IndraLab
Statements
OTUD7B affects cell population proliferation
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OTUD7B activates cell population proliferation.
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OTUD7B activates cell population proliferation. 10 / 27
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"These findings lead us to suggest that the role of OTUD7B in prostate cancer cells may be linked to autophagy through the modulation of the mTOR signaling pathway.Collectively, our current study demonstrated that OTUD7B knockdown inhibits autophagy through activating AKT/mTOR pathway and positively contributes to the extrinsic apoptosis and proliferation of prostate cancer cell."
OTUD7B inhibits cell population proliferation.
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"Using OLco‐regulated gene sets revealed that loss of OTUD7B or LSD1 resulted in a significantly reduced expression of metastatic genes (Figure xref , Supporting Information), providing potential mechanistic clues explaining suppressed metastatic ability due to impaired OTUD7B–LSD1 signaling."
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"As shown in Figure S3A in the Supporting Information, K63R mutation caused significant loss of polyubiquitinated LSD1 signals, whereas K48R displayed very marginal reduction in LSD1 ubiquitination, suggesting LSD1 ubiquitination involves mixed linkage specificity, and predominantly prefers K63‐linked polyubiquitin chains.We next determined whether OTUD7B modulated LSD1 deubiquitination."
"<span class="match term0">OTUD7B</span> is responsible for <span class="match term1">LSD1</span> deubiquitination at K226/277 residues, resulting in dynamic control of <span class="match term1">LSD1</span> binding partner specificity and cellular homeostasis"
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"Therefore, perturbation of OTUD7B–LSD1 axis results in changes in both activating and repressive chromatin modification marks, providing a plausible mechanism for altered gene transcription due to OTUD7B loss.To investigate the contribution of LSD1 deubiquitination by OTUD7B in OTUD7B‐mediated LSD1 genomic distribution and H3K4me2/H3K9me2 enrichment, we analyzed LSD1 binding and H3K4me2/H3K9me2 levels of the selected 11 genes in LSD1 reconstituting cells."
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"The fact that many of these gene hits are linked to cell cycle likely explains the result that the primary functions of OTUD7B or LSD1 in coordinating cell cycle progression.The above ChIP‐seq and RNA‐seq datasets were aligned to explore the potential correlations between OTUD7B‐induced H3K4me2 and LSD1 occupancy changes and changes in gene transcription."
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"OTUD7B or CoREST depletion only resulted in LSD1 degradation in p62 cells, but not in p62 cells (Figure 4E), suggesting that the binding to poly‐Ub chains on LSD1 is indispensable for p62‐mediated LSD1 degradation triggered by the deficiency of OTUD7B or CoREST.We next determined the type of poly‐Ub chains predisposed LSD1 to p62 binding."
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"We next generated OTUD7B reconstituting cell lines by expressing sgRNA‐resistant WT or mutant OTUD7B construct in MDA‐MB‐231 cells depleted of OTUD7B, and found only WT OTUD7B reconstitution rescued LSD1 decrease, excluding a possible off‐target issue during sgRNA‐mediated knockdown, also suggesting the DUB catalytic function of OTUD7B is required for its regulation of LSD1 (Figure 1F)."
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"Collectively, these results demonstrate that K63‐linked ubiquitination of LSD1, triggered by depletion of OTUD7B or CoREST, targets LSD1 to proteasomal degradation via p62.The enhanced interaction between p62 and LSD1 upon OTUD7B loss raised one possibility that p62 may compete with CoREST for binding to ubiquitinated LSD1."
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"In addition to being transcriptionally upregulated by NF-kappaB to promote NIK degradation, leading to p100 stabilization and attenuation of non canonical NF-kappaB signalling, TRAF3 is subject to post-translational stabilisation by means of OTUD7B, which targets TRAF3 for deubiquitination of its K48 linked polyubiquitin chains, thereby preventing NIK accumulation and the processing of p100 [XREF_BIBR, XREF_BIBR]."
