Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Regulation of the oxidative stress response by the E3 ligase TRIP12

ABSTRACT: Regulation of the oxidative stress response by the E3 ligase TRIP12

PROVIDER: PRJNA1182683 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Regulation of the oxidative stress response by the E3 ligase TRIP12

Project description:Centered on the transcription factor NRF2, the oxidative stress response counteracts reactive oxygen species (ROS) to ensure cell and tissue homeostasis. While unstressed cells constantly degrade NRF2, ROS inhibit the respective E3 ligase, CUL3KEAP1, to stabilize NRF2 and elicit antioxidant gene expression. Following ROS clearance, cells must rapidly reinstate NRF2 degradation, but mechanisms underlying this dynamic regulation are poorly understood. Here, we identify TRIP12, an essential E3 ligase dysregulated in Clark-Baraitser Syndrome and Parkinson’s Disease, as a component of the oxidative stress response. TRIP12 is a ubiquitin chain elongation factor that acts after CUL3KEAP1 to extend K29-linked conjugates for efficient NRF2 degradation. TRIP12 accelerates stress response silencing as CUL3KEAP1 is being restored, but limits NRF2 activation during stress. The need for dynamic NRF2 regulation therefore comes at the cost of less responsive stress signaling, suggesting that TRIP12 inhibition could be exploited to bolster the oxidative stress response in neurodegenerative diseases.

2025-08-12 | GSE281184 | GEO

Trip12 deficiency effect on embryonic stem cell line

Project description:Analysis of E14 embryonic stem cells lacking Trip12 ubiquitin ligase activity. We used microarrays to detail the global gene expression profiles affected by Trip12 ubiquitin ligase activity in mouse embryonic stem cell. Total RNA was extracted from wild-type and Trip12 mutant mouse embryonic stem cells and hybridized on Affymetrix microarrays.

2014-01-01 | E-GEOD-27527 | biostudies-arrayexpress

E3 ubiquitin ligase TRIP12 catalyzes non-canonical lysine-independent ubiquitin-ubiquitin linkages in vitro

Project description:Mass spectrometry raw data and proteomic results relating to: E3 ubiquitin ligase TRIP12 catalyzes non-canonical lysine-independent ubiquitin-ubiquitin linkages in vitro

2025-05-23 | MSV000097978 | MassIVE

Transcriptomic profiling of human pancreatic cancer-derived cell lines PANC-1 depleted of TRIP12 mRNA compared to control cells

Project description:TRIP12 (Thyroid hormone Receptor Interacting Protein) is an E3 ubiquitin ligase involved in numerous cellular processes. TRIP12 controls the stability of the PTF1A transcription factor that is implicated in pancreatic cancer initiation. To elucidate the role of TRIP12 on the expression of pancreatic cancer-derived cell lines, Trip12 mRNA expression was inhibited using a shRNA strategy. Transcriptomic profiling of shTrip12-PANC-1 cell s was perfomed and compared to ShScramble control cells.

2024-04-19 | GSE147717 | GEO

Transcriptomic profiling of human pancreatic cancer-derived cell lines MiaPACA-2 depleted of TRIP12 mRNA compared to control cells

Project description:TRIP12 (Thyroid hormone Receptor Interacting Protein) is an E3 ubiquitin ligase involved in numerous cellular processes. TRIP12 controls the stability of the PTF1A transcription factor that is implicated in pancreatic cancer initiation. To elucidate the role of TRIP12 on the expression of pancreatic cancer-derived cell lines, Trip12 mRNA expression was inhibited using a shRNA strategy. Transcriptomic profiling of shTrip12-MiaPACA-2 cell s was perfomed and compared to ShScramble control cells.

2024-04-19 | GSE147549 | GEO

Trip12 deficiency effect on embryonic stem cell line

2014-01-01 | GSE27527 | GEO

Effect of depletion of TRIP12 on gene expression in adult murine pancreatic acinar cells and murine pancreatic cancer cell lines

Project description:To investigate the role of the E3 ubiquitin ligase Thyroid Receptor Interacting Protein 12 (TRIP12) in pancreatic acinar cell identity and pancreatic carcinogenesis, we used genetically engineered mouse models of pancreas-selective Trip12 deletion, mutant Kras (G12D) and mutant P53 (R172H). We performed gene expression analysis using RNA-seq data from adult acinar cells. We established cell lines from murine pancreatic tumors.

2024-04-19 | GSE221587 | GEO

E3 ubiquitin ligase TRIP12 controls protein translation and promotes cancer cell survival via a potential mTOR/G3BP1 nexus

Project description:Mass spectrometry data and proteomic results relating to the manuscript: E3 ubiquitin ligase TRIP12 controls protein translation and promotes cancer cell survival via a potential mTOR/G3BP1 nexus

2025-06-19 | MSV000098264 | MassIVE

E3 ligase TRIP12 affecting EZH2 ubiquitination in ENKTL

Project description:Effects of potential E3 ligase that mediates polyubiquitination of EZH2 in extranodal natural killer T cell lymphoma

2023-10-14 | PXD046145 |

E3 Ubiquitin Ligase TRIP12: Regulation, Structure, and Physiopathological Functions.

Project description:The Thyroid hormone Receptor Interacting Protein 12 (TRIP12) protein belongs to the 28-member Homologous to the E6-AP C-Terminus (HECT) E3 ubiquitin ligase family. First described as an interactor of the thyroid hormone receptor, TRIP12's biological importance was revealed by the embryonic lethality of a murine model bearing an inactivating mutation in the TRIP12 gene. Further studies showed the participation of TRIP12 in the regulation of major biological processes such as cell cycle progression, DNA damage repair, chromatin remodeling, and cell differentiation by an ubiquitination-mediated degradation of key protein substrates. Moreover, alterations of TRIP12 expression have been reported in cancers that can serve as predictive markers of therapeutic response. The TRIP12 gene is also referenced as a causative gene associated to intellectual disorders such as Clark-Baraitser syndrome and is clearly implicated in Autism Spectrum Disorder. The aim of the review is to provide an exhaustive and integrated overview of the different aspects of TRIP12 ranging from its regulation, molecular functions and physio-pathological implications.

| S-EPMC7697007 | 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