Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A CHAF1B-dependent molecular switch in hematopoiesis and leukemia pathogenesis

ABSTRACT: A CHAF1B-dependent molecular switch in hematopoiesis and leukemia pathogenesis

PROVIDER: PRJNA491485 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7865900.fastq.gz	Fastqsanger.gz
	SRR7865910_1.fastq.gz	Fastqsanger.gz
	SRR7865910_2.fastq.gz	Fastqsanger.gz
	SRR7865920.fastq.gz	Fastqsanger.gz
	SRR7865930.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 54

Similar Datasets

A CHAF1B-dependent molecular switch in hematopoiesis and leukemia pathogenesis

Project description:CHAF1B is the p60 subunit of the chromatin assembly factor (CAF1) complex, which is responsible for assembly of H3.1/H4 heterodimers at the replication fork during S phase. Here we report that CHAF1B is required for normal hematopoiesis while its overexpression promotes leukemia. CHAF1B has a pro-leukemia effect by binding chromatin at discrete sites and interfering with occupancy of transcription factors that promote myeloid differentiation, such as CEBPA. Reducing Chaf1b activity by either heterozygous deletion or overexpression of a CAF1 dominant negative allele was sufficient to suppress leukemogenesis in vivo without impairing normal hematopoiesis.

2018-11-12 | GSE120063 | GEO

A CHAF1B-Dependent Molecular Switch in Hematopoiesis and Leukemia Pathogenesis.

Project description:CHAF1B is the p60 subunit of the chromatin assembly factor (CAF1) complex, which is responsible for assembly of histones H3.1/H4 heterodimers at the replication fork during S phase. Here we report that CHAF1B is required for normal hematopoiesis while its overexpression promotes leukemia. CHAF1B has a pro-leukemia effect by binding chromatin at discrete sites and interfering with occupancy of transcription factors that promote myeloid differentiation, such as CEBPA. Reducing Chaf1b activity by either heterozygous deletion or overexpression of a CAF1 dominant negative allele is sufficient to suppress leukemogenesis in vivo without impairing normal hematopoiesis.

| S-EPMC6235627 | biostudies-literature

Sustained fetal hematopoiesis causes juvenile death from leukemia: evidence from a dual-age-specific mouse model

Project description:It is not clear whether disrupted age-specific hematopoiesis contributes to the complex manifestations in leukemia patients who carry identical mutations, particularly in pediatric and adult patients with similar clinical characteristics. By studying a dual-age-specific mouse model, we demonstrate: 1) loss of Pten during the fetal-to-adult hematopoiesis switch (HSC switch) causes sustained fetal hematopoiesis, resulting in death in juvenile leukemia; 2) myeloid-biased hematopoiesis in juvenile mice is associated with the sustained fetal properties of hematopoietic stem cells (HSCs); 3) the age specificity of juvenile myelomonocytic leukemia (JMML) depends on the dosage of Pten and Nf1; 4) single-allelic Pten deletion during the HSC switch causes constitutive activation of mitogen-activated protein kinase (MAPK) in juvenile mice with Nf1 loss of heterozygosity (LOH); and 5) Nf1 LOH causes monocytosis in juvenile mice with Pten haploinsufficiency but does not cause lethality until adulthood. Our data suggest that one copy of Pten is sufficient to maintain an intact negative feedback loop of the Akt pathway and HSC function in reconstitution, despite MAPK being constitutively activated in juvenile mice with Pten+/DNf1LOH. However, two copies of Pten are required to maintain the integrity of the MAPK pathway in juvenile mice with Nf1 haploinsufficiency. Our data indicate that previous investigations of Pten function in wild type mice may not reflect the impact of Pten loss in mice with Nf1 mutations or other genetic defects. We provide a proof-of-concept that disassociated age-specific hematopoiesis contributes to leukemogenesis and pediatric demise.

2020-06-25 | GSE137152 | GEO

The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis.

Project description:The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis.

| PRJNA752569 | ENA

Understanding RNA Biology and Therapeutics in Hematopoiesis and Leukemia

Project description:Understanding RNA Biology and Therapeutics in Hematopoiesis and Leukemia

| PRJNA548599 | ENA

Understanding RNA Biology and Therapeutics in Hematopoiesis and Leukemia

Project description:Understanding RNA Biology and Therapeutics in Hematopoiesis and Leukemia

| PRJNA548601 | ENA

Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis

Project description:This SuperSeries is composed of the following subset Series: GSE16432: MSI2 regulates hematopoiesis and accelerates leukemogenesis GSE22773: Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis (LK and MS12-inducible) GSE22774: Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis (LSK and LK) GSE22775: Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis (Leukemia cell lines) Refer to individual Series

2010-07-21 | E-GEOD-22778 | biostudies-arrayexpress

Oncofetal gene reactivation drives EZH2-mutant myeloid leukemia pathogenesis

Project description:Oncofetal gene reactivation drives EZH2-mutant myeloid leukemia pathogenesis

| PRJNA725836 | ENA

Loss of FOXC1 contributes to the corneal epithelial fate switch and pathogenesis

Project description:Loss of FOXC1 contributes to the corneal epithelial fate switch and pathogenesis

| PRJNA655547 | ENA

The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [CUT&RUN]

Project description:The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [CUT&RUN]

| PRJNA752579 | ENA