| 2010 |
USP10 is a cytoplasmic deubiquitinase that deubiquitinates p53, reversing Mdm2-induced p53 nuclear export and degradation. After DNA damage, USP10 is stabilized and translocates to the nucleus to activate p53; this translocation and stabilization is regulated by ATM-mediated phosphorylation of USP10 at Thr42 and Ser337. |
Co-immunoprecipitation, in vitro deubiquitination assay, subcellular fractionation, ATM kinase assay, site-directed mutagenesis, loss-of-function experiments with defined p53-dependent phenotypic readout |
Cell |
High |
20096447
|
| 2011 |
Beclin1 controls the protein stability of USP10 (and USP13) by regulating their deubiquitinating activities. USP10 mediates deubiquitination of p53, and Beclin1-regulated USP10 activity provides a mechanism linking the tumor suppressors Beclin1 and p53. USP10 and USP13 also deubiquitinate the Beclin1 subunit of Vps34 PI3 kinase complexes, protecting them from degradation. |
Small molecule inhibitor (spautin-1) studies, co-immunoprecipitation, ubiquitination assays, loss-of-function experiments, in-cell protein stability assays |
Cell |
High |
21962518
|
| 2011 |
USP10 directly deubiquitylates the histone variant H2A.Z in vitro and in vivo. USP10 and H2A.Z are both required for transcriptional activation of androgen receptor (AR)-regulated genes (PSA and KLK3); knockdown of USP10 elevates steady-state mono-ubiquitylated H2A.Z and ablates hormone-induced deubiquitylation at AR-regulated gene regulatory regions. |
In vitro deubiquitylation assay, ChIP, sequential ChIP, siRNA knockdown, reporter assays |
Nucleic acids research |
High |
21245042
|
| 2009 |
USP10 is localized in early endosomes in airway epithelial cells and deubiquitinates endocytosed CFTR, promoting its recycling back to the apical membrane rather than lysosomal degradation. siRNA knockdown of USP10 increased ubiquitinated CFTR and lysosomal degradation; dominant-negative USP10-C424A increased ubiquitinated CFTR degradation; overexpression of wt-USP10 decreased ubiquitinated CFTR. |
Activity-based chemical DUB screen, siRNA knockdown, dominant-negative overexpression (C424A mutant), endosomal fractionation, chloride secretion assay, co-immunoprecipitation |
The Journal of biological chemistry |
High |
19398555
|
| 2016 |
USP10 specifically removes ubiquitin from AMPKα to facilitate AMPKα phosphorylation by LKB1. Ubiquitination on AMPKα blocks LKB1-mediated phosphorylation. Under energy stress, AMPK-mediated phosphorylation of USP10 at Ser76 enhances USP10 activity, forming a feedforward loop amplifying AMPK activation. |
In vitro deubiquitination assay, in vitro kinase assay, co-immunoprecipitation, site-directed mutagenesis (Ser76), genetic loss-of-function with metabolic phenotypic readout |
Molecular cell |
High |
26876938
|
| 2013 |
USP10 interacts with SIRT6 and suppresses SIRT6 ubiquitination, protecting SIRT6 from proteasomal degradation. Through stabilizing SIRT6, USP10 antagonizes c-Myc transcriptional activity and inhibits cell-cycle progression. |
Proteomic approach (co-IP/MS), co-immunoprecipitation, ubiquitination assay, cell-cycle analysis, loss-of-function experiments |
Cell reports |
Medium |
24332849
|
| 2013 |
USP10 interacts with NEMO via the scaffold protein MCPIP1 upon genotoxic stress and removes linear polyubiquitin chains from NEMO, resulting in decreased IKK and NF-κB activation. USP10 is required for MCPIP1-mediated inhibition of genotoxic NF-κB activation. |
Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, NF-κB reporter assay, epistasis experiments |
The EMBO journal |
Medium |
24270572
|
| 2015 |
