Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The deubiquitinase USP7 stabilizes Maf proteins to promote myeloma cell survival

ABSTRACT: USP7, as a deubiquitination enzyme, controls ubiquitination and stability of Maf family proteins. USP7 promotes Maf transcriptional activity. Moreover, USP7 is overexpressed in multiple myeloma cells and its expression level is negatively correlated to the survival of myeloma patients.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell

DISEASE(S): Multiple Myeloma

SUBMITTER: Jiefei Tong

LAB HEAD: Mike Moran

PROVIDER: PXD016020 | Pride | 2019-12-16

REPOSITORIES: pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	Biyin-MG1321st.raw	Raw
	Biyin-MG1322nd.raw	Raw
	Biyin-MG1323rd.raw	Raw
	Biyin-MafB1st.raw	Raw
	Biyin-MafB2nd.raw	Raw

Items per page:

1 - 5 of 10

Publications

The deubiquitinase USP7 stabilizes Maf proteins to promote myeloma cell survival.

He Yuanming Y Wang Siyu S Tong Jiefei J Jiang Shuoyi S Yang Ye Y Zhang Zubin Z Xu Yujia Y Zeng Yuanying Y Cao Biyin B Moran Michael F MF Mao Xinliang X

The Journal of biological chemistry 20191210 7

The Maf proteins, including c-Maf, MafA, and MafB, are critical transcription factors in myelomagenesis. Previous studies demonstrated that Maf proteins are processed by the ubiquitin-proteasome pathway, but the mechanisms remain elusive. This study applied MS to identify MafB ubiquitination-associated proteins and found that the ubiquitin-specific protease USP7 was present in the MafB interactome. Moreover, USP7 also interacted with c-Maf and MafA and blocked their polyubiquitination and degrad ...[more]

PMID: 31822558

Similar Datasets

RNAi knockdown of Tip60 and Usp7 in mouse 3T3-L1 adipocytes

Project description:Knockdown of Tip60 or Usp7 in differentiated 3T3-L1 adipocytes

2013-08-28 | E-TABM-1145 | biostudies-arrayexpress

USP7 cooperates with SCML2 to regulate the activity of PRC1

Project description:In this experiment, we sought to identify the distribution of USP7 on chromatin relative to other PRC1 components ChIP-seq for USP7 in 293T-REx cells

2015-06-10 | E-GEOD-61048 | biostudies-arrayexpress

Microarry from Treg with conditional knockout of Usp7

Project description:Microarry from Treg with conditional knockout of Usp7 RNA from three independent samples from FACS sorted CD4+YFP+ Treg of fl-Usp7/Foxp3cre mice, compared to Foxp3cre control (C57BL/6 background).

2015-09-15 | E-GEOD-72988 | biostudies-arrayexpress

USP7 protects TFEB from proteasome-mediated degradation

Project description:The transcription factor EB (TFEB) is a master regulator of lysosomal biogenesis and autophagy. We identify a distinct nuclear interactome of TFEB, with USP7 emerging as a key post-translational modulator of TFEB. Genetic depletion and inhibition of USP7 reveal its critical role in preserving TFEB stability within both nuclear and cytoplasmic compartments. Specifically, USP7 is identified as the deubiquitinase responsible for removing the K48-linked polyubiquitination signal from TFEB at lysine residues K116, K264, and K274, thereby preventing its proteasomal degradation. Functional assays demonstrate the involvement of USP7 in preserving TFEB-mediated transcriptional responses to nutrient deprivation, while also modulating autophagy flux and lysosome biogenesis. As USP7 is a deubiquitinase that protects TFEB from proteasomal degradation, these findings provide the foundation for therapeutic targeting of the USP7-TFEB axis in conditions characterized by TFEB dysregulation and metabolic abnormalities, particularly in certain cancers.

2024-09-17 | PXD055937 | Pride

YG001: A Usp7-Tip60 pathway regulates early adipogenesis

Project description:USP7, a dominant DUB activity in 3T3-L1 adipocytes and in mouse adipose tissue, increases Tip60 protein levels, and deubiquitinates Tip60 both in intact cells and in vitro. Treatment with a pan deubiquitinase (DUB) inhibitor, or knockdown of USP7, decreases adipogenesis. Transcriptome analysis reveals a common set of cell cycle genes to be co-regulated by both Tip60 and USP7. Knock down of either factor results in impaired mitotic clonal expansion, an early step in adipogenesis. These results therefore reveal deubiquitination of a transcriptional coregulator to be a key mechanism in the regulation of early adipogenesis Mature 3T3-L1 adipocytes were subjected to RNAi-mediated knock down with control(C), USP7(U)- or Tip60(T)-specific oligonucleotides. For this, 4 replicates of differentiated 3T3-L1 cells were transfected with Amaxa technology. Two days after transfection cells were washed twice with PBS twice and lysed in 0.5ml Trizol (Invitrogen). mRNA expression of Tip60 and USP7 was assessed by qRT-PCR. Amplified cRNA samples were labeled with either cy3 or cy5 and put on microarray together with and oppositely labeled common reference sample consisting of cRNA derived from undifferentiated 3T3-L1 cells.

