy landscapes

Project description:This dataset supports a multiplexed hydrogen-deuterium exchange mass spectrometry (mHDX-MS) study investigating protein energy landscapes across hundreds of protein domains. Proteins continuously fluctuate between their native states and higher-energy conformations that influence stability, interactions, aggregation, and immunogenicity. However, these excited states remain difficult to characterize experimentally, limiting the development of predictive models for conformational energy landscapes. These data provide a foundation for machine learning approaches to predict protein energy landscapes and enhance biophysical modeling of protein folding and conformational dynamics.

2026-05-25 | PXD061702 | Pride

Transcriptomic analysis of the NA-PHER2 clinical trial

Project description:We performed whole transcriptome RNA sequencing on serial tumour biopsies collected at baseline, Day 14, and after completion of all neoadjuvant therapy from the NA-PHER2 trial. Patients received neoadjuvant treatment with the combined regimen of trastuzumab, pertuzumab, palbociclib with or without addition of fulvestrant. Transcriptomic profiles were generated from 143 samples (Baseline n = 53, Day 14 n = 49, Surgery n = 41) corresponding to 55 of the 58 patients enrolled in NA-PHER2 trial (94.8%). RNA sequencing was performed on total RNA samples derived from formalin-fixed, paraffin-embedded (FFPE) tissue sections. RNA-Seq libraries were produced using NEBNext® Ultra™ II Directional RNA Library Prep Kit. The capture was then performed on cDNA libraries with the Twist Human Core Exome Enrichment System according to supplier recommendations (Twist Bioscience). The obtained eluted-enriched DNA samples was then sequenced on an Illumina NovaSeq as paired-end 100bp reads.

2024-10-31 | E-MTAB-14448 | biostudies-arrayexpress

Low pass whole methylome enzymatic sequencing of 11 T-ALL cell lines untreated and after treatment with different concentrations of 5-azacytidine (AZA), 5-aza-2′-deoxycytidine (DEC) and GSK3685032 (GSK5032) for 3 and 7 days

Project description:Here we performed low coverage whole genome enzymatic-mehtyl-conversion sequencing (EM-seq) of 11 commercially available T-ALL cell lines to evaluate their global DNA methylation profile. We then proceeded to treat ALL-SIL, SUP-T1, LOUCY and JURKAT with varying concentrations (0-3000 nM) of three different hypomethylating agents, 5-azacytidine (AZA), 5-aza-2′-deoxycytidine (DEC) and GSK3685032 (GSK5032), for 3 and 7 days to evaluate their DNA demethylating ability.

2024-10-13 | E-MTAB-14197 | biostudies-arrayexpress

Enzymatic methylation sequencing of LOUCY and SUP-T1 cell lines after treatment with Decitabine (3 days) or GSK3685032 (3 and 7 days)

Project description:Decitabine (DEC) has a known DNA demethylating activity but also cause cytotoxicity through DNA damage. The two differing mechanisms of action confound studies investigating the effect of DNA demethylation in cancer treatment. The novel DNA methyltransferase 1 specific inhibitor GSK-3685032 causes loss of DNA methylation without DNA damage and offers the possibility to examine the molecular consequences of global loss of DNA methylation. EM-seq was used to evaluate the DNA demethylating effects of DEC and GSK-3685032 in LOUCY and SUP-T1 cells treated with 10 nM Decitabine for 3 days or 300 nM of GSK-3685032 for 3 and 7 days.

2024-10-13 | E-MTAB-14202 | biostudies-arrayexpress

RNAseq of human fetal testis treated to a mixture of DEHP/BPA

Project description:Fetal human fetal testes (8-11 weeks post-fertilization [WPF]) were cut into small pieces (~1 mm3 ) and 4-6 pieces/testis (depending of the age or size of the gonad) were insert into the muscle of the left back of two twin female mice. One week after surgery, one mouse was exposed by drinking water to a mixture of BPA (1 µM, CAS no. 80-09-1, Merck) and DEHP (1 µM, CAS no. 117-81-7, Merck) and the other was exposed by drinking water to the vehicle (absolute ethanol [ETOH] diluted at 1/1000000 in water). Mice were exposed during 6-11 weeks (corresponding to the 18 WPF equivalent age) and at the end of exposure, testes were collected and each pieces were cleaned from extracellular matrix and murine muscular tissue. One part of the pieces were used for transcriptome analyses

2026-01-01 | E-MTAB-13835 | biostudies-arrayexpress

Low pass whole methylome enzymatic sequencing of four AML cell lines untreated and after treatment with different concentrations of 5-azacytidine (AZA), 5-aza-2′-deoxycytidine (DEC), Cytarabine (ARAC) and GSK3685032 (GSK5032) for 3 and 7 days

Project description:We conducted low-coverage whole-genome enzymatic methylation sequencing (EM-seq) on four commercially available AML cell lines to assess their global DNA methylation profiles following treatment with varying concentrations (0–3000 nM) of three different hypomethylating agents—5-azacytidine (AZA), 5-aza-2′-deoxycytidine (DEC), and GSK3685032 (GSK5032)—for 3 and 7 days (only GSK5032), as well as Cytarabine (ARAC) for 3 days.