USP10 forms a complex with TANK and MCPIP1 that mediates deubiquitination of TRAF6, suppressing NF-κB activation induced by genotoxic stress and IL-1R/TLR stimulation. CRISPR/Cas9 deletion of TANK enhanced NF-κB activation and inflammatory cytokine production. |
Co-immunoprecipitation, ubiquitination assay, CRISPR/Cas9 deletion, NF-κB reporter assay, cytokine ELISA |
The Journal of biological chemistry |
Medium |
25861989
|
| 2016 |
G3BP1/G3BP2 and USP10 form complexes that mediate stress granule (SG) condensation. G3BP1 phosphomimetic S149E mutant fails to rescue SG formation, while G3BP1-F33W mutant (unable to bind Caprin1 or USP10) rescues SG formation. Caprin1 binding promotes SG formation while USP10 binding to G3BP inhibits SG formation; these two interactions are mutually exclusive. |
Genetic rescue experiments with G3BP1 point mutants, G3BP1/G3BP2 double-knockout cells, stress granule induction assays, co-immunoprecipitation |
The Journal of cell biology |
High |
27022092
|
| 2016 |
USP10 as part of G3BP1-family complexes deubiquitinates monoubiquitinated RPS2, RPS3, and RPS10 on 40S ribosomal subunits stalled at aberrant mRNAs. This rescues modified 40S subunits from lysosomal degradation during ribosome-associated quality control. Knockout of USP10 or G3BP1-family proteins increased lysosomal ribosomal degradation and perturbed ribosomal subunit stoichiometry; K214R substitution in RPS3 rescued these phenotypes. |
CRISPR knockout, ubiquitination assay, ribosomal subunit stoichiometry analysis, rescue with RPS3-K214R mutant, mass spectrometry |
Molecular cell |
High |
31981475
|
| 2017 |
USP10 is required to stabilize oncogenic FLT3 (FLT3-ITD and FLT3-D835Y) by preventing its ubiquitin-mediated proteasomal degradation. Pharmacological or genetic inhibition of USP10 induces FLT3 degradation and shows efficacy in preclinical AML models. |
DUB inhibitor library screen, target deconvolution, co-immunoprecipitation, ubiquitination assay, cell-line and primary patient cell models, mouse xenograft model |
Nature chemical biology |
High |
28967922
|
| 2016 |
RNF168 E3 ligase mediates ubiquitylation of TOP2α, while USP10 acts as the deubiquitylase that negatively regulates TOP2α ubiquitylation and restrains its chromatin association. The opposing actions of RNF168 and USP10 on TOP2α ubiquitylation modulate decatenation activity. |
Co-immunoprecipitation, ubiquitination assay, ChIP, genetic loss-of-function with chromosomal segregation phenotypic readout |
Nature communications |
Medium |
27558965
|
| 2019 |
USP10 interacts with NOTCH1 intracellular domain (NICD1) to slow the ubiquitin-dependent turnover of NICD1. Inactivation of USP10 reduced NICD1 abundance and stability and diminished Notch-induced target gene expression in endothelial cells. Loss of endothelial Usp10 increased vessel sprouting in mice and partially restored patterning defects caused by ectopic NICD1 expression. |
Co-immunoprecipitation, protein stability assay, endothelial-specific Usp10 knockout mouse, in vivo sprouting angiogenesis assay, gene expression analysis |
Science |
High |
30975888
|
| 2019 |
USP10 deubiquitinates and stabilizes KLF4 by blocking its proteasomal degradation. Loss of USP10 in mice downregulates KLF4 and accelerates KrasG12D-driven lung adenocarcinoma. KLF4 in turn facilitates transcription of TIMP3 by binding its promoter. |
siRNA screen of ubiquitin-specific proteases, co-immunoprecipitation, ubiquitination assay, conditional USP10 knockout mouse with KrasG12D, promoter binding by ChIP |
Cell death and differentiation |
High |
31748695
|
| 2019 |
