Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Resolving the function of FoxO6 during Somatic Cell Reprogramming by RNA-seq

ABSTRACT: Resolving the function of FoxO6 during Somatic Cell Reprogramming by RNA-seq

PROVIDER: PRJNA675389 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13009109_1.fastq.gz	Fastqsanger.gz
	SRR13009109_2.fastq.gz	Fastqsanger.gz
	SRR13009110_1.fastq.gz	Fastqsanger.gz
	SRR13009110_2.fastq.gz	Fastqsanger.gz
	SRR13009111_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Resolving the function of FoxO6 during Somatic Cell Reprogramming by RNA-seq

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to explore the function of FoxO6 in reprogramming system Methods: The mRNA profiles of OKS induced reprogramming systems with and without FoxO6 were generated by deep sequencing.

2020-12-31 | GSE161057 | GEO

R-loops Function as a Balance during Somatic Cell Reprogramming

Project description:R-loops Function as a Balance during Somatic Cell Reprogramming

| PRJNA517073 | ENA

R-loops Function as a Balance during Somatic Cell Reprogramming

Project description:R-loop induces genome instability and regulates gene expression. However, regulatory mechanism of R-loop in stem cell biology remains unclear. Here, we mapped the profiling of R-loops during reprogramming process and revealed that R-loops change prior to gene expression and are mainly accumulated and enriched at terminator of genes. Disrupting homeostasis of R-loops via RNaseH1 loss-of-function blocks reprogramming in a medium independent manner. Interestingly, Sox2 but not other Yamanaka factors overcomes the inhibitory effects of RNaseH1 loss on reprogramming. Sox2 forms a complex with Ddx5 and R-loop in cells and common targets for Sox2 and Ddx5 at R-loops are mainly associated with pluripotent genes. Furthermore, Sox2 inhibits the resolving activity of RNA helicase Ddx5 at R-loops to facilitate reprogramming. Together, these results indicate that the importance of R-loops balance for reprogramming and shed light on the regulation Sox2/Ddx5 on R-loops during reprogramming.

2020-06-12 | GSE125644 | GEO

Kdm2b regulates somatic reprogramming through variant PRC1 complex dependent function

Project description:Kdm2b regulates somatic reprogramming through variant PRC1 complex dependent function

| PRJNA369098 | ENA

Study of human macrophage reprogramming toward a pro-resolving profile by efferocytosis

Project description:Inﬂammation is a physiopathological process triggered by infection or tissue damage. Immune system initiates coordinated sequential steps in response to these danger signals. Once the threat has been contained inflammation has to be subsequently shut down. Inflammation resolution is initiated by the reprogramming of pro-inflammatory macrophages toward a pro-resolving profile. This reprogramming is induced in particular by the non-phlogistic engulfment of apoptotic cells, mostly apoptotic neutrophils, a process called efferocytosis. As a matter of fact, macrophages are an essential linchpin regulating both inflammation triggering and sustaining and inflammation resolution. This duality can be achieved through the tremendous plasticity of these innate immune cells. Indeed, depending on microenvironmental signals (cytokines, efferocytosis, growth factors…) macrophages can adopt numerous diverse and sometimes antagonistic phenotypes. The mechanisms governing these transitions remain relatively scattered especially in human. With this project we propose to explore the mechanisms involved in human macrophage reprogramming toward a pro-resolving profile after efferocytosis. The stakes are high due to the estimated prevalence of chronic inflammatory diseases in Western society is 5 to 7%. Chronic inflammation is a burden to patient due to life-long debilitating illness and increased mortality and is also a burden to society due to high costs for therapy and care. Finding new therapies to limit chronic inflammation establishment and persistence is thus a highly valuable goal.

2021-12-01 | E-MTAB-8885 | biostudies-arrayexpress

The Role of Tet1 During Somatic Cell Reprogramming

Project description:Tet1 is a hydroxylase known for its role in the conversion of 5-methylcytosines (5mC) to 5-hydroxymethylcytosines (5hmC) involved in the possible active demethylation process and gene expression regulation. As somatic cell reprogramming involves the re-activation of pluripotency genes and the silencing of somatic ones, it remains unclear the role of Tet1 in the reprogramming process. Here, we performed hMeDIP-seq and RNA-seq during somatic cells reprogramming with Tet1 over expression to invest the effect of Tet1.

2013-03-08 | GSE44935 | GEO

Kdm2b regulates somatic reprogramming through variant PRC1 complex dependent function [RNA-seq]

Project description:Polycomb repressive complex 1 (PRC1) plays essential roles in cell fate determination. Recent studies have found that the composition of mammalian PRC1 is particularly varied and complicated, whereas the function of such variant PRC1 complexes on cell fate determination remains unknown. Here we show that Kdm2b, which recruits a variant PRC1 complex (PRC1.1) to CpG islands (CGIs), elevates Oct4 induced somatic reprogramming. Interaction with PRC1 is critical for Kdm2b’s promotion on the process of induced pluripotency. Furthermore, we find that bone morphogenetic proteins (BMPs) repress Oct4/Kdm2b induced somatic reprogramming selectively. Mechanistically, BMP-Smad pathway attenuates PRC1.1 occupation and H2AK119 ubiquitination on development genes, resulting in the release of meso-endoderm factors such as Sox17 and suppression of somatic reprogramming. These observations reveal that PRC1.1 participates in the establishment of pluripotency as well as cellular differentiation and identify BMP signal as a modulator of PRC1.1 function.

2017-11-19 | GSE93974 | GEO

miRNAs regulated by Gadd45a during somatic cell reprogramming

Project description:Gadd45a can enhance somatic cell reprogramming significantly. To explore the roles of Gadd45a playing in reprogramming, we performed miRNA microarray to identify miRNAs and signals pathways that regulated by Gadd45a. miRNAs expression of MEFs was measured at day8 in reprogramming. Four samples were set: MEFs infected with SKO plus Flag, MEFs infected with SKO plus Gadd45a, MEFs infected with SKOM plus Flag and MEFs infected with SKOM+Ga.

2014-04-22 | E-GEOD-56942 | biostudies-arrayexpress

Genes regulated by Gadd45a during somatic cell reprogramming

Project description:Gadd45a can enhance somatic cell reprogramming significantly. To explore the roles of Gadd45a playing in reprogramming, we performed whole genome microarray to identify genes and signals pathways that regulated by Gadd45a. Genes expression of MEFs was measured at day8 in reprogramming. Three samples were set: MEFs infected with SKO plus Flag, MEFs infected with SKO plus Gadd45a and MEFs infected with SKO plus G39A which is a negative mutant of Gadd45a.

2014-04-22 | E-GEOD-56943 | biostudies-arrayexpress

Transcriptome analysis during somatic cell reprogramming

Project description:By combining deep sequencing with high-throughput quantitative RT-PCR, we reveal that somatic splicing profiles are reorganized to pluripotent splicing profiles during reprogramming from mouse embryonic fibroblasts (MEFs) to induced pluripotent stem (iPS) cells. The splicing pattern in pluripotent stem cells resembles that in testis, and the regulatory regions have specific characters in length and sequence. These results indicate that the dynamic alteration in splicing is an integral part of the molecular network involved in the reprogramming process. Sequencing data from MEF, two iPS cell lines and one ES cell line. RT-PCR data will be represented within Figures or Tables in published manuscripts.

2013-10-17 | E-GEOD-46149 | biostudies-arrayexpress

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