Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

HFD activated FAO mediates intestinal stemness and tumorgenicity II

ABSTRACT: HFD activated FAO mediates intestinal stemness and tumorgenicity II

PROVIDER: PRJNA634507 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11830346.fastq.gz	Fastqsanger.gz
	SRR11830347.fastq.gz	Fastqsanger.gz
	SRR11830348.fastq.gz	Fastqsanger.gz
	SRR11830349.fastq.gz	Fastqsanger.gz
	SRR11830350.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 38

Similar Datasets

HFD activated FAO mediates intestinal stemness and tumorgenicity

Project description:HFD activated FAO mediates intestinal stemness and tumorgenicity

| PRJNA634505 | ENA

HFD activated FAO mediates intestinal stemness and tumorgenicity I

Project description:HFD activated FAO mediates intestinal stemness and tumorgenicity I

| PRJNA634508 | ENA

HFD activated FAO mediates intestinal stemness and tumorgenicity II

Project description:Obesity is an established risk factor for cancer in many tissues such as the gastrointestinal tract. In the mammalian intestine, a pro-obesity high fat diet (HFD) promotes tumorigenesis in part by enhancing intestinal stem cell (ISC) numbers, proliferation and function. Although Ppar (Peroxisome proliferator-activated receptor) nuclear receptor activity has been proposed to mediate some of these effects in HFD ISCs, the exact role that different Ppar family members play in this process is unclear. Here, we find that in loss-of-function in vivo models, both Ppar family members alpha and delta contribute to the HFD response in ISCs. Mechanistically, both PPARs do so by robustly inducing a downstream fatty acid oxidation (FAO) metabolic program. Notably, pharmacologic and genetic disruption of CPT1a (the rate limiting enzyme of FAO) blunts the HFD phenotype in ISCs. Furthermore, just as HFD ISCs depend on CPT1a-mediated FAO, inhibition of CPT1a dampens the pro-tumorigenic consequences of a HFD on early tumor incidence and progression in the intestine. These findings demonstrate that inhibition of a HFD activated FAO program creates a therapeutic opportunity to counter the effects of a HFD on ISCs and intestinal tumorigenesis.

2021-06-01 | GSE151046 | GEO

HFD activated FAO mediates intestinal stemness and tumorgenicity I

2021-06-01 | GSE151045 | GEO

High-fat diet activated fatty acid oxidation mediates intestinal stemness and tumorigenicity

2021-06-01 | GSE167996 | GEO

HFD activated FAO mediates intestinal stemness and tumorgenicity

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

2021-06-01 | GSE151047 | GEO

High-fat diet activated fatty acid oxidation mediates intestinal stemness and tumorigenicity

Project description:High-fat diet activated fatty acid oxidation mediates intestinal stemness and tumorigenicity

| PRJNA705719 | ENA

High-fat diet activated fatty acid oxidation mediates intestinal stemness and tumorigenicity

Project description:High-fat diet activated fatty acid oxidation mediates intestinal stemness and tumorigenicity

| PRJNA692179 | ENA

10nM insulin stimulation of Fao Cells

Project description:To confirm how many and what kind of gene changes within 1 hour treatment of insulin stimulation, we have performed whole genome microarray expression profiling. And we found that 276 genes increased (>2 fold) or decreased (<0.5 fold) 10nM insulin induced gene expression in Fao cells was measured at 0, 15, 30, 45, 60 min.

2014-07-01 | E-GEOD-58302 | biostudies-arrayexpress

Phosphoribotrap-based profiling of activated hypothalamic cells during acute high-fat diet (HFD)-feeding

Project description:To identify novel neurocircuits activated upon short-term HFD feeding, we employed phosphoribotrap-profiling, which allows for the unbiased identification of alterations in neuronal activation via immunoprecipitation of phosphorylated S6 ribosomal protein-tagged ribosomes from hypothalamic extracts of mice exposed to either 3 days of normal chow diet or HFD-feeding. We have analyzed mRNA selectively expressed in hypothalamic cells activated by a either normal chow diet (NCD)-feeding for 3 days or high fat diet (HFD)-feeding for 3 days. 10-week-old male C57/BL6N mice were put either on a normal chow diet or a high fat diet for 3 days. Afterwards, mice were sacrificed by cervical dislocation. The hypothalamus was rapidly dissected using a stainless steel brain matrix and immediately frozen in liquid nitrogen. Hypothalamic tissues were pooled (8 per IP).

2020-04-16 | GSE137737 | 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