USP10 deubiquitinates and stabilizes Smad4, sustaining TGF-β signaling. USP10 directly interacts with Smad4 and cleaves its proteolytic ubiquitin chains, promoting HCC metastasis. Suppression of USP10 inhibits HCC cell migration; reconstitution of Smad4 rescues this defect. |
siRNA library screen of USPs, co-immunoprecipitation, ubiquitination assay, migration assay, rescue experiment with Smad4 |
Molecular oncology |
Medium |
31721429
|
| 2020 |
USP10 directly interacts with YAP and TAZ, deubiquitinates them by reverting their proteolytic ubiquitination, and stabilizes them. Depletion of USP10 enhanced polyubiquitination of YAP/TAZ and promoted their proteasomal degradation, arresting hepatocellular carcinoma proliferation in vitro and in vivo. |
DUB screen (transcriptional activity and protein abundance), co-immunoprecipitation, ubiquitination assay, siRNA knockdown, in vivo xenograft |
Cancer research |
High |
32217697
|
| 2018 |
USP10 interacts with and deubiquitinates G3BP2, maintaining G3BP2 protein stability and reducing its polyubiquitylation. G3BP2-dependent growth activation and p53 nuclear export are repressed by USP10 knockdown, placing USP10 upstream of the G3BP2-p53 axis. |
Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, chromatin immunoprecipitation, cell growth assay |
Molecular cancer research |
Medium |
29378906
|
| 2013 |
HTLV-1 Tax oncoprotein interacts with USP10 and inhibits arsenic-induced stress granule formation by USP10-containing SGs, stimulating ROS production and augmenting ROS-dependent apoptosis. USP10 normally functions to inhibit stress-induced ROS production and apoptosis; Tax attenuates this activity. |
Co-immunoprecipitation, stress granule formation assay, ROS measurement, apoptosis assay |
Blood |
Medium |
23775713
|
| 2019 |
USP10 is a novel deubiquitinase of SKP2; it binds to and deubiquitinates SKP2, preventing its degradation. Stabilized SKP2 in turn mediates K63-linked ubiquitination and activation of Bcr-Abl, creating a USP10/SKP2/Bcr-Abl axis in CML. |
Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, cell proliferation assay in imatinib-sensitive and -resistant CML cells |
Cell discovery |
Medium |
31044085
|
| 2016 |
USP10 interacts with MSH2 and deubiquitinates it both in vitro and in vivo, stabilizing MSH2 protein. Knockdown of USP10 in lung cancer cells exhibits increased cell survival and decreased apoptosis upon treatment with MNNG and 6-TG; these phenotypes are rescued by ectopic MSH2 expression. MSH2 protein level correlates positively with USP10 level. |
Co-immunoprecipitation, in vitro deubiquitination assay, siRNA knockdown, mismatch repair activity assay, cell survival/apoptosis assay, rescue experiment |
The Journal of biological chemistry |
High |
26975374
|
| 2018 |
USP10 mediates deubiquitination of p14ARF, preventing its proteasome-dependent degradation. c-Myc induces USP10 transcription; USP10 then stabilizes p14ARF to enforce oncogene-induced senescence. USP10-null MEFs and primary cells depleted of USP10 bypass c-Myc-induced senescence via p14ARF destabilization. |
Ubiquitination assay, siRNA knockdown, USP10-null MEFs, cell senescence assay (SA-β-gal, proliferation), c-Myc overexpression epistasis |
Cell death and differentiation |
Medium |
29472714
|
| 2017 |
USP10 interacts with integrin β1 and β5; recombinant USP10 removes ubiquitin from these integrin subunits in vitro. Loss of USP10 induces ubiquitin accumulation on β1/β5 integrins, decreasing αv/β1/β5 protein levels and TGFβ activation. Gain of USP10 increases αv/β1/β5 protein levels and fibrotic marker expression. |
Genetic screen, siRNA knockdown, recombinant USP10 in vitro deubiquitination, co-immunoprecipitation, ex vivo cornea organ culture, loss- and gain-of-function with fibrotic marker readout |
