Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SRCAP Mutations Drive Clonal Hematopoiesis Through Epigenetic and DNA Repair Dysregulation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE230155 | GEO | 2023/10/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

SRCAP Mutations Drive Clonal Hematopoiesis Through Epigenetic and DNA Repair Dysregulation [Cut & Run]

Project description:To investigate how Srcap mutations confer mutant hematopoietic stem and progenitor cells (HSPCs) with selective advantage after transplantation We assessed SRCAP chromatin remodeling and corresponding H2A.Z incorporation using Cut-and-run sequencing

2023-10-19 | GSE229864 | GEO

SRCAP Mutations Drive Clonal Hematopoiesis Through Epigenetic and DNA Repair Dysregulation [ATAC-Seq]

Project description:To investigate how Srcap mutations confer mutant hematopoietic stem and progenitor cells (HSPCs) with selective advantage after transplantation We assessed chromatin remodeling and chromatin accessbility before and after transplantation to understand the mechanism of the acquisition of Srcap selective advantage

2023-10-19 | GSE229862 | GEO

SRCAP Mutations Drive Clonal Hematopoiesis Through Epigenetic and DNA Repair Dysregulation [scRNA-Seq]

Project description:To investigate the transcriptomic regulation of Srcap mutant lymphoid-biased expansion after compeititve transplantation

2023-10-19 | GSE230153 | GEO

SRCAP Mutations Drive Clonal Hematopoiesis Through Epigenetic and DNA Repair Dysregulation [RNA-seq]

Project description:To investigate how Srcap mutations confer mutant hematopoietic stem and progenitor cells (HSPCs) with selective advantage after exposure to cellular stressors, transplantation and doxorubicin treatment We established Srcap heterozygous mutant murine model and utilized competitive bone marrow transplantation to assess the transcriptome of donor cells using RNA-seq

2023-10-19 | GSE229865 | GEO

SRCAP Mutations Drive Clonal Hematopoiesis Through Epigenetic and DNA Repair Dysregulation

Project description:SRCAP Mutations Drive Clonal Hematopoiesis Through Epigenetic and DNA Repair Dysregulation

| PRJNA957753 | ENA

SRCAP Mutations Drive Clonal Hematopoiesis Through Epigenetic and DNA Repair Dysregulation [ATAC-Seq]

Project description:SRCAP Mutations Drive Clonal Hematopoiesis Through Epigenetic and DNA Repair Dysregulation [ATAC-Seq]

| PRJNA956472 | ENA

SRCAP Mutations Drive Clonal Hematopoiesis Through Epigenetic and DNA Repair Dysregulation [Cut & Run]

Project description:SRCAP Mutations Drive Clonal Hematopoiesis Through Epigenetic and DNA Repair Dysregulation [Cut & Run]

| PRJNA956487 | ENA

SRCAP Mutations Drive Clonal Hematopoiesis Through Epigenetic and DNA Repair Dysregulation [RNA-seq]

Project description:SRCAP Mutations Drive Clonal Hematopoiesis Through Epigenetic and DNA Repair Dysregulation [RNA-seq]

| PRJNA956488 | ENA

SRCAP Mutations Drive Clonal Hematopoiesis Through Epigenetic and DNA Repair Dysregulation [scRNA-Seq]

Project description:SRCAP Mutations Drive Clonal Hematopoiesis Through Epigenetic and DNA Repair Dysregulation [scRNA-Seq]

| PRJNA957754 | ENA

PPM1D Mutations Drive Clonal Hematopoiesis in Response to Cytotoxic Chemotherapy.

Project description:Clonal hematopoiesis (CH), in which stem cell clones dominate blood production, becomes increasingly common with age and can presage malignancy development. The conditions that promote ascendancy of particular clones are unclear. We found that mutations in PPM1D (protein phosphatase Mn2+/Mg2+-dependent 1D), a DNA damage response regulator that is frequently mutated in CH, were present in one-fifth of patients with therapy-related acute myeloid leukemia or myelodysplastic syndrome and strongly correlated with cisplatin exposure. Cell lines with hyperactive PPM1D mutations expand to outcompete normal cells after exposure to cytotoxic DNA damaging agents including cisplatin, and this effect was predominantly mediated by increased resistance to apoptosis. Moreover, heterozygous mutant Ppm1d hematopoietic cells outcompeted their wild-type counterparts in vivo after exposure to cisplatin and doxorubicin, but not during recovery from bone marrow transplantation. These findings establish the clinical relevance of PPM1D mutations in CH and the importance of studying mutation-treatment interactions. VIDEO ABSTRACT.

| S-EPMC6224657 | biostudies-literature

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