"<span class="match term0">OTUD7B</span> controls non-canonical NF-kappaB activation through deubiquitination of <span class="match term1">TRAF3</span>"
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"Accumulation of NIK induces phosphorylation of the inhibitor of kappa-B kinase α (IKKα), leading to the ubiquitination and processing of p100.19 20 21 56 The inactive precursor protein p100 undergoes proteasome-mediated processing to generate active protein p52, which binds to RelB and translocates to the nucleus.19 20 21 The deubiquitination of TRAF3 by Otud7b inhibits NF-κB activation by preventing TRAF3 proteolysis and NIK accumulation.56 Alternatively, the canonical pathway relies on ubiquitination of RIP1 kinase or TRAF6."
OTUD7B affects apoptotic process
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OTUD7B inhibits apoptotic process.
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OTUD7B inhibits apoptotic process. 10 / 14
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"16
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Molecularly, OTUD7B inhibits LCL161 inhibitor of apoptosis protein antagonist‐induced invasion and migration by binding to and deubiquitinating TRAF3 (tumor necrosis factor receptor‐associated factor 3), thereby inhibiting NIK (NF‐κB‐inducing kinase) and preventing noncanonical NF‐κB activation in lung cancer."
OTUD7B activates apoptotic process.
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OTUD7B activates apoptotic process. 10 / 13
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"This study represents one of several reports showing both negative and positive effects of OTUD7B on tumor cell invasiveness 18, 23, 42, 63, a tumorigenic phenotype which we have not addressed here.We further observed one of the major outcomes associated with the stabilization of p53 via enforced OTUD7B expression involved inducing HCC cell apoptosis, phenocopying the p53 response to cellular insults such as unresolved levels of DNA damage."
reach
"These findings lead us to suggest that the role of OTUD7B in prostate cancer cells may be linked to autophagy through the modulation of the mTOR signaling pathway.Collectively, our current study demonstrated that OTUD7B knockdown inhibits autophagy through activating AKT/mTOR pathway and positively contributes to the extrinsic apoptosis and proliferation of prostate cancer cell."
sparser
"To determine which domains are responsible for the interaction between LEF1 and OTUD7B, we generated three deletion mutants of LEF1: LEF1ΔHMG (High Mobility Group domain deleted, aa 1-804), LEF1ΔCRD (context-dependent regulatory domain deleted, aa 1-201 & 805-1116), and LEF1ΔBCBD (β-catenin binding domain deleted, aa 202-1116) ( xref A) using the MYC-LEF1 plasmid."
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"To determine which domains are responsible for the interaction between LEF1 and OTUD7B, we generated three deletion mutants of LEF1: LEF1ΔHMG (High Mobility Group domain deleted, aa 1-804), LEF1ΔCRD (context-dependent regulatory domain deleted, aa 1-201 & 805-1116), and LEF1ΔBCBD (β-catenin binding domain deleted, aa 202-1116) (Figure 2A) using the MYC-LEF1 plasmid."
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"Third, Cezanne was reported to regulate the stability of p62 [44], so in this study, we did not show the results of p62.In conclusion, this study showed a new network connecting Cezanne, autophagy, and Osimertinib resistance, and in consideration of the wide effect and complexity of autophagy, further study is needed to explore the effect of autophagy induced by Cezanne on other cellular functions."
sparser
"Others have shown retinoic acid (RA) treatment increases OTUD7B levels in HCC xref while we observed that OTUD7B was subject to transcriptional repression by p53: the latter finding further suggests that p53 establishes negative feedback towards tuning the cellular levels of OTUD7B. It is further noteworthy to consider how the wiring of the OTUD7B-p53 relationship may dovetail with the well-known Mdm2-p53 regulatory circuit."
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"Thus, OTUD7B physically associates with p53 through dual interfaces within the p53 TAD (1-60) and DBD (98-292) regions.Additional characterization using nuclear-cytoplasmic separation showed a biased distribution of OTUD7B within the cytoplasm of HCC cells while p53 occurred both in the cytoplasm and nucleus (Figure 1I)."
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"For example, the cell growth-regulating nucleolar protein LYAR suppresses IFN production by targeting phosphorylated IRF3 [13], OTUD7B deubiquitinates SQSTM1/p62 and promotes IRF3 degradation to inhibit antiviral immunity [14], and the prolyl isomerase PIN1 negatively regulates the innate antiviral response by proteasome-dependent degradation of IRF3 [15]."