Journal of cell science |
Medium |
28851806
|
| 2005 |
USP10 is part of DNA-bound androgen receptor (AR) complexes in nuclear extracts. Interaction with AR confirmed by GST pull-down. USP10 localizes in both nucleus and cytoplasm. Overexpression of catalytically active, but not enzymatically inactive, USP10 stimulates AR transactivation at AREs, SREs, and MMTV promoter; siRNA knockdown of USP10 impairs MMTV androgen response. |
Nuclear extract purification, GST pull-down, fluorescence microscopy, cell-based transactivation reporter assay, siRNA knockdown |
Molecular and cellular endocrinology |
Medium |
16368182
|
| 2017 |
Crystal structure of UbV.7.2 (ubiquitin variant inhibitor) was solved and provided the molecular basis for enhanced affinity and specificity for USP7. UbVs were also identified that bound USP10 with high affinity and inhibited its deubiquitination activity, validating the catalytic site of USP10 as a druggable interface. |
Phage-displayed UbV library, crystal structure determination (for USP7 UbV), in vitro deubiquitination inhibition assay, cell death assay |
Journal of molecular biology |
Medium |
28587923
|
| 2018 |
USP10 interacts with HDAC6 and deubiquitinates and stabilizes HDAC6. Reintroduction of either USP10 or HDAC6 into USP10-knockdown NSCLC cells with null p53 restores cisplatin resistance, defining a USP10-HDAC6-cisplatin resistance axis. |
Co-immunoprecipitation, ubiquitination assay, siRNA/genetic knockdown, rescue experiment with USP10 or HDAC6, xenograft model |
Cell death & disease |
Medium |
32382008
|
| 2014 |
USP10 interacts with T-bet transcription factor in the nucleus, directly inhibits T-bet ubiquitination, and increases T-bet protein expression. Quercetin, a reported T-bet inhibitor, targets USP10 to promote T-bet proteasomal degradation. |
Co-immunoprecipitation, ubiquitination assay, overexpression, inhibitor treatment (quercetin) |
Biochemical and biophysical research communications |
Low |
24845384
|
| 2021 |
USP10 deubiquitinates LC3B, reversing monoubiquitination-mediated proteasomal degradation of LC3B. CRISPR-Cas9 KO of USP10 reduces both LC3B-I and LC3B-II levels through increased ubiquitination and proteasomal degradation, leading to slower degradation of autophagy receptors SQSTM1 and NBR1 and increased aggresome-like structures. |
CRISPR-Cas9 knockout screen, biochemical ubiquitination assay, proteasome inhibitor experiments, autophagy receptor degradation assay |
The Journal of biological chemistry |
High |
33577797
|
| 2018 |
USP10 interacts with p62 (ubiquitin receptor) and the USP10-p62 interaction augments p62-dependent ubiquitinated protein aggregation and aggresome formation, thereby inhibiting apoptosis. USP10-p62-induced protein aggregates inhibit proteasome activity, further increasing ubiquitinated protein levels. USP10 co-localizes with α-synuclein in Lewy bodies in Parkinson disease brains. |
Co-immunoprecipitation, aggresome formation assay, proteasome activity assay, immunohistochemistry of PD brain tissue |
iScience |
Medium |
30469013
|
| 2019 |
USP10 is a critical factor for the formation of Tau/TIA1/USP10-positive stress granules in neuronal cells. Depletion of USP10 severely attenuates TIA1/Tau-positive SG formation induced by proteasome inhibition or TIA1 overexpression. Overexpression of USP10 without stress stimuli induces TIA1/Tau/USP10-positive SGs in a deubiquitinase-independent manner. |
siRNA knockdown, overexpression with catalytically inactive control, immunofluorescence of SG formation, immunohistochemistry of AD brain tissue |
