USP29 Data Analysis

HGNC Gene Name
ubiquitin specific peptidase 29
HGNC Gene Symbol
USP29
Identifiers
hgnc:18563 NCBIGene:57663 uniprot:Q9HBJ7
Orthologs
mgi:1888998 rgd:1306648
INDRA Statements
deubiquitinations all statements
Pathway Commons
Search for USP29
Number of Papers
46 retrieved on 2022-05-22

DepMap Analysis

The Dependency Map (DepMap) is a genome-wide pooled CRISPR-Cas9 knockout proliferation screen conducted in more than 700 cancer cell lines spanning many different tumor lineages. Each cell line in the DepMap contains a unique barcode, and each gene knockout is assigned a “dependency score” on a per cell-line basis which quantifies the rate of CRISPR-Cas9 guide drop. It has been found that proteins with similar DepMap scores across cell lines, a phenomenon known as co-dependent genes, have closely related biological functions. This can include activity in the same or parallel pathways or membership in the same protein complex or the same pathway.

We identified the strongest seven co-dependent genes (“Symbol”) for DUBs and ran GO enrichment analysis. We used Biogrid, IntAct, and Pathway Commons PPIDs, and the NURSA protein-protein interaction databases (PPIDs) to determine whether co-dependent genes interact with one another. The “Evidence” column contains the PPIDs in which the interaction appears as well as whether there is support for the association by an INDRA statement. As another approach to identify potential interactors, we looked at proteomics data from the Broad Institute's Cancer Cell Line Encyclopedia (CCLE) for proteins whose expression across ~375 cell lines strongly correlated with the abundance of each DUB; it has previously been observed that proteins in the same complex are frequently significantly co-expressed. The correlations and associated p-values in the CCLE proteomics dataset are provided. And, we determined whether co-dependent genes yield similar transcriptomic signatures in the Broad Institute's Connectivity Map (CMap). A CMap score greater than 90 is considered significantly similar.

DepMap Correlations

Symbol Name DepMap Correlation Evidence CCLE Correlation CCLE Z-score CCLE p-value (adj) CCLE Significant CMAP Score CMAP Type

Dependency GO Term Enrichment

Gene set enrichment analysis was done on the genes correlated with USP29using the terms from Gene Ontology and gene sets derived from the Gene Ontology Annotations database via MSigDB.

Using the biological processes and other Gene Ontology terms from well characterized DUBs as a positive control, several gene set enrichment analyses were considered. Threshold-less methods like GSEA had relatively poor results. Over-representation analysis with a threshold of of the top 7 highest absolute value Dependency Map correlations yielded the best results and is reported below.

GO Identifier GO Name GO Type p-value p-value (adj.) q-value

Transcriptomics

The following table shows the significantly differentially expressed genes after knocking out USP29 using CRISPR-Cas9.

Knockout Differential Expression

Symbol Name log2-fold-change p-value p-value (adj.)
PSMB1 proteasome 20S subunit beta 1 3.59e-01 2.39e-07 8.39e-04
RPLP1 ribosomal protein lateral stalk subunit P1 7.38e-01 2.20e-07 8.39e-04
RPS12 ribosomal protein S12 1.06e+00 2.00e-07 8.39e-04
RPS27A ribosomal protein S27a 8.21e-01 4.08e-06 8.58e-03
RPS4X ribosomal protein S4 X-linked 1.01e+00 3.98e-06 8.58e-03
MT1E metallothionein 1E 5.19e-01 7.34e-06 9.94e-03
RPS4XP11 ribosomal protein S4X pseudogene 11 1.04e+00 8.10e-06 9.94e-03
RPL7A ribosomal protein L7a 6.45e-01 4.57e-05 4.81e-02
RPS26 ribosomal protein S26 3.53e-01 5.21e-05 4.98e-02

Gene Set Enrichment Analysis

There were too few differentially expressed genes to run a meaningful GSEA.

Literature Mining

INDRA was used to automatically assemble known mechanisms related to USP29 from literature and knowledge bases. The first section shows only DUB activity and the second shows all other results.

Deubiquitinase Activity

psp cbn pc bel_lc signor biogrid lincs_drug tas hprd trrust ctd vhn pe drugbank omnipath conib crog dgi | rlimsp isi tees geneways eidos trips medscan sparser reach
USP29 deubiquitinates TP53. 3 / 3
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USP29 is transcriptionally activated following oxidative stress and then mediates p53 deubiquitination.