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"For example, the cell growth-regulating nucleolar protein LYAR suppresses IFN production by targeting phosphorylated IRF3 [13], OTUD7B deubiquitinates SQSTM1/p62 and promotes IRF3 degradation to inhibit antiviral immunity [14], and the prolyl isomerase PIN1 negatively regulates the innate antiviral response by proteasome-dependent degradation of IRF3 [15]."
sparser
"LSD1 protein expression oscillates during cell cycle, low in G1 and high in G2/M. [ xref ] Similar expression patterns were observed with OTUD7B. [ xref ] We therefore set out to investigate if OTUD7B–p62 axis is responsible for LSD1 ubiquitination and degradation throughout the cell cycle."
Sal-miR-1 affects OTUD7B
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Sal-miR-1 inhibits OTUD7B.
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"OTUD7B downregulation by Sal-miR-1 and 3 attenuates KLF4 protein levels To clarify which substrate is regulated and deubiquitinated by OTUD7B in the context of VSMC migration and adhesion , we used 3 protein-protein interaction prediction databases ( Cytoscape : http://apps.cytoscape.org/apps/agilentliteraturesearch; inBio-Map : https://www.intomics.com/inbio/map.html#search; Genemania : http://genemania.org ) to search for putative proteins interacting with OTUD7B ."
eidos
"Importantly , OTUD7B downregulation by Sal-miR-1 and 3 results in a reduction in KLF4 protein level , which in turn relieves KLF4 repression of the expression of SM alpha-actin , SM22alpha , and SMMHC , thus facilitating VSMC contractile gene ( VSMC differentiation gene ) expression ."
eidos
"Sal-miR-1 and 3 abrogate OTUD7B upregulation by thrombin via targeting the OTUD7B 3'UTR Because plant-derived miRNAs are known to be capable of regulating mammalian gene expression by binding to the 3 ' UTR of target genes 19 , 29 , we utilized the bioinformatic databases miRanda ( http://www.microrna.org/microrna/home.do ) , Targetscan ( http://www.targetscan.org/vert_72/ ) and RNAhybrid ( https://bibiserv.cebitec.uni-bielefeld.de/rnahybrid/ ) to predict Sal-miR-1 and 3 targets ( Figure S3A , Table S1 ) ."
Sal-miR-1 decreases the amount of OTUD7B.
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Sal-miR-1 activates OTUD7B.
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"Using OLco‐regulated gene sets revealed that loss of OTUD7B or LSD1 resulted in a significantly reduced expression of metastatic genes (Figure xref , Supporting Information), providing potential mechanistic clues explaining suppressed metastatic ability due to impaired OTUD7B–LSD1 signaling."
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"TRAF3 and TRAF2 could recruit cIAP1/2 to catalyze K48‐linked ubiquitination and subsequent degradation of NIK.11, 12 NLRP12 or OTUD7B stabilizes TRAF3 and subsequently accelerates NIK degradation.13, 14 Lastly, IKKα and TBK1 may induce NIK phosphorylation‐dependent degradation.15, 16 In contrast to NIK, little is known about how the downstream subunit p100/p52 is regulated."
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"As shown in Fig. 3B, in the immunoprecipitate pulled down by the Flag antibody, the His-Ub level in the group with overexpression of HA-OTUD7B was markedly lower than that in the group without overexpression of HA-OTUD7B, indicating that OTUD7B reduced the ubiquitination level of Flag-FOXM1."
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"OTUD7B mediated cleavage of K63 linked polyubiquitin chains on GbetaL appears to be a common mechanism to promote mTORC2 and AKT signalling, as knockdown of OTUD7B downregulated AKT (pS473) and conferred chemosensitivity to cancer cells with elevated mTORC2 and AKT signalling due to oncogenic events such as PTEN deletion, PIK3CA, EGFR or KRAS mutations (XREF_FIG)."
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"The interaction between OTUD7B and ERα suggested that ERα might be a substrate of OTUD7B, and therefore we evaluated the possibility of ERα deubiquitylation by OTUD7B. It was found that OTUD7B deletion dramatically decreased ERα protein level, and this effect could be reversed by addition of the proteasome inhibitor MG132 or overexpression of OTUD7B-WT, but not its catalytically inactive mutant OTUD7B C194S (Fig. xref )."
