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Inhibition of Phosphoinositide-3-kinase signaling promotes the stem cell state of trophoblast

ABSTRACT: Inhibition of Phosphoinositide-3-kinase signaling promotes the stem cell state of trophoblast

PROVIDER: PRJNA515820 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8454030.fastq.gz	Fastqsanger.gz
	SRR8454031.fastq.gz	Fastqsanger.gz
	SRR8454032.fastq.gz	Fastqsanger.gz
	SRR8454033.fastq.gz	Fastqsanger.gz
	SRR8454034.fastq.gz	Fastqsanger.gz

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Inhibition of Phosphoinositide-3-kinase signaling promotes the stem cell state of trophoblast

Project description:We found that PI3K inhibition increased the expression of stem cell markers in trophoblast stem cells (TSCs). To better understand the PI3K inhibited cells, we compared untreated TSCs with cells treated with PI3K inhibitor ZSTK474 for 3h, 6h and 3 days.

2019-05-30 | GSE125301 | GEO

Phosphatidylinositol 3-kinase modulation of trophoblast cell differentiation

Project description:Rcho-1 trophoblast stem cells can be maintained in a trophoblast stem cell state or induced to differentiate into trophoblast giant cells. During the differentiation process the PI3K pathway is constitutively activated. Microarray analysis of stem, differentiated and differentiated Rcho-1 trophoblast stem cells treated with the PI3K inhibitor LY294002.

2010-09-15 | GSE21938 | GEO

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Project description:FLT3 is a receptor tyrosine kinase that is frequently mutated in AML. Inhibition of FLT3 induces myeloid differentiation in AML patients. We identified a role of FLT3 inhibition in decreasing EZH2 expression. To assess the impact of this regulation on PRC2 function, we performed H3K27me3 ChIP-Seq in a FLT3 mutated human AML cell line.

2024-01-03 | GSE243857 | GEO

MAP3K4 Kinase Activity Controls Chromatin Remodelers for Transitions Between Epithelial and Mesenchymal Phenotypes in Trophoblast Stem Cells [ChIP-Seq]

Project description:MAP3K4 is a serine/threonine kinase that regulates epithelial to mesenchymal transition (EMT). Trophoblast stem (TS) cells lacking MAP3K4 kinase activity (TSKI4 cells) are in an intermediate state of EMT, having reduced epithelial and increased mesenchymal marker expression. Reduced epithelial gene expression in TSKI4 cells was due to loss of H2BK5 promoter acetylation catalyzed by the histone acetyltransferase CBP. Herein, we show that MAP3K4 also regulates the ubiquitination and degradation of the deacetylase HDAC6. Due to the loss of MAP3K4 kinase activity, TSKI4 cells have elevated HDAC6 expression and activity. Knockdown of HDAC6 in TSKI4 cells restores epithelial features, defining HDAC6 as a key regulator of EMT controlled by MAP3K4. HDAC6 promotes EMT by directly deacetylating H2BK5 on promoters of tight junction genes claudin6 and occludin, inhibiting their expression. Thus, MAP3K4 is a master regulator that coordinates chromatin modifiers, CBP and HDAC6, to regulate the transition between epithelial and mesenchymal states.

2017-03-07 | GSE92394 | GEO

MAP3K4 Kinase Activity Controls Chromatin Remodelers for Transitions Between Epithelial and Mesenchymal Phenotypes in Trophoblast Stem Cells [RNA-Seq]

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Glycolysis Promotes Phosphoinositide 3-Kinase Signaling In Support of T Helper 17 Cell-Mediated Autoimmunity

Project description:T helper (Th) cell differentiation is driven by antigen and accessory signals that activate phosphoinositide 3-kinase (PI3K) to induce transcriptional and metabolic reprogramming including aerobic glycolysis (the Warburg effect). Here, we show that ATP generated through glycolysis fuels PI3K signaling to promote pathogenic Th17 cell responses. Mice with T cell-specific ablation of the glycolytic enzyme lactate dehydrogenase A (LDHA) were resistant to Th17 cell-mediated experimental autoimmune encephalomyelitis in association with defective T cell activation, migration, proliferation, and differentiation. LDHA deficiency crippled the cellular redox balance and inhibited ATP production causing attenuated phosphoinositide (3,4,5)-trisphosphate generation, and diminished activation of the Akt kinase and phosphorylation of its transcription factor target Foxo1. Th17 cell-specific expression of an Akt-insensitive Foxo1 mutant recapitulated the Th17 cell differentiation defects caused by LDHA deficiency. Thus, PI3K signaling and glycolytic bioenergetics constitute a positive feedback regulatory circuit essential for Th17 cell-mediated autoimmunity.

2021-03-27 | GSE164959 | GEO

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