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USP29 can also deubiquitinate p53 in response to oxidative stress.
USP29 deubiquitinates CGAS-K464R. 2 / 2
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In support of this notion, we found that USP29 deubiquitinated cGAS (K464R) but did not affect the ubiquitination of cGAS (K271R).

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In this context, we noted that USP29 inhibited ubiquitination of cGAS (K464R) but not cGAS (K271R) after HSV-1 infection, and that knockout of USP29 potentiated ubiquitination of cGAS (K464R) but not cGAS (K271R) before or after HSV-1 infection.
USP29 deubiquitinates CLSPN. 1 / 1
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USP29 controls the stability of checkpoint adaptor Claspin by deubiquitination
USP29 deubiquitinates H2AC20. 1 / 1
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Both USP44 and USP29 promoted efficient deubiquitylation of histone H2A
USP29 deubiquitinates CGAS. 1 / 1
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USP29 deubiquitinates cGAS in the presence or absence of HSV-1 infection.
USP29 leads to the deubiquitination of CDC25A. 1 / 1
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The presence of USP29 effectively blocked polyubiquitination of Cdc25A and extended its half-life.

Other Statements

psp cbn pc bel_lc signor biogrid lincs_drug tas hprd trrust ctd vhn pe drugbank omnipath conib crog dgi | rlimsp isi tees geneways eidos trips medscan sparser reach
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Neuron-specific USP29 knockout significantly diminished, whereas USP29 overexpression aggravated cerebral I/R-induced oxidative stress, apoptosis, and neurological dysfunction in mice.

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We also demonstrated that USP29 depletion hampers the colony formation and increases apoptosis of HCT116 cells.

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During stress, USP29 removes the polyubiquitin chain from p53 thus stabilizing it and induces p53 dependent apoptosis.

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In addition, OGD/R-induced oxidative stress and neuronal apoptosis were also attenuated by USP29 silence but exacerbated by USP29 overexpression in vitro.

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Our findings for the first time identify that USP29 upregulation during cerebral I/R may contribute to oxidative stress, neuronal apoptosis, and the progression of cerebral I/R injury and that inhibition of USP29 may help to develop novel therapeutic strategies to treat cerebral I/R injury.
AIMP2 affects USP29
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AIMP2 activates USP29.
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AIMP2 activates USP29. 3 / 3
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Knockdown of parkin increased the level of AIMP2, leading to ultimately USP29 and MYBBP1A accumulation in SH-SY5Y cells.

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These results suggest that AIMP2 upregulates USP29 and MYBBP1A in the absence of parkin activity, contributing to PD pathogenesis.

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USP29 is induced by JTV1 and FBP driven transcription in response to oxidative stress, and was also shown to be important for the full activation of PUMA and apoptosis [XREF_BIBR].
AIMP2 increases the amount of USP29.
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AIMP2 increases the amount of USP29. 2 / 2
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USP29 is expressed by JTV1 and FBP transcriptional factors.
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JTV1 co-activates FBP to induce USP29 transcription and stabilize p53 in response to oxidative stress.
USP29 affects CGAS
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USP29 activates CGAS.
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USP29 activates CGAS. 3 / 3
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In contrast, cGAS was still degraded in Usp29 m/m MLFs (half-life ~ 8h) after HSV-1 infection, which was due to inefficient induction of cGas transcription and accelerated degradation of basal and newly synthesized cGAS caused by the absence of USP29.

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These data together suggest that USP29 deconjugates K48 linked polyubiquitin chains from cGAS and thereby inhibits the proteasomal degradation of cGAS.

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In addition, we found that TRIM38 and USP29 interacts with cGAS independently, suggesting that TRIM38 mediated sumoylation and USP29 mediated deubiquitination of cGAS cooperatively regulate the stability of cGAS.
USP29 increases the amount of CGAS.
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USP29-C298A increases the amount of CGAS. 1 / 1
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In addition, reconstitution of USP29 but not USP29 (C298A) into Usp29 m/m MEFs restored the protein levels of cGAS with or without HSV-1 infection and cGAMP production after cytoplasmic DNA challenge.
USP29 increases the amount of CGAS. 1 / 1
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In addition, reconstitution of USP29 but not USP29 (C298A) into Usp29 m/m MEFs restored the protein levels of cGAS with or without HSV-1 infection and cGAMP production after cytoplasmic DNA challenge.
USP29 affects IFNB1
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USP29 decreases the amount of IFNB1.
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USP29 decreases the amount of IFNB1. 2 / 2
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Interestingly, we found that knockdown of USP29 significantly impaired various cytoplasmic DNA induced expression of IFNB, TNF, and IP10 but had little effect on cGAMP induced expression of IFNB, TNF, and IP10.