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"Besides, the enzymatic activity mutant Cezanne (C194S and H358R, Cezanne CH) could not decrease PIK3C3 ubiquitination (Fig. 4B), further confirming the deubiquitination effect of Cezanne on PIK3C3.To explore the motif or molecule basis of Cezanne and PIK3C3, we constructed plasmids composed of different part of these two proteins shown in Fig. 4C and Supplementary Fig. 1E."
sparser
"Furthermore, immunoblot analysis of lysates from Hek 293 T cells transfected with K48-Ub, Myc-tagged PIK3C3 fragments showed the ubiquitination of V2 fragment of PIK3C3 was inhibited by Cezanne which indicated that the actual K48-linked ubiquitination lysine residue of PIK3C3 might locate at this fragment (Fig. xref )."
sparser
"The interaction between OTUD7B and ERα suggested that ERα might be a substrate of OTUD7B, and therefore we evaluated the possibility of ERα deubiquitylation by OTUD7B. It was found that OTUD7B deletion dramatically decreased ERα protein level, and this effect could be reversed by addition of the proteasome inhibitor MG132 or overexpression of OTUD7B-WT, but not its catalytically inactive mutant OTUD7B C194S (Fig. xref )."
sparser
"To determine which domains are responsible for the interaction between LEF1 and OTUD7B, we generated three deletion mutants of LEF1: LEF1ΔHMG (High Mobility Group domain deleted, aa 1-804), LEF1ΔCRD (context-dependent regulatory domain deleted, aa 1-201 & 805-1116), and LEF1ΔBCBD (β-catenin binding domain deleted, aa 202-1116) ( xref A) using the MYC-LEF1 plasmid."
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"To determine which domains are responsible for the interaction between LEF1 and OTUD7B, we generated three deletion mutants of LEF1: LEF1ΔHMG (High Mobility Group domain deleted, aa 1-804), LEF1ΔCRD (context-dependent regulatory domain deleted, aa 1-201 & 805-1116), and LEF1ΔBCBD (β-catenin binding domain deleted, aa 202-1116) (Figure 2A) using the MYC-LEF1 plasmid."
OTUD7B affects Neoplasm Metastasis
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OTUD7B activates Neoplasm Metastasis.
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OTUD7B inhibits Neoplasm Metastasis.
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OTUD7B affects Neoplasm Invasiveness
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OTUD7B activates Neoplasm Invasiveness.
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OTUD7B inhibits Neoplasm Invasiveness.
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OTUD7B inhibits Neoplasm Invasiveness. 5 / 5
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"16
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Molecularly, OTUD7B inhibits LCL161 inhibitor of apoptosis protein antagonist‐induced invasion and migration by binding to and deubiquitinating TRAF3 (tumor necrosis factor receptor‐associated factor 3), thereby inhibiting NIK (NF‐κB‐inducing kinase) and preventing noncanonical NF‐κB activation in lung cancer."
OTUD7B affects Hypertrophy
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OTUD7B inhibits Hypertrophy.
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OTUD7B activates Hypertrophy.
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OTUD7B is modified
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"Others have shown retinoic acid (RA) treatment increases OTUD7B levels in HCC xref while we observed that OTUD7B was subject to transcriptional repression by p53: the latter finding further suggests that p53 establishes negative feedback towards tuning the cellular levels of OTUD7B. It is further noteworthy to consider how the wiring of the OTUD7B-p53 relationship may dovetail with the well-known Mdm2-p53 regulatory circuit."
reach
"Thus, OTUD7B physically associates with p53 through dual interfaces within the p53 TAD (1-60) and DBD (98-292) regions.Additional characterization using nuclear-cytoplasmic separation showed a biased distribution of OTUD7B within the cytoplasm of HCC cells while p53 occurred both in the cytoplasm and nucleus (Figure 1I)."
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"Our co-immunoprecipitation experiments showed induced interaction of OTUD7b with TRAF2 upon TNF stimulation (Fig. xref ), Since proteasomal degradation of the substrate is mediated either by K11- or K48-linked polyubiquitin chains, we next determined K48- and K11-linked polyubiquitin chains on TRAF2."