Scientific reports |
Medium |
31332267
|
| 2021 |
USP10 promotes clearance of TDP-43-positive stress granules and thereby inhibits aberrant cytoplasmic aggregation of TDP-43/TDP-35 in neuronal cells. Depletion of USP10 increases insoluble TDP-35 in the cytoplasm. TDP-35 interacts with USP10 in an RNA-binding-dependent manner. |
siRNA knockdown, overexpression, stress granule clearance assay, solubility fractionation, co-immunoprecipitation, immunohistochemistry of ALS patient tissue |
Molecular and cellular biology |
Medium |
35007165
|
| 2019 |
USP10 interacts with Raf-1 and promotes its deubiquitination, stabilizing Raf-1 protein (without affecting mRNA), which activates downstream MEK/ERK signaling. USP10 overexpression promotes proliferation, migration, and inhibits apoptosis of endometrial stromal cells via Raf-1/MEK/ERK; effects are blocked by MEK inhibitor PD-98059. |
Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, overexpression, MEK inhibitor rescue, proliferation/apoptosis/migration assays |
American journal of physiology. Cell physiology |
Medium |
30281322
|
| 2018 |
USP10 interacts with SIRT6 and inhibits its ubiquitination and degradation in the liver. USP10 deficiency exacerbates HFD-induced metabolic dysfunction; SIRT6 overexpression reverses USP10 deficiency effects; SIRT6 deficiency counteracts USP10 overexpression benefits, placing USP10 upstream of SIRT6 in hepatic metabolism. |
Co-immunoprecipitation, ubiquitination assay, hepatocyte-specific USP10 knockout and overexpression mouse models, genetic epistasis with SIRT6 |
Hepatology |
High |
29698567
|
| 2019 |
USP10 deubiquitinates and stabilizes Musashi-2 (MSI2) through direct interaction, preventing its proteasomal degradation, and thereby promotes colon cancer cell proliferation. |
Co-immunoprecipitation, ubiquitination assay, protein stability assay, cell proliferation assay |
FEBS letters |
Low |
30604502
|
| 2017 |
USP10 is the major DUB required for stabilization of SYK. USP10 inhibition leads to proteasome-mediated SYK degradation and potentiates anti-leukemic effects of FLT3 inhibition. |
Co-immunoprecipitation, ubiquitination assay, USP10 inhibitor treatment, cell viability assay |
British journal of cancer |
Medium |
32015510
|
| 2016 |
USP10 directly interacts with and stabilizes PTEN through deubiquitination in lung cancer cells. Co-immunoprecipitation confirmed the interaction; ubiquitination/deubiquitination assays confirmed the mechanism. Pro-cancerous effects of USP10 deficiency are abolished by PTEN re-introduction. |
Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, PTEN rescue experiment, in vivo allograft |
Molecular and cellular biochemistry |
Medium |
28852924
|
| 2021 |
USP10 interacts with PTEN and removes TRIM25-mediated K63-linked polyubiquitination of PTEN, restoring PTEN phosphatase activity and reducing PIP3 production, thereby inhibiting AKT/mTOR signaling. The inactive C424A mutant of USP10 fails to reverse PTEN ubiquitination. |
Co-immunoprecipitation, ubiquitination assay with K63-specific chains, C424A inactive mutant, PIP3 measurement, AKT/mTOR signaling assay, NSCLC proliferation assay |
The Journal of biological chemistry |
High |
34416231
|
| 2022 |
USP10 deubiquitinates and stabilizes ANLN (anillin) by removing K11- and K63-linked ubiquitin chains, preventing APC/C-Cdh1-mediated degradation. USP10 and Cdh1 form a functional complex with ANLN in a non-competitive manner to balance ANLN levels. USP10 promotes contractile ring assembly at the cytokinetic furrow and cytokinesis through ANLN stabilization. |
