Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide maps of Qki-5, Srebp2, and Pol II in oligodendrocytes

ABSTRACT: Genome-wide maps of Qki-5, Srebp2, and Pol II in oligodendrocytes

PROVIDER: PRJNA604792 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11016645_1.fastq.gz	Fastqsanger.gz
	SRR11016645_2.fastq.gz	Fastqsanger.gz
	SRR11016646_1.fastq.gz	Fastqsanger.gz
	SRR11016646_2.fastq.gz	Fastqsanger.gz
	SRR11016647_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Genome-wide maps of Qki-5, Srebp2, and Pol II in oligodendrocytes

Project description:We found the genome-wide co-localization of Qki-5 and Srebp2. Notably, the genomic distribution analysis revealed that Qki-5 and Srebp2 highly co-occupied the regions of the promoter/transcription start site (TSS), where active transcription was taken place in a oligodendrocyte-specific manner, which was indicated by Pol II binding events. GO analysis of the genes whose promoters were co-bound by Qki-5, Srebp2, and Pol II showed a significant enrichment of the Srebp2-mediated cholesterol biosynthesis pathway, and Qki depletion led to reduced recruitment of Srebp2 and Pol II on the promoters of the genes involved in cholesterol biosynthesis. These data suggest Qki-5 as a potential transcription co-activator of Srebp2-mediated cholesterol biosynthesis in oligodendrocytes.

2021-05-10 | GSE144756 | GEO

Genome-wide maps of QKI-5, SREBP2, and POL II in eye lens cells

Project description:We found the genome-wide co-binding of QKI-5 and SREBP2. Notably, the genomic distribution analysis revealed that the co-binding events between QKI-5 and SREBP2 highly occurred at the regions of the promoter/transcription start site (TSS), where active transcription was taken place in a lens cell-specific manner, which was indicated by POL II binding events. Cellular pathway analysis of the genes whose promoters were co-bound by QKI-5, SREBP2, and POL II showed a significant enrichment of the SREBP2-medaited cholesterol biosynthesis pathway, and QKI depletion led to reduced co-occupancies of SREBP2 and POL II on the promoters of the genes involved in cholesterol biosynthesis. These data suggest QKI-5 as a potential transcription co-activator mediating SREBP2-dependent cholesterol biosynthesis in eye lens cells.

2021-01-29 | GSE144757 | GEO

Genome-wide maps of QKI-5, SREBP2, and POL II in eye lens cells

Project description:Genome-wide maps of QKI-5, SREBP2, and POL II in eye lens cells

| PRJNA604795 | ENA

Genome-wide maps of Qki-5 and PPARb in mouse oligodendrocytes

Project description:Genome-wide maps of Qki-5 and PPARb in mouse oligodendrocytes

| PRJNA522428 | ENA

Genome-wide maps of Qki-5 and PPARb in mouse oligodendrocytes

Project description:We found that there is a big overlap between the Qki5- and PPARb-binding events by ChIP-seq. Interestingly, the genomic distribution analyses of Qki-5- and PPARβ-binding events showed significant enrichment at the regions of the promoter/transcription start site (TSS) which were indicated by Pol II-binding events. The strong preference of the promoter/TSS co-occupancy suggested that Qki-5 might play an important role in PPARβ-mediated transcriptional regulation of its downstream genes.

2020-01-05 | GSE126577 | GEO

QKI and miR-155 in inflammation and leukemogenesis

Project description:Transcription profiling by array of siRNA against Quaking (QKI) transcripts to identify transcripts that are modulated by QKI activity. MiR-155 is an oncogene and we report here that it targets QKI transcripts. Therefore, we believe that QKI acts as a tumor suppressor gene in different leukemias. We ablated the expression of QKI transcripts using siRNAs in order to further elucidate the effects of QKI in leukemogenesis, and how miR-155 and QKI functionally interact with each other.

2016-01-17 | E-MTAB-2375 | biostudies-arrayexpress

Genomewide analysis of QKI-dependent alternative splicing

Project description:To identify QKI targets, we performed QKI knockdown in BEAS2B cells and analyzed alternative splicing patterns by high-throughput RNA sequencing. The mRNA profiles of control- and QKI-knockdown BEAS2B cells were generated by deep sequencing using Illumina GAIIx sequencer.

2014-04-14 | E-GEOD-55215 | biostudies-arrayexpress

Effects of Intestine-specifc SREBP2 overactivation on gene expression in mouse jejnum

Project description:The active form of the SREBP2 transcription factor was specifically overexpressed in the intesitne. This was achieved by generating transgenic mouse model (designated as ISR2) in which the transgene represents the N-terminal active SREBP2 transcription factor driven by the villin promoter. In this project, we investigated the effects of overactivation of SREBP2 on gene expression in mouse jejunum Gene expression profile in the jejunum of ISR2 was compared to gene expression profile in the jejunum of their wild type littermates.

2013-10-26 | E-GEOD-51736 | biostudies-arrayexpress

Qki regulates myelinogenesis through Srebp2-dependent cholesterol biosynthesis.

Project description:Myelination depends on timely, precise control of oligodendrocyte differentiation and myelinogenesis. Cholesterol is the most abundant component of myelin and essential for myelin membrane assembly in the central nervous system. However, the underlying mechanisms of precise control of cholesterol biosynthesis in oligodendrocytes remain elusive. In the present study, we found that Qki depletion in neural stem cells or oligodendrocyte precursor cells in neonatal mice resulted in impaired cholesterol biosynthesis and defective myelinogenesis without compromising their differentiation into Aspa+Gstpi+ myelinating oligodendrocytes. Mechanistically, Qki-5 functions as a co-activator of Srebp2 to control transcription of the genes involved in cholesterol biosynthesis in oligodendrocytes. Consequently, Qki depletion led to substantially reduced concentration of cholesterol in mouse brain, impairing proper myelin assembly. Our study demonstrated that Qki-Srebp2-controlled cholesterol biosynthesis is indispensable for myelinogenesis and highlights a novel function of Qki as a transcriptional co-activator beyond its canonical function as an RNA-binding protein.

| S-EPMC8139834 | biostudies-literature

RNA-seq profiles of WT and Qk-KO freshly isolated oligodendrocytes

Project description:Lipid-rich myelin forms insulating axon-wrapping multilayers essential for neural function, but how mature myelin maintains its structural lipid components remains obscure. Here we identify Quaking (Qki) as a major regulator of myelin lipid homeostasis. Qki depletion in adult myelinating oligodendrocytes disrupted myelin lipid metabolism and caused demyelination, resulting in progressive neurological deficits that could be partially rescued by high-fat diet. Mechanistically, Qki serves as a coactivator of the PPARb-RXRa complex, which controls transcription of lipid-metabolism genes, particularly those for fatty acid desaturation and elongation. Treatment of Qki-depleted mice with PPARb or RXR agonists alleviated neurological disability and significantly extended mouse survival. Furthermore, a subset of lesions from patients with primary progressive multiple sclerosis were characterized by preferential reduction of myelin lipids and activities of lipid-metabolism pathways. Together, our findings demonstrate that continuous lipid synthesis is indispensable for mature myelin maintenance and highlight an underappreciated role of lipid metabolism in demyelinating diseases.

2020-01-04 | GSE125581 | 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