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"In addition, loss of the active catalytic site C194 showed reduction in binding of OTUD7b to TRAF2 upon TNF stimulation, presumably by disruption of the TRAF binding region spanning the catalytic domain of OTUD7b.The in vivo function of OTUD7b in infectious diseases has been sparsely studied."
sparser
"In line with our data after long-term exposure to TNF (Fig. xref ), we observed (i) enhanced proteasomal degradation of TRAF2 (Fig. xref ), (ii) TNF-induced OTUD7b-TRAF2 interaction (Fig. xref ) (iii) increased levels of K48-linked polyubiquitin chains on TRAF2 (Fig. xref ), (iv) interaction of TRAF2 with RIPK1 and OTUD7b with RIPK1 (Fig. xref ), and consequently, (v) reduced K63-linked polyubiquitination of RIPK1 (Fig. xref )."
sparser
"Increased Lys11-linkage ubiquitination due to lack of Cezanne DUB activity compromises the recruitment of Rap80/BRCA1-A. Cezanne2 interacts with Cezanne, facilitating Cezanne in the recruitment of Rap80/BRCA1-A, Rad18, and 53BP1, in cellular resistance to ionizing radiation and DNA repair."
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"Thus, it is likely that Cezanne and Cezanne2 form a complex and that the DUB activity of both of these two proteins is required for promoting Rap80/Abraxas/BRCA1, Rad18, and 53BP1 recruitment.Due to the role of Cezanne and Cezanne2 in the recruitment of the Rap80/BRCA1-A complex, Rad18, and 53BP1, we examined their roles in DNA damage repair and cellular resistance to IR."
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"Activation of HIF1α in response to dimethyloxallyl glycine, desferrioxamine or CoCl did not influence Cezanne expression (Online Fig. III) and silencing of HIF1α or HIF2α did not suppress Cezanne expression in hypoxic EC (Online Fig. IV), indicating that induction of Cezanne by hypoxia is HIF-independent."
sparser
"Our co-immunoprecipitation experiments showed induced interaction of OTUD7b with TRAF2 upon TNF stimulation (Fig. xref ), Since proteasomal degradation of the substrate is mediated either by K11- or K48-linked polyubiquitin chains, we next determined K48- and K11-linked polyubiquitin chains on TRAF2."
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"In addition, loss of the active catalytic site C194 showed reduction in binding of OTUD7b to TRAF2 upon TNF stimulation, presumably by disruption of the TRAF binding region spanning the catalytic domain of OTUD7b.The in vivo function of OTUD7b in infectious diseases has been sparsely studied."
sparser
"In line with our data after long-term exposure to TNF (Fig. xref ), we observed (i) enhanced proteasomal degradation of TRAF2 (Fig. xref ), (ii) TNF-induced OTUD7b-TRAF2 interaction (Fig. xref ) (iii) increased levels of K48-linked polyubiquitin chains on TRAF2 (Fig. xref ), (iv) interaction of TRAF2 with RIPK1 and OTUD7b with RIPK1 (Fig. xref ), and consequently, (v) reduced K63-linked polyubiquitination of RIPK1 (Fig. xref )."
OTUD7B affects inflammatory response
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OTUD7B inhibits inflammatory response. 8 / 8
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"Our observation that endogenous Cezanne can reduce inflammation and injury in response to ischemia-reperfusion has important implications for therapeutic targeting of inflammation during transplantation of vascularised organs, bypass grafting, percutaneous coronary intervention of arteries and other procedures that involve reperfusion."
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"The evidence suggests that there was a strong correlation between the release of CA125 and IFN-γ in psoriatic patients.Since A20, CYLD and Cezanne negatively regulate the inflammatory response in autoimmune and cancer diseases, their mRNA levels were examined by quantitative real-time PCR."
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"These studies propose that OTUD7B suppresses tumor progression in HCC although the underlying molecular mechanisms and cause of OTUD7B downregulation in HCC are largely unknown.HCC is one of the most common malignant tumors, ranking sixth in incidence and second in mortality rate among cancers worldwide."