2025-04-10 | E-MTAB-14969 | biostudies-arrayexpress

GLORI mapping of m⁶A sites in human primary CD8⁺ T cells under activation and METTL3 inhibition

Project description:Glyoxal and nitrite-mediated deamination of unmethylated adenosines (GLORI) was applied to human primary CD8⁺ T cells subjected to in vitro activation with αCD3/αCD28 beads. To identify N⁶-methyladenosine (m⁶A) sites at single-nucleotide resolution and to test their dependence on METTL3, we generated GLORI libraries from non-activated (NoAct) CD8⁺ T cells, Day1-activated T cells treated for 24 hours with a competitive METTL3 inhibitor (4 μM), and Day5-activated T cells treated with the same inhibitor for 5 days. These datasets provide high-resolution m⁶A maps and allow comparison of m⁶A regulation in the presence or absence of METTL3 activity during distinct states of CD8⁺ T cell activation.

2025-10-15 | E-MTAB-15649 | biostudies-arrayexpress

In Utero Cigarette Smoke Affects Allergic Airway Disease But Does Not Alter the Lung Methylome

Project description:Introduction: Prenatal and postnatal cigarette smoke exposure enhances the risk of developing asthma. Despite this as well as other smoking related risks, 11% of women still smoke during pregnancy. We hypothesized that cigarette smoke exposure during prenatal development generates long lasting differential methylation altering transcriptional activity that correlates with disease. Methods: In a house dust mite (HDM) model of allergic airway disease, we measured airway hyperresponsiveness (AHR) and airway inflammation between mice exposed prenatally to cigarette smoke (CS) or filtered air (FA). DNA methylation and gene expression were then measured in lung tissue. Results: We demonstrate that HDM-treated CS mice develop a more severe allergic airway disease compared to HDM-treated FA mice including increased AHR and airway inflammation. While DNA methylation changes between the two HDM-treated groups failed to reach genome-wide significance, 99 DMRs had an uncorrected p-value < 0.001. 6 of these 99 DMRs were selected for validation, based on the immune function of adjacent genes, and only 2 of the 6 DMRs confirmed the bisulfite sequencing data. Additionally, genes near these 6 DMRs (Lif, Il27ra, Tle4, Ptk7, Nfatc2, and Runx3) are differentially expressed between HDM-treated CS mice and HDM-treated FA mice. Conclusions: Our findings confirm that prenatal exposure to cigarette smoke is sufficient to modify allergic airway disease, however, it is unlikely that specific methylation changes account for the exposure-response relationship. These findings highlight the important role in utero cigarette smoke exposure plays in the development of allergic airway disease. Lung DNA methylation profiles of mice exposed in utero to cigarette smoke (CS) then treated with house dust mite (HDM, n = 8) or saline (n = 6), or exposed in utero to filtered air (FA) then treated with HDM (n = 9) or saline (n = 6)

2015-11-19 | E-GEOD-71718 | biostudies-arrayexpress

RNA-seq of NK cells from blood samples of HV and AML patients

Project description:CD56neg CD16+ Natural Killer (NK) cells have been reported to expand in chronic diseases and acute myeloid leukemia (AML). However, their biological role is still unclear. Using bulk RNA-sequencing, we compared gene expression profile of CD56neg CD16+ NK cells with conventional CD56bright, CD56dim CD16- and CD56dim CD16+ NK cells from blood samples of HV and AML patients. RNA-seq unveiled that CD56neg CD16+ NK cells were mature circulating NK cells with functional capacities. Taken together, our results suggest that CD56neg CD16+ NK cells are a relevant target for future NK-cell-based immunotherapies.

2024-12-20 | E-MTAB-14569 | biostudies-arrayexpress

Whole genome DNA methylation of undifferentiated spermatogonia of postnatal day 14 (P14) wild-type and Spocd1-K464A (does not interact with TPR) homozygous mutant mice

Project description:In the male mouse germline, PIWI-interacting RNAs (piRNAs), bound by the PIWI protein MIWI2 (PIWIL4), guide the DNA methylation of young active transposable elements (TEs) through SPOCD1. We find that SPOCD1 interacts with the nuclear pore protein TPR, and that this interaction is required to prevent SPOCD1 and its known binding partners SPIN1 and C19ORF84 from being incorporated into constitutive heterochromatin. We perform enzymatic methylation sequencing of undifferentiated spermatogonia from wild-type mice and mice carrying the K464A mutation in SPOCD1, which prevents interaction with TPR. The mutant mice display a stochastic failure of young LINE1 methylation.

2025-11-12 | E-MTAB-14862 | 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