Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The CDP-Etn pathway accelerates mesenchymal-to-epithelial transition in somatic cell reprogramming

ABSTRACT: the CDP-Etn pathway accelerates mesenchymal-to-epithelial transition in somatic cell reprogramming

PROVIDER: PRJNA476964 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7405190_1.fastq.gz	Fastqsanger.gz
	SRR7405190_2.fastq.gz	Fastqsanger.gz
	SRR7405191_1.fastq.gz	Fastqsanger.gz
	SRR7405191_2.fastq.gz	Fastqsanger.gz
	SRR7405186_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

the CDP-Etn pathway accelerates mesenchymal-to-epithelial transition in somatic cell reprogramming

Project description:Metabolic reprogramming has emerged as key regulators of cell fate decisions. Whereas the glucose and amino acid metabolism have been extensively documented, the roles of lipid metabolism in pluripotency remain largely unexplored. Here, we report that the CDP-Ethanolamine (CDP-Etn) pathway for phosphatidylethanolamine synthesis is required for somatic cell reprogramming at the early stage. Mechanistically, the CDP-Etn pathway inhibits NF-κB signaling and mesenchymal genes in a Pebp1 dependent manner, resulting in accelerated mesenchymal-to-epithelial transition and enhanced reprogramming. In addition, we show that phospholipids are critical for the growth of mESC though without effects on pluripotency. Our study reveals an unforeseen connection between phospholipids, cell migration and pluripotency and highlights the importance of phospholipids in cell fate transitions.

2019-08-25 | GSE116080 | GEO

Obesity Accelerates Endothelial-to-Mesenchymal Transition in Adipose Tissue of Mice and Humans

Project description:Obesity Accelerates Endothelial-to-Mesenchymal Transition in Adipose Tissue of Mice and Humans

| PRJNA1006048 | ENA

Epigenomic reprogramming during epithelial to mesenchymal transition

Project description:This SuperSeries is composed of the following subset Series: GSE27968: DNA methylation data from AML12 cells during EMT GSE28291: Genome-scale epigenetic reprogramming during epithelial to mesenchymal transition Refer to individual Series

2011-07-03 | E-GEOD-28581 | biostudies-arrayexpress

Oocyte Specific Homeobox 1 (Obox1) Facilitates Somatic Cell Reprogramming by Promoting Mesenchymal-to-Epithelial Transition and Mitigating Cell Hyper-proliferation

Project description:Mammalian oocytes possess fascinating unknown factors, which can reprogram terminally differentiated germ cells (sperm) or somatic cells into totipotent embryos. Here, we demonstrate that oocyte specific homeobox 1 (Obox1), an oocyte-specific factor, can markedly enhance the generation of induced pluripotent stem cells (iPSCs) from mouse fibroblasts in a proliferation-independent manner and can replace Sox2 to achieve pluripotency. Overexpression of Obox1 can greatly promote mesenchymal-to-epithelial transition (MET) at early stage of OSKM-induced somatic cell reprogramming and meanwhile, the cell hyper-proliferation can be significantly slowed down. Subsequently, the proportion of Thy1 negative cells and Oct4-GFP positive cells increased dramatically. Further analysis of gene expression and targets of Obox1 during reprogramming indicates that the expression of Obox1 can promote epithelial genes expression and repress cell cycle-related genes expression. Taken together, we conclude that the oocyte-specific factor Obox1 serves as a strong activator for somatic cell reprogramming through promoting the MET and mitigating cells hyper-proliferation.

2017-09-21 | GSE97859 | GEO

Loss of ATM accelerates pancreatic cancer formation and epithelial–mesenchymal transition

Project description:Pancreatic ductal adenocarcinoma (PDAC) is associated with accumulation of particular oncogenic mutations and recent genetic sequencing studies have identified ataxia telangiectasia-mutated (ATM) mutations in PDAC cohorts. Here we report that conditional deletion of ATM in a mouse model of PDAC induces a greater number of proliferative precursor lesions coupled with a pronounced fibrotic reaction. ATM-targeted mice display altered TGFβ-superfamily signalling and enhanced epithelial-to-mesenchymal transition (EMT) coupled with shortened survival. Notably, our mouse model recapitulates many features of more aggressive human PDAC subtypes. Particularly, we report that low expression of ATM predicts EMT, a gene signature specific for Bmp4 signalling and poor prognosis in human PDAC. Our data suggest an intimate link between ATM expression and pancreatic cancer progression in mice and men. KC (Atm+/+) and AKC (Atm-/-) mouse pancreata at 5 weeks old (n= 3 KC; n= 3 AKC) or 10 weeks old (n=3 KC; n=4 AKC) were subjected to microarray analysis.

2015-08-07 | E-GEOD-68808 | biostudies-arrayexpress

SS18 regulates pluripotent-somatic transition through phase separation

Project description:The transition from pluripotent to somatic states marks a critical event in mammalian development, but remains largely unresolved. Here we report the identification of SS18 as a regulator for pluripotent to somatic transition or PST by CRISPR-based whole genome screens. Mechanistically, SS18 forms microscopic condensates in nuclei through a C-terminal intrinsically disordered region (IDR) rich in tyrosine, which, once mutated, no longer form condensates nor rescue SS18-/- defect in PST. Yet, the IDR alone is not sufficient to rescue the defect even though it can form condensates indistinguishable from the wild type protein. We further show that its N-terminal 70aa is required for PST by interacting with BAF complex, and remains functional even swapped onto unrelated IDRs or even an artificial 24 tyrosine polypeptide. Finally, we show that SS18 mediates BAF assembly through phase separation to regulate PST. These studies suggest that SS18 plays a role in the pluripotent to somatic interface and undergoes liquid-liquid phase separation through a unique tyrosine-based mechanism.

2021-05-23 | PXD026208 |

Tet1 as a Negative Regulator of 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 regulation1-5.M-BM- As somatic cell reprogramming involves the re-activation of pluripotency genes and the silencing of somatic ones6, it remains unclear whether Tet1 plays a positive or negative role in the reprogramming process. Here we show that Tet1 deficiency enhances reprogramming and its overexpression impairs reprogramming. Mechanistically, we demonstrated that Tet1 represses the early obligatory process of mesenchymal to epithelial transition (MET) during reprogramming7,8. Thus, our findings not only define a negative role for Tet1 in somatic cell reprogramming, but also suggest that the Tet enzymes regulate cell fate through distinctive mechanisms. Examination of genome DNA hmC modifications in 2 conditions: individually overexpressed Tet1CD or Tet2CD during MEF reprogramming; Examination of mRNA levels in five different conditions: individually overexpressed DR or Tet1CD or Tet1CDmut or Tet2CD or Tet2CDmut, during MEF reprogrammig.

2013-03-08 | E-GEOD-44935 | biostudies-arrayexpress

Architecture of Epigenetic Reprogramming Following Twist1 Mediated Epithelial-Mesenchymal Transition

Project description:Architecture of Epigenetic Reprogramming Following Twist1 Mediated Epithelial-Mesenchymal Transition

| PRJNA230687 | ENA

Progesterone inhibits epithelial-to-mesenchymal transition in endometrial cancer

Project description:This SuperSeries is composed of the following subset Series: GSE29435: Progesterone inhibits epithelial-to-mesenchymal transition in endometrial cancer: cell line data GSE29436: Progesterone inhibits epithelial-to-mesenchymal transition in endometrial cancer: patient data Refer to individual Series

2012-01-26 | E-GEOD-29437 | biostudies-arrayexpress

Loss of ATM accelerates pancreatic cancer formation and epithelial–mesenchymal transition

2015-08-07 | GSE68808 | GEO