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"RNF26 played a role in EGFR‐driven cell proliferation by ubiquitinating Sqstm1, [ xref ] while mutation of Sqstm1 at K420 led to abnormal ubiquitination and thus inhibited autophagy. [ xref ] TRIM21 could bind to the PB1 domain to ubiquitinate K7, hindering the oligomerization of Sqstm1 and inhibiting its function. [ xref ] CUL5‐ASB6 complex promoted the ubiquitination of Sqstm1 for degradation to inhibit cell proliferation and autophagy. [ xref ] In addition, RNF166 and NEDD4 activated autophagy through ubiquitination of Sqstm1. [ xref ] KEAP1‐CUL3 ubiquitinated Sqstm1 at the site of K420 within the UBA domain, improved the efficiency of substrate transport to the autophagosome, enhanced selective autophagic flux, and accelerated the degradation of target proteins. [ xref ] The ubiquitin‐specific peptidase USP8 acted as a negative regulator of autophagy by deubiquitinating Sqstm1 at K420. [ xref ] The deubiquitinating enzyme OTUD7B interacted with IRF3 to remove the polyubiquitin chain at the K7 site of Sqstm1 to enhance the oligomerization for the block of antiviral immune response. [ xref ] In this study, we found that RNF6, an E3 ubiquitin ligase, mediated the ubiquitination of Sqstm1 at K314 to promote autophagy."
OTUD7B affects pathway
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OTUD7B affects osimertinib
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OTUD7B activates osimertinib. 6 / 6
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"The IC50 assay also proved the resistance of Osimertinib induced by Cezanne and the addition of CQ significantly decreased the Osimertinib resistance in LUAD cell lines, PC9 and HCC827 cells (Fig. 1F, G), which suggested Cezanne promoted Osimertinib resistance and autophagy played a vital role (Fig. 8)."
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"To investigate the connection between Cezanne and Osimertinib resistance in LUAD, analysis of the expression of Cezanne using the GEO data was conducted, which showed that Cezanne expression elevated in the Osimertinib-treated PC9 cells (Fig. 1A) and Osimertinib-resistant HCC827, H1975 cells (Fig. 1B, C)."
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"Therefore, our results suggested that Cezanne contributed to Osimertinib resistance in LUAD cells.Autophagy activation is related to Osimertinib resistance in several types of tumors [6], and our study indicated that the autophagy inhibitor CQ could inhibit the Osimertinib resistance induced by Cezanne (Fig. 1F, G), which suggested Cezanne promoted Osimertinib resistance in an autophagy-dependent way."
OTUD7B affects migration
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"mTOR is the catalytic subunit of two complexes, mTORC1 and mTORC2.65 mTORC1 comprises mTOR, a regulatory protein associated with mTOR (Raptor) and mammalian lethal with Sec13 protein 8 (mLST8, also referred to as GβL).65 In contrast, mTORC2 comprises mTOR, rapamycin insensitive companion of mTOR (Rictor), and GβL.65 Otud7b has been reported to promote mTORC2 signaling through the deubiquitination of GβL."
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"Given that binding of p110alpha subunit to Ras and subsequent activation of PI3K is required for the development and maintenance of Kras driven lung tumours XREF_BIBR, XREF_BIBR, we further assessed whether Otud7b promoted mTORC2 and Akt signalling is causally related to Kras induced lung tumorigenesis."
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"Pathologically, OTUD7B mediated activation of mTORC2 and AKT signalling may be a critical molecular event down-stream of the RAS and PI3K pathway to favour Kras LA2 -driven lung tumorigenesis, suggesting that OTUD7B may be a potential therapeutic target against diseases harbouring hyperactivated PI3K and mTOR signalling such as cancer."
OTUD7B affects cell differentiation
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OTUD7B activates cell differentiation.
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OTUD7B inhibits cell differentiation.
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OTUD7B inhibits cell differentiation. 2 / 2
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OTUD7B affects Stomach Neoplasms
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OTUD7B affects KLF4 protein
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"KLF4 negatively regulates NMHC IIA expression , and downregulation of KLF4 by Sal-miR-1 and 3 reduces KLF4 repression of the expression of NMHC IIA and thus increases NMHC IIA expression level Because Sal-miR-1 and 3 downregulated KLF4 protein levels by attenuating OTUD7B expression , we sought to determine KLF4 target genes associated with induction of VSMC migration ."
