Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The essential clathrin adaptor protein complex-2 is tumor suppressive specifically in vivo

ABSTRACT: The essential clathrin adaptor protein complex-2 is tumor suppressive specifically in vivo

PROVIDER: PRJNA975168 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24687100_1.fastq.gz	Fastqsanger.gz
	SRR24687100_2.fastq.gz	Fastqsanger.gz
	SRR24687101_1.fastq.gz	Fastqsanger.gz
	SRR24687101_2.fastq.gz	Fastqsanger.gz
	SRR24687102_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 288

Similar Datasets

The essential clathrin adaptor protein complex-2 is tumor suppressive specifically in vivo [CRISPR Screen]

Project description:The essential clathrin adaptor protein complex-2 is tumor suppressive specifically in vivo [CRISPR Screen]

| PRJNA1224449 | ENA

The essential clathrin adaptor protein complex-2 is tumor suppressive specifically in vivo

Project description:The microenvironment is a rich source of new cancer targets. While whole-genome CRISPR/Cas9 screens have identified vulnerabilities in cultured cells, it is a challenge to use this approach in tumors to interrogate the microenvironment. To this end, we screened a panel of pancreatic cancer lines grown in culture versus as tumors with a phosphatidylinositol metabolism CRISPR/Cas9 library. This revealed the Adaptor Protein complex-2 (AP2) of clathrin-mediated endocytosis behaves as common essential in culture but tumor suppressive in vivo. These polar-opposite phenotypes were attributed to different microenvironments. In culture, AP2 loss reduces endocytosis of transferrin and iron import. In tumors, alternative iron transport pathways allow pro-tumor signaling to manifest. In the most sensitive case, AP2 loss reprograms the plasma membrane proteome, retaining integrins on the surface leading to downregulation of the tumor-suppressor PTEN. Analysis of human tumors suggests a similar tumor suppressive activity. AP2 may foreshadow other proteins unique to the tumor-microenvironment.

2024-12-12 | GSE233173 | GEO

The essential clathrin adaptor protein complex-2 is tumor suppressive specifically in vivo [CRISPR Screen]

2025-02-21 | GSE289756 | GEO

The essential clathrin adapter protein complex-2 is tumor suppressive specifically in vivo.

Project description:The microenvironment is a rich source of new cancer targets. We thus used a targeted single-guide RNA library to screen a panel of human pancreatic cancer lines for genes uniquely affecting tumorigenesis. Here we show inactivation of the Adapter Protein complex-2 of clathrin-mediated endocytosis reduces cell growth in vitro, but completely oppositely, promotes tumor growth in vivo. In culture, loss of the complex reduces transferrin endocytosis and iron import required for cell fitness. In tumors, alternative iron transport pathways allow pro-tumor effects of Adapter Protein complex-2 loss to manifest. In the most sensitive case, this is attributed to reprogramming the plasma membrane proteome, retaining integrins on the surface leading to Focal Adhesion Kinase phosphorylation and induction of proliferative signals. Adapter Protein complex-2 function in tumorigenesis is thus dependent upon the microenvironment, behaving as a common essential gene in culture via iron import, but as a tumor suppressor in tumors via integrin trafficking.

| S-EPMC11885535 | biostudies-literature

Mitochondrial complex III is essential for regulatory T cell suppressive function

Project description:Mitochondrial complex III is essential for regulatory T cell suppressive function

| PRJNA493083 | ENA

Mitochondrial complex III is essential for regulatory T cell suppressive function. [DNA methylation/RRBS]

Project description:Regulatory T cells (Treg cells), a distinct subset of CD4+ T cells, are necessary for the maintenance of immune self-tolerance and homeostasis. Recent studies have demonstrated that Treg cells display a unique metabolic profile characterized by an increase in mitochondrial metabolism relative to other CD4+ effector subsets. Furthermore, the Treg cell lineage-defining transcription factor, Foxp3, has been shown to promote respiration; however, it remains unknown whether the mitochondrial respiratory chain is required for Treg cell suppressive capacity, stability, and survival. Here we report that Treg cell-specific ablation of mitochondrial respiratory chain complex III results in the development of a fatal inflammatory disease early in life, without impacting Treg cell number. Mice lacking complex III specifically in Treg cells displayed a loss of Treg cell suppressive capacity without altering Treg cell proliferation and survival. Treg cells deficient in complex III display decreased expression of genes associated with Treg function while maintaining stable FOXP3 expression. Complex III-null Treg cells displayed increased DNA methylation at the loci of differentially down-regulated genes without a global increase in DNA methylation. Loss of complex III in Treg cells resulted in buildup of the metabolites 2-hydroxyglutarate (2-HG) and succinate that can function as inhibitors of α-ketoglutarate (α−KG)-dependent dioxygenase reactions such as the ten-eleven translocation (TET) family of DNA demethylases. Thus, Treg cells require mitochondrial respiration to maintain immune regulatory gene expression and suppressive function.

2018-12-18 | GSE120451 | GEO

Mitochondrial complex III is essential for regulatory T cell suppressive function. [gene expression/RNA-seq]

2018-12-18 | GSE120449 | GEO

Mitochondrial complex III is essential for regulatory T cell suppressive function. [DNA methylation/RRBS]

Project description:Mitochondrial complex III is essential for regulatory T cell suppressive function. [DNA methylation/RRBS]

| PRJNA493088 | ENA

Mitochondrial complex III is essential for regulatory T cell suppressive function. [gene expression/RNA-seq]

Project description:Mitochondrial complex III is essential for regulatory T cell suppressive function. [gene expression/RNA-seq]

| PRJNA493086 | ENA

Adaptor candidates

Project description:IP of candidate adaptor Ada5/Gdi1, tagged with HA, versus Mock (untagged) replicates. IP associated RNA was assayed. A replicate experimental design type is where a series of replicates are performed to evaluate reproducibility or as a pilot study to determine the appropriate number of replicates for a subsequent experiments. GeneticModification: HA-tagged candidate gene or control replicate_design

2012-11-15 | E-GEOD-33747 | 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