2013-08-28 | E-GEOD-28587 | biostudies-arrayexpress

Molecular basis of USP7 inhibition by selective small molecule inhibitors

Project description:Modification by ubiquitin controls the stability of most cellular proteins, and deregulation contributes to a variety of human diseases such as cancer. Deubiquitinases (DUBs) remove ubiquitin from proteins, and the inhibition of DUBs has been recognized as a therapeutic strategy to induce degradation of specific proteins, a concept extendable to ‘undruggable’ targets such as transcription factors. However, this potential has remained untapped; specific small molecule inhibitors for DUBs are scarce and insights into mechanisms of action are limited. Ubiquitin specific protease (USP) 7 stabilises the oncogenic E3 ligase MDM2 that destabilises the tumour suppressor p53 and inhibition of USP7 results in MDM2 degradation and p53 re-activation in a variety of cancers. We here present two small molecule inhibitors, FT671 and FT827, that inhibit USP7 with nanomolar affinity and display exquisite specificity towards USP7 in vitro and in cells. USP7-inhibitor co-crystal structures reveal that both compounds target the auto-inhibited apo-form of USP7 and bind in proximity to the misaligned catalytic triad in a dynamic hydrophobic pocket that serves as the binding site for the ubiquitin C-terminus. The unique auto-inhibited conformation of apo USP7 differs from other USP DUBs, explaining compound selectivity. Consistent with USP7 target engagement in cells, FT671 destabilises MDM2, stabilises p53 and results in transcription of p53 target genes, induction of the tumour suppressor p21, and tumour growth inhibition in vivo.

2018-04-05 | PXD006418 | Pride

USP7 shRNA knock-down in T-ALL cells [Jurkat_HSB2_shRNA_RNA-seq]

Project description:RNAseq analysis of USP7 shRNA KD in T-ALL cell lines. USP7 shRNAs lentivirus was generated by co-transfecting 293T cells with shRNA vectors (OriGene or Sigma). T-ALL cells were transduced with USP7 shRNA lentivirus and sorted for GFP positive cells five days after transduction or selected by puromycin.

2021-03-09 | GSE148522 | GEO

USP7 represses lineage differentiation genes in mouse embryonic stem cells by both catalytic and non-catalytic activity

Project description:USP7, a ubiquitin-specific peptidase (USP), plays an important role in many cellular processes through its catalytic deubiquitination of various substrates. However, its nuclear function to shape the transcriptional network in mouse embryonic stem cells (mESCs) remains poorly understood. Here, we report that USP7 maintains mESCs identity through both catalytic activity-dependent and -independent repression of lineage differentiation genes. Usp7 depletion attenuates SOX2 level and derepresses lineage differentiation genes thereby compromising mESCs pluripotency. Mechanistically, USP7 deubiquitinates and stabilizes SOX2 to repress mesoendodermal (ME) lineage genes. Moreover, USP7 assembles into RYBP-variant Polycomb repressive complex 1 and contributes to Polycomb chromatin-mediated repression of ME lineage genes in a catalytic activity-dependent manner. Importantly, USP7 deficient in its deubiquitination function is able to maintain RYBP binding to chromatin for repressing primitive endoderm-associated genes. Overall, our study demonstrates that USP7 harbors both catalytic and non-catalytic activity to repress different lineage differentiation genes thereby revealing a previously unrecognized role in controlling gene expression for maintaining mESCs identity.

2023-07-20 | PXD039633 | Pride

USP7 is a tumor-specific WNT activator for APC-mutated colorectal cancer by mediating B-catenin deu

Project description:The tumor suppressor gene adenomatous polyposis coli (APC) is mutated in most colorectal cancers (CRC) resulting in constitutive Wnt activation. To understand the Wnt-activating mechanism of APC mutation, we applied CRISPR/Cas9 technology to engineer various APC-truncated isogenic lines. We find that the β-catenin inhibitory domain (CID) in APC represents the threshold for pathological levels of Wnt activation and tumor transformation. Mechanistically, CID-deleted APC truncation promotes β-catenin deubiquitination through reverse binding of β-TrCP and USP7 to the destruction complex. USP7 depletion in APC-mutated CRC inhibits Wnt activation by restoring β-catenin ubiquitination, drives differentiation and suppresses xenograft tumor growth. Finally, the Wnt-activating role of USP7 is specific to APC mutations, thus can be used as tumor-specific therapeutic target for most CRCs.

2017-11-09 | PXD007947 | Pride

Transcriptome profiling in USP7 inhibitor (P22077)-treated H1299 and HeLa cells

Project description:To investigate the molecular pathway signature responsive to pharmacological inhibition of USP7, we analyzed transcriptome in P22077 (a USP7 selective inhibitor)-treated H1299 and HeLa cells.

2023-09-30 | GSE213931 | 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