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"Other phenotypic features consistent with apoptosis observed upon overexpressing OTUD7B in HCC cells were the condensation and fragmentation of nuclear chromatin 49 as detected by flow cytometry and confocal microscopy, respectively (Figure 7F-G), while examination of cleaved caspase 3 staining in HCC xenografts showed that OTUD7B overexpression also increased HCC cell apoptosis rates in vivo (Figure 7H)."
reach
"This study represents one of several reports showing both negative and positive effects of OTUD7B on tumor cell invasiveness 18, 23, 42, 63, a tumorigenic phenotype which we have not addressed here.We further observed one of the major outcomes associated with the stabilization of p53 via enforced OTUD7B expression involved inducing HCC cell apoptosis, phenocopying the p53 response to cellular insults such as unresolved levels of DNA damage."
sparser
"The luciferase reporter containing wildtype TCF/LEF binding sites (TOPflash) and mutated TCF/LEF binding sites (FOPflash) was transfected with SFB-USP36 or SFB-OTUD7B. Compared to FOPflash luciferase levels, both USP36 and OTUD7B increased the luciferase activities (TOPflash), but OTUD7B significantly enhanced LEF1 activity to a greater extent (6.64-fold) than USP36 did (2.04-fold) ( xref C)."
sparser
"Next, we generated three deletion mutants of OTUD7B: OTUD7BΔZnF (Zinc Finger domain deleted, aa 1-1077), OTUD7BΔOTU (Ovarian Tumor domain deleted, aa 1-564 & 1078-2532), and OTUD7BNt (UBA domain-containing, 1-564) using the SFB-OTUD7B plasmid ( xref C) and attempted to identify the LEF1-binding region on OTUD7B. Similarly, we co-transfected these constructs and full-length MYC-LEF1 into HEK293T cells and pulled down full-length and mutant SFB-OTUD7B with S-protein agarose beads."
sparser
"RNF26 played a role in EGFR‐driven cell proliferation by ubiquitinating Sqstm1, [ xref ] while mutation of Sqstm1 at K420 led to abnormal ubiquitination and thus inhibited autophagy. [ xref ] TRIM21 could bind to the PB1 domain to ubiquitinate K7, hindering the oligomerization of Sqstm1 and inhibiting its function. [ xref ] CUL5‐ASB6 complex promoted the ubiquitination of Sqstm1 for degradation to inhibit cell proliferation and autophagy. [ xref ] In addition, RNF166 and NEDD4 activated autophagy through ubiquitination of Sqstm1. [ xref ] KEAP1‐CUL3 ubiquitinated Sqstm1 at the site of K420 within the UBA domain, improved the efficiency of substrate transport to the autophagosome, enhanced selective autophagic flux, and accelerated the degradation of target proteins. [ xref ] The ubiquitin‐specific peptidase USP8 acted as a negative regulator of autophagy by deubiquitinating Sqstm1 at K420. [ xref ] The deubiquitinating enzyme OTUD7B interacted with IRF3 to remove the polyubiquitin chain at the K7 site of Sqstm1 to enhance the oligomerization for the block of antiviral immune response. [ xref ] In this study, we found that RNF6, an E3 ubiquitin ligase, mediated the ubiquitination of Sqstm1 at K314 to promote autophagy."
sparser
"The luciferase reporter containing wildtype TCF/LEF binding sites (TOPflash) and mutated TCF/LEF binding sites (FOPflash) was transfected with SFB-USP36 or SFB-OTUD7B. Compared to FOPflash luciferase levels, both USP36 and OTUD7B increased the luciferase activities (TOPflash), but OTUD7B significantly enhanced LEF1 activity to a greater extent (6.64-fold) than USP36 did (2.04-fold) ( xref C)."
sparser
"Next, we generated three deletion mutants of OTUD7B: OTUD7BΔZnF (Zinc Finger domain deleted, aa 1-1077), OTUD7BΔOTU (Ovarian Tumor domain deleted, aa 1-564 & 1078-2532), and OTUD7BNt (UBA domain-containing, 1-564) using the SFB-OTUD7B plasmid ( xref C) and attempted to identify the LEF1-binding region on OTUD7B. Similarly, we co-transfected these constructs and full-length MYC-LEF1 into HEK293T cells and pulled down full-length and mutant SFB-OTUD7B with S-protein agarose beads."
sparser
"LSD1 protein expression oscillates during cell cycle, low in G1 and high in G2/M. [ xref ] Similar expression patterns were observed with OTUD7B. [ xref ] We therefore set out to investigate if OTUD7B–p62 axis is responsible for LSD1 ubiquitination and degradation throughout the cell cycle."