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Knockdown of USP29 by these two shRNAs significantly inhibited HSV-1-induced expression of IFNB, TNF, IL6, and IP10 in THP-1 cells (The # 2 shRNA was used for the following experiments and similar results were observed with # 1 shRNA).
USP29 increases the amount of IFNB1.
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USP29-C298A increases the amount of IFNB1. 1 / 1
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XREF_FIG, reconstitution of wild-type USP29 but not the inactive mutant USP29 (C298A) into Usp29 m/m MLFs fully restored the expression of Ifnb, Ifna4, Tnf, or Il6.
USP29 increases the amount of IFNB1. 1 / 1
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XREF_FIG, reconstitution of wild-type USP29 but not the inactive mutant USP29 (C298A) into Usp29 m/m MLFs fully restored the expression of Ifnb, Ifna4, Tnf, or Il6.
USP29 activates IFNB1.
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USP29 activates IFNB1. 1 / 1
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In addition, knockdown of USP29 significantly impaired the production of IFN-beta, IFN-alpha, IL-6, and TNF after infection of HSV-1 or transfection of various DNA ligands.
Infections affects USP29
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Sequence analysis of USP29 promoter ( -5000 bp ~ +100 bp ) failed to identify any recognizable IRF , NF-kappaB , or STAT binding sites , indicating that the transcriptional regulation of USP29 by viral infection is different from that of OTUD4 , USP25 or INKIT previously reported.37 ,40,41 In this context , it has been shown that transcription factors JTV1 and FBP co-activate USP29 transcription in response to oxidative stress and that one of the evolutionarily conserved sequence elements ( CSE1 ) on Usp29 promoter suppresses its transcription.39 ,42 Because USP29 interacted with cGAS and was upregulated by HSV-1 infection , we investigated its role in regulating HSV-1 - or cytoplasmic DNA-triggered innate immune signaling .

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Sequence analysis of USP29 promoter ( -5000 bp ~ +100 bp ) failed to identify any recognizable IRF , NF-kappaB , or STAT binding sites , indicating that the transcriptional regulation of USP29 by viral infection is different from that of OTUD4 , USP25 or INKIT previously reported.37 ,40,41 In this context , it has been shown that transcription factors JTV1 and FBP co-activate USP29 transcription in response to oxidative stress and that one of the evolutionarily conserved sequence elements ( CSE1 ) on Usp29 promoter suppresses its transcription.39 ,42 USP29 promotes HSV-1-triggered innate antiviral signaling in THP-1 cells Because USP29 interacted with cGAS and was upregulated by HSV-1 infection , we investigated its role in regulating HSV-1 - or cytoplasmic DNA-triggered innate immune signaling .

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39 , 42 USP29 promotes HSV-1-triggered innate antiviral signaling in THP-1 cells Because USP29 interacted with cGAS and was upregulated by HSV-1 infection , we investigated its role in regulating HSV-1-or cytoplasmic DNA-triggered innate immune signaling .

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Our results suggest that HSV-1 infection upregulated USP29 , which might be responsible for increased USP29-cGAS association after HSV-1 infection .
USP29 affects CLSPN
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USP29 activates CLSPN.
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USP29 activates CLSPN. 2 / 3
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A recent report indicates that USP29 promotes CLASPIN (not CHK1) stability, ensuring CHK1 activation in response to UV irradiation.

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The deubiquitinases USP9X and USP29 promote Claspin stabilization during the S phase, and thus, adequate replication fork progression, by opposing its proteasomal degradation [23,24].
USP29 increases the amount of CLSPN.
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USP29 increases the amount of CLSPN. 1 / 1
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In contrast, knockdown of endogenous USP29 (TOV21G cells transfected with sh-USP29) did not reduce the Claspin protein expression (data not shown).
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Biologically, ectopic expression of USP29 promotes gastric cancer cell migration, and depletion of Snail abolishes USP29 mediated cell migration; and USP29 can be induced by major EMT and metastatic inducing factors such as TGFbeta, TNFalpha, and hypoxia.

