Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PLAG1 and USF2 Co-regulate Expression of Musashi-2 in Human Hematopoietic Stem and Progenitor Cells

ABSTRACT: PLAG1 and USF2 Co-regulate Expression of Musashi-2 in Human Hematopoietic Stem and Progenitor Cells

PROVIDER: PRJNA437125 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6810050.fastq.gz	Fastqsanger.gz
	SRR6810060.fastq.gz	Fastqsanger.gz
	SRR6810051.fastq.gz	Fastqsanger.gz
	SRR6810052.fastq.gz	Fastqsanger.gz
	SRR6810053.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

PLAG1 and USF2 Co-regulate Expression of Musashi-2 in Human Hematopoietic Stem and Progenitor Cells

Project description:MSI2, which is expressed predominantly in hematopoietic stem and progenitor cells (HSPCs), enforces HSPC expansion when overexpressed and is upregulated in myeloid leukemias indicating its regulated transcription is critical to balanced self-renewal and leukemia restraint. Despite this, little is understood of the factors that enforce appropriate physiological levels of MSI2 in the blood system. Here we define a promoter region that reports on endogenous expression of MSI2 and identify USF2 and PLAG1 as transcription factors whose promoter binding drives reporter activity. We show that these factors co-regulate, and are required for, efficient transactivation of endogenous MSI2. Coincident overexpression of USF2 and PLAG1 in primitive cord blood cells enhanced MSI2 transcription and yielded cellular phenotypes, including expansion of CD34+ cells in vitro, consistent with that achieved by direct MSI2 overexpression. Global ChIP-seq analyses confirm a preferential co-binding of PLAG1 and USF2 at the promoter of MSI2, as well as regulatory regions corresponding to genes with roles in HSPC homeostasis. PLAG1 and USF2 cooperation is thus an important contributor to stem cell-specific expression of MSI2 and represents novel HSPC-specific transcriptional circuitry.

2018-03-15 | GSE111469 | GEO

PLAG1 and USF2 Co-regulate Expression of Musashi-2 in Human Hematopoietic Stem and Progenitor Cells.

Project description:MSI2, which is expressed predominantly in hematopoietic stem and progenitor cells (HSPCs), enforces HSPC expansion when overexpressed and is upregulated in myeloid leukemias, indicating its regulated transcription is critical to balanced self-renewal and leukemia restraint. Despite this, little is understood of the factors that enforce appropriate physiological levels of MSI2 in the blood system. Here, we define a promoter region that reports on endogenous expression of MSI2 and identify USF2 and PLAG1 as transcription factors whose promoter binding drives reporter activity. We show that these factors co-regulate, and are required for, efficient transactivation of endogenous MSI2. Coincident overexpression of USF2 and PLAG1 in primitive cord blood cells enhanced MSI2 transcription and yielded cellular phenotypes, including expansion of CD34+ cells in vitro, consistent with that achieved by direct MSI2 overexpression. Global chromatin immunoprecipitation sequencing analyses confirm a preferential co-binding of PLAG1 and USF2 at the promoter of MSI2, as well as regulatory regions corresponding to genes with roles in HSPC homeostasis. PLAG1 and USF2 cooperation is thus an important contributor to stem cell-specific expression of MSI2 and HSPC-specific transcriptional circuitry.

| S-EPMC5998603 | biostudies-literature

USF2 interacted proteins in HEK293T cells

Project description:We found that USF2 is repressor of lysosomal genes. To find the interacting co-repressor complex of USF2, we performed USF2 complex purification and mass spectrography.

2024-09-11 | PXD050434 | Pride

Plag1 in the mouse Epididymis

Project description:RNA sequencing of Plag1 mouse epididymides. 5 each of Plag1 WT, HET and KO whole epididymis tissues were sequenced.

2019-11-19 | GSE140576 | GEO

Effects of KD USF2 on gene expressions in C2C12

Project description:USF2 has emerged as a key player in various cellular processes, including cell cycle regulation， apoptosi, metabolism, and response to cellular stress. In the context of muscle biology, the role of USF2 is not clear. To elucidate the functional significance of USF2, we conducted knockdown (KD) experiments targeting USF2 in C2C12 myoblast cells. The KD of USF2 resulted in the differential expression of a set of genes, and functional enrichment analysis of genes affected by KD of USF2 were performed.