Co-immunoprecipitation, ubiquitination assay (K11 and K63-specific), cytokinesis assay, USP10 inhibitor (F806), complex formation analysis with Cdh1 mutant |
Cell death and differentiation |
Medium |
36526897
|
| 2019 |
USP10 interacts with TAK1 directly and promotes protection against cerebral ischemia-reperfusion injury. USP10 KO mice show elevated NF-κB signaling, JNK-MAPK activation, and increased apoptosis after cerebral I/R, demonstrating USP10's inhibitory role on TAK1-mediated inflammatory signaling. |
USP10 knockout mouse, cerebral I/R injury model, co-immunoprecipitation, NF-κB and JNK pathway analysis, apoptosis assay |
Biochemical and biophysical research communications |
Medium |
31301769
|
| 2021 |
USP10 interacts with NEMO in macrophages; USP10 inhibition accelerates NEMO degradation. USP10 stabilizes NEMO by deubiquitination, maintaining NF-κB activation in LPS-induced sepsis. Suppressing USP10 attenuated inflammatory responses and improved survival in LPS-induced sepsis mice. |
Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, spautin-1 inhibitor, NF-κB translocation assay, cytokine ELISA, in vivo sepsis model |
Inflammation research |
Medium |
37436447
|
| 2023 |
USP10 binds to Axin1 via conserved motifs and stabilizes Axin1 through K48-linked deubiquitination. Additionally, USP10 physically tethers Axin1 and β-catenin and promotes phase separation for β-catenin suppression in a manner independent of enzymatic activity. In APC-truncated CRC, USP10 binds to β-catenin directly (via unstructured N-terminus) and increases β-catenin stability. |
Unbiased DUB screen, in vitro binding assay, computational modelling, ubiquitination assay (K48-specific), phase separation assay, USP10 enzymatic mutant, CRC organoid model, xenograft |
Cell chemical biology / Oncogene |
High |
37611590 39443725
|
| 2019 |
TRAF4 interacts with USP10 and blocks p53 access to USP10, resulting in p53 destabilization and enhanced fibroblast proliferation in keloids. TRAF4 acts independently of its E3 ubiquitin ligase activity in this process. |
Co-immunoprecipitation, p53 ubiquitination assay, siRNA knockdown, rescue experiment (p53 knockdown), keloid fibroblast proliferation assay |
The Journal of investigative dermatology |
Medium |
30940456
|
| 2022 |
USP10 deubiquitinates RUNX1 and stabilizes it, maintaining mesenchymal subtype properties in glioblastoma. USP10 knockdown inhibits RUNX1 and results in loss of mesenchymal properties. |
Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, overexpression, in vivo xenograft, GBM subtype gene expression analysis |
Cell death & disease |
Medium |
36949071
|
| 2022 |
USP10 deubiquitinates and stabilizes AID (activation-induced cytidine deaminase), which specifically stabilizes nuclear AID protein. USP10 translocates into the nucleus after AKT-mediated phosphorylation at T674 within its NLS domain. BCR and TLR1/2 signals synergistically promote this phosphorylation. USP10 deficiency in B cells decreased AID protein levels and reduced neutralizing antibody production after vaccination. |
Co-immunoprecipitation, ubiquitination assay, nuclear localization imaging, kinase assay, USP10-conditional B cell knockout, vaccination challenge |
Signal transduction and targeted therapy |
Medium |
34983926
|
| 2023 |
USP10 directly interacts with PABPC1 and decreases K27/K29-linked ubiquitination of the RRM2 domain of PABPC1. Deubiquitinated PABPC1 couples more CLK2 mRNA and eIF4G1, increasing CLK2 translation efficiency and promoting pancreatic cancer tumor growth. |
Co-immunoprecipitation, mass spectrometry, ubiquitination assay (K27/K29-specific), polysome/mRNA association assay, in vivo xenograft and PDX model |