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Collectively , these data indicate that Snail is a crucial substrate for USP29 to promote cell migration and USP29 / SCP1 complex may be new therapeutic targets to treat metastatic cancer .

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Deubiquitinase USP29 promotes gastric cancer cell migration by cooperating with phosphatase SCP1 to stabilize Snail protein.
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Pirinixic acid decreases the amount of USP29.
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Pirinixic acid decreases the amount of USP29. 2 / 2
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Pirinixic acid activates USP29.
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USP29 affects TNF
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USP29 decreases the amount of TNF.
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USP29 decreases the amount of TNF. 2 / 2
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Knockdown of USP29 by these two shRNAs significantly inhibited HSV-1-induced expression of IFNB, TNF, IL6, and IP10 in THP-1 cells (The # 2 shRNA was used for the following experiments and similar results were observed with # 1 shRNA).

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Interestingly, we found that knockdown of USP29 significantly impaired various cytoplasmic DNA induced expression of IFNB, TNF, and IP10 but had little effect on cGAMP induced expression of IFNB, TNF, and IP10.
USP29 activates TNF.
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USP29 activates TNF. 1 / 1
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In addition, knockdown of USP29 significantly impaired the production of IFN-beta, IFN-alpha, IL-6, and TNF after infection of HSV-1 or transfection of various DNA ligands.
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USP29 activates Autoimmunity.
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Author Correction : USP29 maintains the stability of cGAS and promotes cellular antiviral responses and autoimmunity .

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USP29 maintains the stability of cGAS and promotes cellular antiviral responses and autoimmunity .
USP29 inhibits Autoimmunity.
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USP29 deficiency alleviates autoimmunity in Trex1 - / - mice Consistent with the results obtained with USP29 knockout cells , we found that the protein levels of cGAS were substantially lower in various organs such as heart , liver , kidney and spleen from Usp29m / m mice than in those from Usp29 + / + mice ( Fig. 7a ) .

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Biologically, ectopic expression of USP29 promotes gastric cancer cell migration, and depletion of Snail abolishes USP29 mediated cell migration; and USP29 can be induced by major EMT and metastatic inducing factors such as TGFbeta, TNFalpha, and hypoxia.

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Biologically , ectopic expression of USP29 promotes gastric cancer cell migration , and depletion of Snail abolishes USP29-mediated cell migration ; and USP29 can be induced by major EMT and metastatic inducing factors such as TGFbeta , TNFalpha , and hypoxia .
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To further substantiate our conclusion that USP29 positively regulates antiviral immunity by stabilizing cGAS, we reconstituted an empty vector or cGAS into Usp29 +/+ or Usp29 m/m MLFs and examined HSV-1-triggered signaling in these cells.

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46 In this study, we demonstrated that USP29 deconjugated K48 linked polyubiquitin chains from K271 of cGAS in resting cells or after HSV-1 infection, which stabilized cGAS to produce cGAMP and activate MITA mediated antiviral immunity as well as autoimmunity (Supplementary information, FigS7e).
USP29 affects TP53
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USP29 activates TP53. 2 / 2
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This is also consistent with the observations that human USP29 might modulate the protein levels of p53 [XREF_BIBR].

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During stress, USP29 removes the polyubiquitin chain from p53 thus stabilizing it and induces p53 dependent apoptosis.
USP29 affects Neoplasms
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In conclusion , our study shows that elevated expression of USP29 promotes malignancy in CRC , suggesting that USP29 could be a promising target for colon cancer therapy .

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Systemic knockout of Usp29 depleted MYC and HIF1α in MYC-driven neuroblastoma and B cell lymphoma, inhibited critical metabolic targets and significantly prolonged survival of tumor-bearing mice.
USP29 affects CXCL10
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USP29 decreases the amount of CXCL10. 2 / 2
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Knockdown of USP29 by these two shRNAs significantly inhibited HSV-1-induced expression of IFNB, TNF, IL6, and IP10 in THP-1 cells (The # 2 shRNA was used for the following experiments and similar results were observed with # 1 shRNA).