2024-01-01 | GSE244161 | GEO

Plag1 overexpression cooperates with Evi1 overexpression and Gata1s mutation in leading to M7 leukemia

Project description:The goal of this study is to develop a Plag1 signature and determine how its overexpression contributes to leukemogenesis. To study this, we transduced an immortalized (but not transformed) cell line (derived from Gata1s mutant fetal liver progenitor through insertional mutagenesis) by Plag1-expressing retrovirus. This turned a non-transformed cell line to a leukemogenic cell line. To study whether Plag1 overexpression led to deregulation of signaling pathways that may contribute to leukemic transformation, we generated microarray gene expression profiles of this cell line transduced with either Plag1 or the empty vector. We generated gene expression profiles by microarray from stable cell lines transduced with either the empty vector or the Plag1-expressing vector.

2010-08-01 | E-GEOD-16679 | biostudies-arrayexpress

Microarray analysis of differential gene expression of whole testis extracts from transgenic Musashi-2 and transgenic Musashi-1 over-expression mice

2014-07-12 | GSE59358 | GEO

Genome binding/occupancy profiling of USF2 under glucose starvation and changes in H3K27ac based on the presence of USF2

Project description:Intricate regulation of lysosome and autophagy processes is essential for maintaining cellular homeostasis and basal metabolism. While the consequences of disrupting or attenuating lysosome and autophagy systems have been extensively studied, little is known about the impact of hyper-activation of lysosomal and autophagy genes on homeostasis. Our research uncovers previously unknown transcriptional repression mechanism by upstream stimulatory factor 2 (USF2), which inhibits lysosomal and autophagy genes in nutrient-rich conditions. USF2 binds to the CLEAR motif within lysosomal genes along with HDAC1, which diminishes H3K27 acetylation levels, restrains chromatin accessibility, and lowers lysosomal gene expression. Under starvation, USF2 competes with TFEB, a master transcriptional activator of lysosomal and autophagy genes, to bind target gene promoters in phosphorylation-dependent manner. Phosphorylation of the S155 site by GSK3b plays a pivotal role in controlling USF2's DNA binding activity for the repression of lysosomal genes while GSK3b-mediated phosphorylation of TFEB enhances its cytoplasmic retention. Applying these discoveries has potential for treating diseases associated with protein aggregation, including alpha-1 antitrypsin deficiency. These findings demonstrate that the USF2 repression mechanism could be a potent therapeutic strategy for various lysosome and autophagy-related diseases.

2024-08-06 | GSE252310 | GEO

Microarray analysis of differential gene expression of whole testis extracts from transgenic Musashi-2 and transgenic Musashi-1 over-expression mice

Project description:Analysis of testis-specific over-expression of Musashi-1 and Musashi-2 at gene expression level. The hypothesis tested in the present study was that testis-specific over-expression of Musashi-1/Musashi-2 would result in differential gene expression profiles from the Wildtype control. Results provide important information of the genes affected by Musashi-2 overexpression during spermatogenesis. Total RNA obtained from whole adult testis of transgenic testis-specfic Musashi-1 and Musashi-2 overexpression mice compared to Wildtype (control) littermates. 4 replicates, 16 samples, 2 comparisons: Wt (Musashi-1) vs. TgMsi1 & Wt (Musashi-2) vs. TgMsi2

2014-07-12 | E-GEOD-59358 | biostudies-arrayexpress

Maternal Plag1 deficiency delays two-cell stage embryo development and embryonic genome activation [Embryos]

Project description:Pleomorphic adenoma gene 1 (PLAG1) encodes a transcription factor involved in cancer and growth. We study the role of PLAG1 in preimplantation embryos using STRT RNA-seq of single embryos from wild type and knockout mothers (both mated with wild type studs). The lack of maternal Plag1 led to delayed mouse 2-cell stage embryo development, compensatory expression of Plag1 from the paternal allele, and dysregulation of 1,089 genes. Half of these genes displayed a pattern of delayed activation and play roles in ribosome biogenesis and protein synthesis. These mouse genes further showed a significant overlap with human EGA genes with similar ontology, and an enrichment of the PLAG1 de novo motif. We conclude that Plag1 affects EGA through retrotransposons influencing ribosomes and protein synthesis, a mechanism that might also explain its roles in cancer and growth

2019-06-20 | GSE111039 | 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