Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteome changes upon knockdown of ubiquitin E3 ligases

ABSTRACT: Proteome analysis upon knockdown of UBR1, UBR2, UBR4, UBR5, KCMF1, UBE4B, TRIP12

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

SUBMITTER: Takuya Tomita

LAB HEAD: Yasushi Saeki

PROVIDER: PXD066132 | Pride | 2025-08-18

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	20250501_Ding_Zoom_20SPD_DIA.msf	Msf
	20250501_Ding_Zoom_20SPD_DIA.pep.xml	Pepxml
	20250501_Ding_Zoom_20SPD_DIA_HCT116_siControl-1.raw	Raw
	20250501_Ding_Zoom_20SPD_DIA_HCT116_siControl-2.raw	Raw
	20250501_Ding_Zoom_20SPD_DIA_Ub-GFP_siControl-1.raw	Raw

Items per page:

1 - 5 of 21

Similar Datasets

Interactome of Ub-GFP and Ub-GFP-tail

Project description:Immunoprecipitation of Ub-GFP and Ub-GFP-tail expressed in HCT116 cells using GFP-Trap.

2025-08-18 | PXD066134 | Pride

Interactome analysis of GST-UFD1-NBM

Project description:GST pull-down assay using crude extracts from HCT116 cells to analyze the selectivity of the UFD1-NBM peptide in a cellular context.

2025-06-03 | PXD063521 | Pride

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

RNAi Screening for Ubiquitin Ligases that Regulate Myofiber Size Identifies a Key Role for UBR4 in Myofiber Hypertrophy in Drosophila and Mice

Project description:Sequencing of RNA isolated from the tibialis anterior muscles of 6 month old C57BL/6J mice that had been injected and electroporated with either a control non-targeting siRNA (NT) or two different UBR4 targeting siRNA sequences (UBR4 siRNA5 and siRNA7) to deplete UBR4. Muscles were harvested 7 days after electroporation and showed significant loss of UBR4 coincident with hypertrophy of type 2A and 2X myofibers.

2019-03-01 | GSE126922 | GEO

Identification of defective proteins trapped by TanGIBLE

Project description:To identify an uncharacterized endogenous defective protein pool, we immunoprecipitated Flag-tagged TanGIBLE from HeLa cell extracts, and co-immunoprecipitated proteins werer subjected to LC-MS/MS analysis.

2024-12-25 | PXD057470 | Pride

Downregulation of calcium-activated potassium channels drives cortical excitability dysfunction in a model of Itgb3-associated autism

Project description:Layer V pyramidal neurons, particularly pyramidal tract (PT) neurons, are essential for cortical output. Genetic studies have linked ITGB3, the gene encoding the cell-adhesion molecule β3 integrin, to autism spectrum disorder (ASD), yet its role in brain function remains poorly understood. Here, we investigate β3 integrin function in the prefrontal cortex, revealing its selective regulation of PT neuron excitability. β3 integrin modulates action potential (AP) discharge through its interaction with Ca2+-activated SK2 channels. Genetic ablation of Itgb3 reduces SK2 channel surface expression, impairing the gain, adaptation and precision of AP discharge in PT neurons. Phosphoproteomic analysis reveals altered protein kinase A (PKA)-dependent phosphorylation of Tau in Itgb3 KO mice, while PKA inhibition restores SK2 channel currents, linking phosphorylation changes to excitability defects. These findings identify a novel β3 integrin-dependent signaling pathway as a selective key modulator of PT neuron function, and provide insight into the cellular mechanisms linking dysfunction in cortical output to ASD.