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Interestingly, we found that knockdown of USP29 significantly impaired various cytoplasmic DNA induced expression of IFNB, TNF, and IP10 but had little effect on cGAMP induced expression of IFNB, TNF, and IP10.
USP29 affects CRC
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USP29 activates CRC. 2 / 2
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USP29 knockdown significantly decreased CRC cell proliferation in vitro.

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In conclusion, our study shows that elevated expression of USP29 promotes malignancy in CRC, suggesting that USP29 could be a promising target for colon cancer therapy.
USP29 affects cell
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USP29 inhibits cell.
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USP29 inhibits cell. 1 / 1
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The absence of USP29 , and thus of HIF1alpha transcriptional activity , reduces the levels of aerobic glycolysis and restores sensitivity to Sorafenib in Sorafenib-resistant HCC cells in vitro and in xenograft transplantation mouse models in vivo .
USP29 activates cell.
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USP29 activates cell. 1 / 1
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USP29 knockdown significantly decreased CRC cell proliferation in vitro .
USP29 affects TREX1
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USP29 inhibits TREX1.
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USP29 inhibits TREX1. 1 / 1
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In addition, knockout of USP29 in Trex1 -/- background rescued developmental retardation of Trex1 -/- mice.
USP29 activates TREX1.
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USP29 activates TREX1. 1 / 1
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Consistently, knockout of USP29 results in constitutive degradation of cGAS and eliminates the autoimmune phenotypes in Trex1 -/- mice.
USP29 affects IL6
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USP29 decreases the amount of IL6.
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USP29 decreases the amount of IL6. 1 / 1
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Knockdown of USP29 by these two shRNAs significantly inhibited HSV-1-induced expression of IFNB, TNF, IL6, and IP10 in THP-1 cells (The # 2 shRNA was used for the following experiments and similar results were observed with # 1 shRNA).
USP29 activates IL6.
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USP29 activates IL6. 1 / 1
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In addition, knockdown of USP29 significantly impaired the production of IFN-beta, IFN-alpha, IL-6, and TNF after infection of HSV-1 or transfection of various DNA ligands.
FUBP1 affects USP29
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FUBP1 increases the amount of USP29.
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FUBP1 increases the amount of USP29. 1 / 1
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JTV1 co-activates FBP to induce USP29 transcription and stabilize p53 in response to oxidative stress.
FUBP1 activates USP29.
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FUBP1 activates USP29. 1 / 1
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USP29 is induced by JTV1 and FBP driven transcription in response to oxidative stress, and was also shown to be important for the full activation of PUMA and apoptosis [XREF_BIBR].
FBP1 affects USP29
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FBP1 increases the amount of USP29.
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FBP1 increases the amount of USP29. 1 / 1
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FBP1 promotes transcription of the USP29 gene through binding to FUSE.
FBP1 activates USP29.
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FBP1 activates USP29. 1 / 1
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It will be interesting to examine whether DX2 also competes with AIMP2 and p38 for binding to FBP1 and inhibits FBP1 mediated induction of USP29, which in turn, may have destabilizing effect on p53.
2,3,7,8-tetrachlorodibenzodioxine increases the amount of USP29.
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2,3,7,8-tetrachlorodibenzodioxine decreases the amount of USP29.
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Thimerosal affects USP29
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Thimerosal decreases the amount of USP29. 1 / 1
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Methylmercury chloride decreases the amount of USP29. 1 / 1
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Hsa-miR-335-5p decreases the amount of USP29. 1 / 1
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Cadmium dichloride increases the amount of USP29. 1 / 1
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No evidence text available
Bisphenol F affects USP29
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Bisphenol F increases the amount of USP29. 1 / 1
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No evidence text available
Bisphenol A affects USP29
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Bisphenol A decreases the amount of USP29. 1 / 1
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Benzo[a]pyrene increases the amount of USP29. 1 / 1
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No evidence text available
USP29 affects sorafenib
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Together, the data demonstrate that, as a DUB of HIF1alpha, USP29 promotes Sorafenib resistance in HCC cells, in parts by upregulating glycolysis, thereby opening new avenues for therapeutically targeting Sorafenib resistant HCC in patients.

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The absence of USP29, and thus of HIF1alpha transcriptional activity, reduces the levels of aerobic glycolysis and restores sensitivity to Sorafenib in Sorafenib resistant HCC cells in vitro and in xenograft transplantation mouse models in vivo.