Cancer letters |
Medium |
37757903
|
| 2023 |
USP10 interacts with and deubiquitinates MOF (KAT8) acetyltransferase at lysine 410, protecting it from proteasomal degradation. Stabilized MOF promotes H4K16ac enrichment at the ANXA2 promoter in a JUN-dependent manner, activating ANXA2/Wnt signaling and ESCC progression. |
Co-immunoprecipitation, ubiquitination assay, specific lysine mutagenesis (K410), H4K16ac ChIP, functional ESCC tumor model |
Oncogene |
Medium |
38317006
|
| 2025 |
USP10 binds to XAB2 and deubiquitinates K48-linked polyubiquitination at K593 of XAB2, stabilizing it and preventing proteasomal degradation. Nuclear USP10 expression increases in CRC cells treated with oxaliplatin. Stabilized XAB2 upregulates ANXA2 transcriptionally by binding the ANXA2 promoter, promoting DNA damage repair and oxaliplatin resistance. |
Co-immunoprecipitation, mass spectrometry, ubiquitination site MS, ubiquitin assay, dual-luciferase reporter, ChIP-qPCR, xenograft model |
Journal of experimental & clinical cancer research |
Medium |
40069750
|
| 2023 |
USP10 interacts with NICD1 (Notch1 intracellular domain) and deubiquitinates it, stabilizing NICD1 and promoting K11/K48-linked polyubiquitination-mediated degradation when disrupted by N1DARP microprotein. N1DARP competitively disrupts USP10-N1ICD interaction, accelerating N1ICD proteasomal degradation. |
Co-immunoprecipitation, ubiquitination assay (K11/K48-specific), competition binding assay, pancreatic cancer organoid model, KPC mouse model |
Cell discovery |
Medium |
37714834
|
| 2020 |
USP10 interacts with CD36 scavenger receptor and stabilizes CD36 protein by cleaving poly-ubiquitin on CD36, promoting foam cell formation. USP10 inhibition promotes CD36 degradation and suppresses lipid uptake and foam cell formation by macrophages. |
Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, Oil Red O staining, immunofluorescence |
Aging |
Low |
33197885
|
| 2019 |
USP10 interacts with the EMT transcription factor Slug/SNAI2, identified in a genome-wide siRNA DUB screen, and mediates its proteasomal degradation. Genetic knockdown of USP10 decreases Slug levels and reduces cancer cell migration; overexpression elevates Slug and Vimentin. |
Genome-wide siRNA DUB screen, co-immunoprecipitation, protein stability assay, migration assay |
Biochemical and biophysical research communications |
Low |
29803676
|
| 2023 |
DCAF7 acts as a scaffold protein facilitating the interaction between USP10 and G3BP1, leading to USP10-mediated removal of K48-linked ubiquitin moieties from Lys76 of G3BP1, preventing its proteasomal degradation and promoting stress granule-like structure formation and NPC chemoresistance. |
Co-immunoprecipitation, ubiquitination assay (K48-specific, K76 site mapping), siRNA knockdown, stress granule formation assay, in vitro and in vivo chemoresistance model |
Advanced science |
Medium |
38973296
|
| 2023 |
USP10 interacts with ZEB1 and promotes its proteasomal degradation by modifying its ubiquitination. ERK phosphorylates USP10 at Ser236, impairing the USP10-ZEB1 interaction and enabling ZEB1 protein stabilization. MEK-ERK inhibition blocks USP10 phosphorylation and enhances USP10-ZEB1 interaction, suppressing ZEB1-mediated metastasis. |
Co-immunoprecipitation, ubiquitination assay, MEK inhibitor, USP10 phospho-site identification, colorectal cancer metastasis mouse tail-vein injection model |
Molecular cancer research |
Medium |
36940483
|
| 2023 |
USP10 interacts with AMPK-phosphorylated state and potentiates deubiquitination and stabilization of Axin1 (K48-linked), linking the LKB1/AMPK axis to Wnt/β-catenin suppression. AMPK phosphorylation of USP10 also strengthens USP10 binding to β-catenin, supporting its phase transition and suppression. |
