Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TXNIP loss

ABSTRACT: TXNIP loss

PROVIDER: PRJNA923024 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23054920_1.fastq.gz	Fastqsanger.gz
	SRR23054920_2.fastq.gz	Fastqsanger.gz
	SRR23054921_1.fastq.gz	Fastqsanger.gz
	SRR23054921_2.fastq.gz	Fastqsanger.gz
	SRR23054922_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

TXNIP loss expands Myc transcriptome

Project description:TXNIP loss expands Myc transcriptome

| PRJNA923027 | ENA

TXNIP loss increases Myc genomic occupancy [ChIP-seq]

Project description:Our RNA sequencing result demonstrated that TXNIP loss increased the levels of Myc-dependent transcription. To determine whether TXNIP regulates global Myc genomic occupancy, we performed Myc ChIP-seq on parental 231 and 231:TKO cells.

2023-02-07 | GSE208412 | GEO

TXNIP loss does not increase chromatin accessibility for Myc binding.

Project description:Our Myc ChIP sequencing result demonstrated that TXNIP loss increased Myc genomic occupancy levels. To determine whether TXNIP loss increased Myc genomic occupancy through increasing chromatin accessibility for Myc binding, we performed assay for transposase-accessible chromatin with sequencing (ATAC-seq) on parental 231 and 231:TKO cells.

2023-02-07 | GSE222672 | GEO

TXNIP loss expands Myc transcriptome [RNA-seq]

Project description:TXNIP loss expands Myc transcriptome [RNA-seq]

| PRJNA859857 | ENA

TXNIP loss expands Myc transcriptome

Project description:To examine the generality of our finding where the gene expression profile of TXNIP knockout in MDA-MB-231 cells resembles of that Myc overexpression transcriptional program, our lab has generated TXNIP null HCC70 (HCC70:TKO) and MB135 (MB135:TKO) cells. We characterized the gene exrpession programs of these cells by RNA-seq.

2023-02-07 | GSE222693 | GEO

TXNIP loss increases Myc genomic occupancy [ChIP-seq]

Project description:TXNIP loss increases Myc genomic occupancy [ChIP-seq]

| PRJNA859844 | ENA

TXNIP loss expands Myc transcriptome [RNA-seq]

Project description:To better understand how TXNIP in the contributes to the poor prognosis of triple-negative breast cancers, our lab has generated TXNIP null MDA-MB-231 cells (231:TKO). We characterized the gene exrpession programs of these cells by RNA-seq. To determine the Myc-dependence of the transcriptional programs of 231:TKO cells, we used an siRNA RNA approach to reduce Myc levels.

2023-02-07 | GSE208415 | GEO

Secretome from TXNIP knockout human colorectal cell line (DLD1)

Project description:Chemotherapy, the standard of care treatment for cancer patients with advanced disease, has been increasingly recognised to activate host immune responses to produce durable outcomes. Here, in colorectal adenocarcinoma (CRC) we identify oxaliplatin-induced Thioredoxin Interacting Protein (TXNIP), a MondoA-dependent tumor suppressor gene, as a negative regulator of Growth/Differentiation Factor 15 (GDF15). GDF15 is a negative prognostic factor in CRC and promotes the differentiation of regulatory T cells (Tregs), which inhibit CD8 T cell activation. Intriguingly, multiple models including patient-derived tumor organoids demonstrate that the loss of TXNIP and GDF15 responsiveness to oxaliplatin is associated with advanced disease or chemotherapeutic resistance, with transcriptomic or proteomic GDF15/TXNIP ratios showing potential as a prognostic biomarker. These findings illustrate a potentially common pathway where chemotherapy-induced epithelial oxidative stress drives local immune remodelling for patient benefit, with disruption of this pathway seen in refractory or advanced cases.

2024-08-12 | PXD051666 | Pride

TXNIP loss does not increase chromatin accessibility for Myc binding.

Project description:TXNIP loss does not increase chromatin accessibility for Myc binding.

| PRJNA922999 | ENA

TXNIP mediates LAT1/SLC7A5 endocytosis to limit amino acid uptake in cells entering quiescence

Project description:Entry and exit from cellular quiescence require dynamic adjustments in nutrient acquisition, yet the mechanisms by which quiescent cells downregulate amino acid (AA) transport remain poorly understood. Here we show that cells entering quiescence selectively target plasma membrane-resident AA transporters for endocytosis and lysosomal degradation. This process matches AA uptake with reduced translational demand and promotes survival during extended periods of quiescence. Mechanistically, we identify the α-arrestin TXNIP as a key regulator of this metabolic adaptation, since it mediates the endocytosis of the SLC7A5-SLC3A2 (LAT1-4F2hc) AA transporter complex in response to reduced AKT signaling. To promote transporter ubiquitination, TXNIP interacts with NEDD4L and other HECT-type ubiquitin ligases. Loss of TXNIP disrupts this regulation, resulting in dysregulated AA uptake, sustained mTORC1 signaling, and ultimately cell death under prolonged quiescence. The characterization of a novel TXNIP loss-of-function variant in a patient with a severe metabolic disease further supports its role in nutrient homeostasis and human health. Together, these findings highlight TXNIP's central role in controlling nutrient acquisition and metabolic plasticity with implications for quiescence biology and diseases.

2025-12-08 | PXD066527 | Pride

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