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USP29 knockdown significantly decreased CRC cell proliferation in vitro.
USP29 affects cell cycle
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Altogether , our results implied that USP29 promoted cell cycle progression and oncogenic transformation by regulating protein turnover of Cdc25A .
USP29 affects USP29
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USP29 activates USP29. 1 / 1
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Collectively , these data indicate that Snail is a crucial substrate for USP29 to promote cell migration and USP29 / SCP1 complex may be new therapeutic targets to treat metastatic cancer .
USP29 affects THP-1 Cells
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39 , 42 USP29 promotes HSV-1-triggered innate antiviral signaling in THP-1 cells Because USP29 interacted with cGAS and was upregulated by HSV-1 infection , we investigated its role in regulating HSV-1-or cytoplasmic DNA-triggered innate immune signaling .
USP29 affects SNAI1
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USP29 activates SNAI1. 1 / 1
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Deubiquitinase USP29 promotes gastric cancer cell migration by cooperating with phosphatase SCP1 to stabilize Snail protein.
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Our findings for the first time identify that USP29 upregulation during cerebral I / R may contribute to oxidative stress , neuronal apoptosis , and the progression of cerebral I / R injury and that inhibition of USP29 may help to develop novel therapeutic strategies to treat cerebral I / R injury .
USP29 affects Mice
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USP29 activates Mice. 1 / 1
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Systemic knockout of Usp29 depleted MYC and HIF1α in MYC-driven neuroblastoma and B cell lymphoma, inhibited critical metabolic targets and significantly prolonged survival of tumor-bearing mice.
USP29 affects IFNA
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USP29 activates IFNA. 1 / 1
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In addition, knockdown of USP29 significantly impaired the production of IFN-beta, IFN-alpha, IL-6, and TNF after infection of HSV-1 or transfection of various DNA ligands.
USP29 affects HIF1A
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USP29 activates HIF1A. 1 / 1
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USP29 mediated HIF1alpha stabilization is associated with Sorafenib resistance of hepatocellular carcinoma cells by upregulating glycolysis.
USP29 affects FUBP1
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USP29 increases the amount of FUBP1. 1 / 1
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JTV1 co-activates FBP to induce USP29 transcription and stabilize p53 in response to oxidative stress.
TNF affects USP29
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TNF inhibits USP29. 1 / 1
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Interestingly, the levels of cGAS and the expression of Tnf, Il6, Il12p40 and Ifit3 were significantly decreased in Trex1 -/- Usp29 m/m BMDCs compared to Trex1 -/- BMDCs (Supplementary information, Fig.S7d).
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In this context , a previous study has shown that oxidative stress induces JTV1-FBP association to co-activate transcription of USP29.39 Whether and how HSV-1 infection promotes oxidative stress to activate transcription of USP29 requires further investigations .
N-nitrosomorpholine increases the amount of USP29. 1 / 1
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No evidence text available
MACROH2A1 affects USP29
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MACROH2A1 increases the amount of USP29. 1 / 1
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It is plausible that macroH2A1 knockdown might have down-regulated the transcription of Peg3 and Usp29 through other unknown transcription factors like USF2.
IL6 affects USP29
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IL6 inhibits USP29. 1 / 1
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Interestingly, the levels of cGAS and the expression of Tnf, Il6, Il12p40 and Ifit3 were significantly decreased in Trex1 -/- Usp29 m/m BMDCs compared to Trex1 -/- BMDCs (Supplementary information, Fig.S7d).
IFIT3 affects USP29
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IFIT3 inhibits USP29. 1 / 1
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Interestingly, the levels of cGAS and the expression of Tnf, Il6, Il12p40 and Ifit3 were significantly decreased in Trex1 -/- Usp29 m/m BMDCs compared to Trex1 -/- BMDCs (Supplementary information, Fig.S7d).
HNF1B affects USP29
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HNF1B activates USP29. 1 / 1
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However, USP29, a DUB that closely related to USP28, could not be induced by HNF-1beta.
CGAS affects USP29
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CGAS inhibits USP29. 1 / 1
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Interestingly, the levels of cGAS and the expression of Tnf, Il6, Il12p40 and Ifit3 were significantly decreased in Trex1 -/- Usp29 m/m BMDCs compared to Trex1 -/- BMDCs (Supplementary information, Fig.S7d).
4,4'-sulfonyldiphenol increases the amount of USP29. 1 / 1
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