2025-10-13 | PXD056477 | Pride

Chlorin e6-loaded nanostructured lipid carriers targeted by angiopep-2: Advancing photodynamic therapy in glioblastoma

Project description:Glioblastoma (GBM) is a highly aggressive brain tumor known for its resistance to standard treatments. Despite surgery being a primary option, its invasive nature often leads to incomplete removal and high recurrence rates. Photodynamic therapy (PDT) holds promise as an adjunctive treatment, but safety concerns and the need for high-power lasers have limited its widespread use. Our research addresses these challenges by introducing a novel PDT approach using chlorin e6 enclosed in nanostructured lipid carriers (Ang-Ce6-NLCs) and targeted to GBM with the angiopep-2 peptide. Remarkably, a single 5-min irradiation session with LEDs at 660 nm and low power density (10 mW/cm²) proved effective against GBM, while reducing safety risks associated with high-power lasers. Encapsulation improves Ce6 stability and performance in physiological environments, while angiopep-2 targeting enhances delivery to GBM cells, maximizing treatment efficacy and minimizing off-target effects. Our findings demonstrate that Ang-Ce6-NLCs-mediated PDT brings about a significant reduction in GBM cell viability, increased oxidative stress, reduced tumor migration, and enhanced apoptosis. Overall, such treatment holds potential as a safe and efficient GBM therapy, using low-power LED light to minimize harm to surrounding healthy tissue while maximizing tumor treatment.

2024-10-02 | PXD053482 | Pride

Early IGF-1 receptor inhibition in mice mimics preterm human brain disorders and reveals a new therapeutic target

Project description:Besides recent advances in neonatal care, preterm newborns still develop sex-biased behavioural alterations. Preterms fail to receive placental insulin-like growth factor-1 (IGF-1), a major fetal growth hormone in utero, and low IGF-1 serum levels correlate with preterm poor neurodevelopmental outcomes. Here, we mimicked IGF-1 deficiency of preterm newborns in mice by perinatal administration of an IGF-1 receptor antagonist. This resulted in sex-biased brain microstructural, functional, and behavioural alterations, resembling those of ex-preterm children, which we characterized performing parallel mouse/human behavioural tests. Pharmacological enhancement of GABAergic tonic-inhibition by the FDA-approved drug ganaxolone rescued functional/behavioural alterations in mice. Establishing an unprecedented mouse model of prematurity, our work dissects the mechanisms at the core of abnormal behaviours and identifies a new, readily-translatable therapeutic strategy for preterm brain disorders.

2024-06-16 | PXD047222 | Pride

Early IGF-1 receptor inhibition in mice mimics preterm human brain disorders and reveals a new therapeutic target

2024-06-16 | PXD047704 | Pride

Expression data from 17 day old testes of wild type and UBR2-/- mice

Project description:Ubiquitylation of histones provides an important mechanism regulating chromatin remodeling and gene expression. Recent studies have revealed ubiquitin ligases involved in histone ubiquitylation, yet the responsible enzymes and the function of histone ubiquitination in spermatogenesis remain unclear. Here we show that the ubiquitin ligase UBR2, one of the recognition E3 components of the N-end rule proteolytic pathway, localizes to meiotic chromatin regions, including unsynapsed axial elements linked to chromatin inactivation, and mediates, in combination with the ubiquitin-conjugating enzyme HR6B, the ubiquitination of histone H2A. UBR2 interacts with HR6B and H2A and promotes the HR6B-H2A interaction and the HR6B-to-H2A transfer of ubiquitin. UBR2 and ubiquitinated H2A (uH2A) spatiotemporally mark meiotic chromatin regions subject to transcriptional silencing, and UBR2-deficient spermatocytes fail to induce the ubiquitination of H2A during meiosis. UBR2-deficient spermatocytes are profoundly impaired in transcriptional silencing of genes linked to unsynapsed axes of the X and Y chromosomes. We propose a model, in which UBR2 on axial elements of the X-Y pair enables HR6B on the linked chromatin domain to repeat histone ubiquitination cycles while scanning a string of nucleosomes. Our results suggest that histone ubiquitination in germ cells may be mediated by E3-E2 pairs distinct from those in somatic cells, providing a new insight into chromatin remodeling and gene expression regulation.

2009-12-31 | GSE18824 | 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