Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors [single cell RNA-Seq]

ABSTRACT: Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors [single cell RNA-Seq]

PROVIDER: PRJNA779928 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16928942.fastq.gz	Fastqsanger.gz
	SRR16928943.fastq.gz	Fastqsanger.gz

Items per page:

1 - 2 of 2

Similar Datasets

Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors.

Project description:Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors.

| PRJNA779920 | ENA

Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors [bulk RNA-Seq]

Project description:Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors [bulk RNA-Seq]

| PRJNA779929 | ENA

Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors [bulk RNA-Seq]

Project description:Cancers of the gastrointestinal tract including esophageal adenocarcinomas, colorectal cancers, and cancers of the gastric cardia are common comorbidities of obesity. Excessive delivery of macronutrients to the cells lining the gut can increase one’s risk for these cancer by inducing imbalances in the rate of intestinal stem cell proliferation vs. differentiation, which can produce polyps and other aberrant growths. We demonstrate that serine palmitoyltransferase (SPT), which diverts dietary fatty and amino acids into the sphingolipid biosynthesis pathway, is a critical modulator of intestinal stem cell homeostasis. SPT and other enzymes in the biosynthetic pathway are upregulated in human colon tumors. These enzymes produce sphingolipids that serve as pro-stemness signals that stimulate peroxisome-proliferator activated receptor alpha (PPARa)-mediated induction of fatty acid binding protein-1. This increases fatty acid uptake and oxidation and enhances the stemness program. Serine palmitoyltransferase thus serves as a critical link between dietary macronutrients, epithelial regeneration, and cancer risk.

2022-11-01 | GSE188674 | GEO

Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors [single cell RNA-Seq]

2022-11-01 | GSE188675 | GEO

Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors.

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-11-01 | GSE188676 | GEO

Yeast Serine palmitoyl transferase interaction proteomics

Project description:ALFA pulldowns of the Lcb1 subunit of the yeast serine palmitoyltransferase. Wt Lcb1 is compared to a mutant lacking the trans membrane helix 1 of Lcb1 and to control pulldowns lackingthe ALFA tag on Lcb1.

2024-09-12 | PXD048754 | Pride

High-fat diet enhances stemness and tumorigenicity of intestinal progenitors

Project description:Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we find that high fat diet (HFD)-induced obesity augments the numbers and function of Lgr5+ intestinal stem cells (ISCs) of the mammalian intestine. Like HFD, ex vivo treatment of intestinal organoid cultures with palmitic acid (PA), a constituent of the HFD, enhances the self-renewal potential of these organoid bodies. Mechanistically, HFD induces a robust peroxisome proliferator-activated receptor delta (PPAR-delta signature in intestinal stem and progenitor cells and pharmacologic activation of PPAR-delta recapitulates the effects that HFD has on these cells. Interestingly, HFD- and agonist-activated PPAR-delta signaling endows organoid-initiating capacity to non-stem cells and enforced PPAR-delta signaling permits these non-stem cells to form in vivo tumors upon loss of the tumor suppressor Apc. These findings highlight how diet-modulated PPAR-delta activation alters not only the function of intestinal stem and progenitor cells but also their capacity to initiate tumors. mRNA profiles of intestinal stem cells (GFP-Hi) and progenitors (GFP-Low) from WT or HFD fed mice were generated by deep sequencing using HiSeq 2000.

2016-02-16 | E-GEOD-67324 | biostudies-arrayexpress

Serine/Threonine Phosphorylation of RUNX1 Promotes Megakaryocytic Fate in Megakaryocyte-Erythroid Progenitors

Project description:Serine/Threonine Phosphorylation of RUNX1 Promotes Megakaryocytic Fate in Megakaryocyte-Erythroid Progenitors

| PRJNA974359 | ENA

Effect of D-serine on gene expression in Neuro2a cells

Project description:Serine metabolism provides essential metabolites for cellular growth and proliferation, and also produces neurotransmitters. However, how serine metabolism coordinates with functional development of neurons remains unclear. We report neurotransmitter D-serine inhibit growth of immature cells. Metabolomic analysis of neural progenitors revealed that D-serine decreases glycine synthesis thereby diminishes one-carbon metabolism, in which L-serine is a crucial carbon donor. D-serine inhibits one-carbon metabolism by competing transport of cytosolic L-serine to mitochondria, which restrains proliferation and triggers apoptosis of neural progenitors as well as neural tumor cells, but not mature neurons, in vitro and ex vivo. This RNA-seq data supports the idea that D-serine inhibits polarization and growth/proliferation of immature neurons and further indicate that immature neurons counteracts D-serine-induced cellular stress through enhancing mitochondrial function, including energy synthesis.

2024-12-01 | GSE268106 | GEO

High-fat diet enhances stemness and tumorigenicity of intestinal progenitors.

Project description:Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we show that high-fat diet (HFD)-induced obesity augments the numbers and function of Lgr5(+) intestinal stem cells of the mammalian intestine. Mechanistically, a HFD induces a robust peroxisome proliferator-activated receptor delta (PPAR-δ) signature in intestinal stem cells and progenitor cells (non-intestinal stem cells), and pharmacological activation of PPAR-δ recapitulates the effects of a HFD on these cells. Like a HFD, ex vivo treatment of intestinal organoid cultures with fatty acid constituents of the HFD enhances the self-renewal potential of these organoid bodies in a PPAR-δ-dependent manner. Notably, HFD- and agonist-activated PPAR-δ signalling endow organoid-initiating capacity to progenitors, and enforced PPAR-δ signalling permits these progenitors to form in vivo tumours after loss of the tumour suppressor Apc. These findings highlight how diet-modulated PPAR-δ activation alters not only the function of intestinal stem and progenitor cells, but also their capacity to initiate tumours.

| S-EPMC4846772 | biostudies-literature

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