Co-immunoprecipitation, ubiquitination assay, AMPK kinase assay, phase separation assay, colorectal cancer organoid and xenograft model |
FEBS letters |
Medium |
37873736
|
| 2019 |
USP10 interacts with NLRP7 and catalyzes its deubiquitination at K379, stabilizing NLRP7 protein and promoting colorectal cancer progression and M2 macrophage polarization via CCL2. |
Co-immunoprecipitation, mass spectrometry, ubiquitination assay, K379R mutagenesis, in vivo tumor model, macrophage polarization assay |
Journal of experimental & clinical cancer research |
Medium |
33838681
|
| 2021 |
USP10 stabilizes GSK3β through deubiquitination; stabilized GSK3β in turn promotes ULK1 transcription by increasing ULK1 promoter activity, thereby driving ULK1-mediated autophagy, cell proliferation, and invasion in osteosarcoma. |
Co-immunoprecipitation, ubiquitination assay, ULK1 promoter reporter, GSK3β activity assay, siRNA knockdown, xenograft model |
Cell & bioscience |
Medium |
39218913
|
| 2023 |
USP10 interacts with and deubiquitinates FOXQ1, promoting its protein stability. USP10-mediated FOXQ1 stabilization activates CREB5/NF-κB signaling to alleviate sepsis-induced acute kidney injury. |
Co-immunoprecipitation, ubiquitination assay, overexpression/knockdown, rescue experiment, in vivo CLP model |
Biochimica et biophysica acta. Molecular basis of disease |
Low |
38960057
|
| 2024 |
AEG-1 recruits USP10 to remove K48-linked polyubiquitin chains at Lys425 of PARP1, preventing PARP1 proteasomal degradation and facilitating homologous recombination-mediated DNA double-strand break repair, conferring radioresistance in esophageal squamous cell carcinoma. |
Co-immunoprecipitation, ubiquitination assay (K48-specific, K425 site mapping), siRNA knockdown, DNA damage (γH2AX, comet assay), in vivo xenograft |
Cancer letters |
Medium |
37838281
|
| 2024 |
NDR1 inhibits ubiquitination-mediated PD-L1 degradation via the deubiquitinase USP10; USP10 deubiquitinates PD-L1, stabilizing it and promoting immune escape in prostate cancer. |
Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, CD8+ T cell co-culture model |
Cell communication and signaling |
Low |
39227807
|
| 2023 |
KIF15 recruits USP10 to PGK1 and promotes USP10-mediated deubiquitination of PGK1, stabilizing PGK1 and enhancing glycolysis in pancreatic cancer. KIF15 interacts with both PGK1 and USP10 via its coil2 domain. |
Co-immunoprecipitation, mass spectrometry, ubiquitination assay, KIF15 truncation mapping, glycolytic capacity measurement (ECAR/OCR), in vivo xenograft |
Cell death & disease |
Medium |
36807568
|
| 2020 |
Wu-5 directly interacts with and inactivates USP10 in vitro (IC50 = 8.3 µM), confirming its catalytic activity as a cysteine protease DUB. Overexpression of USP10 abrogates Wu-5-induced FLT3-ITD degradation and cell death, placing USP10 directly upstream of FLT3-ITD stability. |
In vitro enzymatic inhibition assay, overexpression rescue, cell viability assay |
Acta pharmacologica Sinica |
Medium |
32694757
|
| 2024 |
PPM1B directly interacts with YBX1 and dephosphorylates YBX1 at serine 314; this dephosphorylation affects USP10-mediated deubiquitination of YBX1, resulting in decreased YBX1 protein stability. Thus USP10 deubiquitinates YBX1, and this is regulated by PPM1B-mediated phosphorylation state of YBX1. |
Co-immunoprecipitation, overexpression/silencing experiments, ubiquitination assay, S314 mutagenesis, PANoptosis assay, oxaliplatin resistance assay |
Cancer letters |
Low |
38364962
|