Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [EM]

ABSTRACT: Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [EM]

PROVIDER: PRJNA1029948 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells

Project description:Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells

| PRJNA1029939 | ENA

Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [FLI1_EM]

Project description:Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [FLI1_EM]

| PRJNA1029949 | ENA

Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [WES]

Project description:Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [WES]

| PRJNA1029950 | ENA

Aberrant DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [CUT&RUN]

Project description:Aberrant DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [CUT&RUN]

| PRJNA1128593 | ENA

Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [YX-FLI1_EM]

Project description:Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [YX-FLI1_EM]

| PRJNA1047085 | ENA

Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [EM]

Project description:Background: Familial platelet disorder (FPD) is an autosomal dominant disease caused by a heterozygous germline mutation inRUNX1. FPD patients show not only thrombocytopenia with platelet dysfunction, but also a high level of developing hematological malignancies, strongly suggesting that FPD is in a precancerous state. However, the DNA methylation status of FPD has not yet been elucidated due to no animal models for FPD and the difficulty in obtaining FPD patient-derived samples. Results: We found that differentiation efficiencies into HPCs and megakaryocytes was reduced in the FPD-mimicking cells, which were established by genome editing for human iPS cells as a FPD-model, compared with those of wild-type cells. The FPD-mimicking HPCs were subjected to DNA methylation analysis, and the HPCs showed the distinct DNA methylation patterns compared to wild-type HPCs. Furthermore, we demonstrated a putative causative transcription factor of the differential DNA hypermethylation, which are involved in both promoting the binding site-directed DNA demethylation and regulating megakaryopoiesis.

2024-02-26 | GSE245765 | GEO

Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [FLI1_EM]

2024-02-26 | GSE245769 | GEO

Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [WES]

2024-02-26 | GSE245770 | GEO

Differential DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [YX-FLI1_EM]

2024-02-26 | GSE249049 | GEO

Aberrant DNA methylation occurs in RUNX1 heterozygous mutations harboring hematopoietic progenitor cells [CUT&RUN]

Project description:Background: Familial platelet disorder with associated myeloid malignancies (FPDMM) is an autosomal dominant disease caused by a heterozygous germline mutation inRUNX1. The patients with FPDMM show not only thrombocytopenia with platelet dysfunction, but also a high level of developing hematological malignancies, strongly suggesting that FPDMM is in a precancerous state. However, the DNA methylation status of FPDMM has not yet been elucidated due to no animal models for FPDMM and the difficulty in obtaining the patient-derived samples. Results: We found that differentiation efficiencies into HPCs and megakaryocytes was reduced in the FPDMM-mimicking cells, which were established by genome editing for human iPS cells as a FPDMM-model, compared with those of wild-type cells. The FPDMM-mimicking HPCs were subjected to DNA methylation analysis, and the HPCs showed the distinct DNA methylation patterns compared to wild-type HPCs. Furthermore, we identified FLI1 as a putative causative transcription factor of the differential DNA hypermethylation involved in both promoting the binding site-directed DNA demethylation and regulating megakaryopoiesis.

2024-07-01 | GSE270829 | 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