Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DNA methylation profiles in 3 mutant iN cells and wt iN cells (control, empty vector) at 2 days

ABSTRACT: To investigate temporal DNA methylation changes occurring during NPC maintenance in later times via genomic DNA methylation measurement by Infinium MethylationEPIC BeadChip assay, we introduced IDH1-R132H, KRAS-G12C, and TP53-R273C, mutations separately into NPCs at day 0, with dox induction for 10 days to overexpress the oncogenes. After 10 days of induction, we differentiated the NPCs into iN cells for two more days, in order to investigate the epigenetic change during differentiation at increase temporal resolution.

ORGANISM(S): Homo sapiens

PROVIDER: GSE268471 | GEO | 2025/05/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

DNA methylation profiles in 3 mutant NPCs and wt NPCs (control, empty vector) at 10 days

Project description:To investigate temporal DNA methylation changes occurring during human neural progenitor cells (NPCs) maintenance in later times via genomic DNA methylation measurement by Infinium MethylationEPIC BeadChip assay, we introduced IDH1-R132H, KRAS-G12C, and TP53-R273C mutations separately into NPCs at day 0, with dox induction for 10 days to overexpress the oncogenes. After 10 days of induction, we investigated the DNA methylation profiles in NPCs, in order to investigate the epigenetic change during oncogene induction.

2025-05-01 | GSE268469 | GEO

DNA methylation profiles in seven mutant NPCs and wt NPCs (control, empty vector) at 2 days

Project description:To investigate temporal DNA methylation changes occurring during human neural progenitor cells (NPCs) maintenance in early times via genomic DNA methylation measurement by Infinium MethylationEPIC BeadChip assay, we introduced IDH1-R132H, KRAS-G12C, TP53-R273C, BRAF-V600E, NRAS-Q61R, HRAS-Q61R, and SOX17-S403I mutations separately into NPCs at day 0, with dox induction for 2 days to overexpress the oncogenes. After 2 days of induction, we investigated the DNA methylation profiles in NPCs, in order to investigate the epigenetic change during oncogene induction.

2025-05-01 | GSE268464 | GEO

DNA methylation profiles in seven mutant NPCs and wt NPCs (control, empty vector) at 2 days [LM17-Lm24]

2025-05-01 | GSE268467 | GEO

DNA methylation profiles in 3 mutant NPCs and wt NPCs (control, empty vector) at 10 days

Project description:DNA methylation profiles in 3 mutant NPCs and wt NPCs (control, empty vector) at 10 days

| PRJNA1117425 | ENA

DNA methylation profiles in seven mutant NPCs and wt NPCs (control, empty vector) at 2 days

Project description:DNA methylation profiles in seven mutant NPCs and wt NPCs (control, empty vector) at 2 days

| PRJNA1117414 | ENA

DNA methylation profiles in seven mutant NPCs and wt NPCs (control, empty vector) at 2 days [LM17-Lm24]

Project description:DNA methylation profiles in seven mutant NPCs and wt NPCs (control, empty vector) at 2 days [LM17-Lm24]

| PRJNA1117422 | ENA

DNA methylation alterations and transcriptional gene silencing induced by IDH1 R132H mutation

Project description:This SuperSeries is composed of the following subset Series: GSE31126: DNA methylation alterations and transcriptional gene silencing induced by IDH1 R132H mutation [Affymetrix] GSE31133: DNA methylation alterations and transcriptional gene silencing induced by IDH1 R132H mutation [Illumina] Refer to individual Series

2012-08-12 | E-GEOD-31134 | biostudies-arrayexpress

Idh1-R132H mutation increases murine hematopoietic progenitors and alters epigenetics.

Project description:Mutations in the IDH1 and IDH2 genes encoding isocitrate dehydrogenases are frequent in human glioblastomas1 and cytogenetically normal acute myeloid leukemias (AML)2. These alterations are gain-of-function mutations in that they drive the synthesis of the M-bM-^@M-^\oncometaboliteM-bM-^@M-^] R-2-hydroxyglutarate (2HG)3. It remains unclear how IDH1 and IDH2 mutations modify myeloid cell development and promote leukemogenesis. Here we report the characterization of conditional knock-in mice in which the most common IDH1 mutation, Idh1-R132H, is inserted into the endogenous murine Idh1 locus and is expressed in cells of the hematopoietic (Vav-KI) or more specifically in cells of the myeloid (LysM-KI) lineage. These mutants show increased numbers of early hematopoietic progenitors and develop splenomegaly and anemia with extramedullary hematopoiesis, suggesting a dysfunctional bone marrow niche. Furthermore, LysM-KI cells exhibit both hypermethylated histones and changes to DNA methylation similar to those observed in human IDH1/2-mutant AML. Thus, our study is the first to describe the generation of conditional Idh1-R132H-KI mice. Furthermore, our study is also the first report showing the induction of a leukemic DNA methylation signature in a modeled system and sheds light on the mechanistic links between IDH1 mutation and human AML. DNA methylation profiling in LSK cells from IDH1-R132H knock-in mice vs. control mice

2012-07-22 | E-GEOD-38687 | biostudies-arrayexpress

Transcriptome of early postnatal brain development of eIF2B-R132H/R132H mutant mice relative to wild-types.

Project description:Genome-wide mRNA expression in brains of wild-type and eIF2B-R132H/R132H mutant mice (Geva et al., BRAIN 133 (8), 2010) profiled at postnatal (P) days 1, 18 and 21 to reflect the early proliferative stage prior to white matter establishment (P1) and the peak of oligodendrocye differentiation and myelin synthesis (P18 and P21). 3 biological replicates (whole brain without the cerebellum) from each wild-type and eIF2B-R132H/R132H mutant mice at 3 postnatal (P) days 1, 18 and 21 were used for RNA extraction and hybridization on Affymetrix microarrays.

2011-11-14 | E-GEOD-32201 | biostudies-arrayexpress

Transcriptome-wide analysis of CRISPR-edited iPSC-derived glioma models

Project description:CRISPR-edited human induced pluripotent stem cell (iPSC)-derived glioma models provide a robust platform to investigate the biology of these aggressive tumors in an isogenic background or to test possible treatments in preclinical settings. We created iPSC12 lines that carry different combinations of glioma driver mutations using CRISPR/Cas9 genome editing technology, including TP53-/-, ATRX-/-, IDH1-R132H/WT, PTEN-/-, CDKN2A/B-/-, TERT promoter(TERTp) C228T/WT, MTAP-/-, and overexpression (OE) of EGFRvIII oncogenic isoform. Edited iPSCs were then differentiated into neural progenitor cells (NPC) using a small molecule protocol. We cultured the edited NPCs in 3D organoid with an FBS-containing differentiation medium. After 14 days, different genotypes of NPCs formed organoids were harvest and RNAs were isolated and subjected to RNA-seq analysis. To create an in vivo model system, NPCs with different genotypes were intracranially transplanted into athymic mice. Mice were sacrificed when pathologic symptoms developed resulting from tumor burden or 120 days post brain transplantation. RNAs were extracted from the tumor region of brain tissue sections and subjected to RNA-seq analysis. Our study showed that the iPSC-based model of gliomas displayed distinct mutation-dependent variation in transcriptome, which recapitulated the gene expression signatures of human gliomas.

2024-05-15 | GSE212671 | 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