reach
"However, the public CHIP data from the Cistrome project (http://cistrome.org/) showed that POLR2A, rather than CTCF, binds the transcription start site of PIK3C2A (Fig. 5K) and we chose POLR2A as the candidate TF.CO-IP assay in Hek 293T cells, IP with anti-Cezanne, validated the binding of Cezanne and POLR2A (Fig. 5L)."
sparser
"In this study, with the help of a public database and LC-MS/MS analysis, we identified a transcription factor, called POLR2A, which might be the mediator between Cezanne and PIK3C2A. Indeed, Cezanne could bind and stabilize POLR2A and deubiquitinate the K48-linked ubiquitination of POLR2A (Fig. xref )."
OTUD7B affects fatty acid metabolic process
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OTUD7B inhibits fatty acid metabolic process.
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OTUD7B inhibits fatty acid metabolic process. 2 / 2
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OTUD7B activates fatty acid metabolic process.
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OTUD7B affects conjugation
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OTUD7B inhibits conjugation. 4 / 4
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"Instead, in the absence of Cezanne, HA K11-linked ubiquitin (an HA-tagged ubiquitin K11 mutant in which all of the lysine residues except lysine 11 are mutated to arginine) conjugation increased, consistent with a role of Cezanne DUB activity in antagonizing K11-conjugation on damaged chromatin (Fig. 4C; Paul and Wang 2017)."
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"Since it has been shown that Cezanne K11-DUB activity not only functions toward K11-chains but also extends to K11-linkage within K11/K63- and K11/Lys48-branched chains (Mevissen et al. 2016), it is likely that at least one of the functions of Cezanne is to prevent K11-conjugation on K63-chains forming mixed K63/K11-chains to protect the “purity” of K63-chains."
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"However, the public CHIP data from the Cistrome project (http://cistrome.org/) showed that POLR2A, rather than CTCF, binds the transcription start site of PIK3C2A (Fig. 5K) and we chose POLR2A as the candidate TF.CO-IP assay in Hek 293T cells, IP with anti-Cezanne, validated the binding of Cezanne and POLR2A (Fig. 5L)."
sparser
"In this study, with the help of a public database and LC-MS/MS analysis, we identified a transcription factor, called POLR2A, which might be the mediator between Cezanne and PIK3C2A. Indeed, Cezanne could bind and stabilize POLR2A and deubiquitinate the K48-linked ubiquitination of POLR2A (Fig. xref )."
OTUD7B affects Dendritic Cells
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4
OTUD7B affects Cell Survival
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3
OTUD7B inhibits Cell Survival.
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1
OTUD7B inhibits Cell Survival. 1 / 2
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1
reach
"Among those tested including the apoptosis inhibitor Z-VAD-FMK (Z-VAD), the programmed necrosis inhibitor necrostatin-1 (Nec-1), the ferroptosis inhibitor ferrostatin-1 (Ferr-1), the necroptosis inhibitor Disulfiram, the cuproptosis inhibitor tetrathiomolybdate (TTM), and the autophagy inhibitor CQ; however, cell viability reductions caused by OTUD7B overexpression were only restored by the addition of the apoptosis inhibitor Z-VAD (Figure 7A-B)."
OTUD7B activates Cell Survival.
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OTUD7B activates Cell Survival. 2 / 2
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2
Sulforaphane affects OTUD7B
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2
1
MiR-500 affects OTUD7B
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3
Bisphenol A affects OTUD7B
3
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3
OTUD7B binds.
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2
OTUD7B translocates.
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1
OTUD7B affects signal transduction
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3
reach
"OTU deubiquitinase 7B (OTUD7B) deubiquitinates lysine-specific demethylase 1 (LSD1) to decrease histone H3 lysine 4 (H3K4)/H3K9 methylation, thereby sustaining breast cancer metastasis potential 103.Overexpression of miR-7 in BCSCs decreases endothelial cell adhesion molecule (ESAM) expression by targeting RelA and inhibits tumorigenesis and distant lung metastasis 104."
reach
"OTU deubiquitinase 7B (OTUD7B) deubiquitinates lysine-specific demethylase 1 (LSD1) to decrease histone H3 lysine 4 (H3K4)/H3K9 methylation, thereby sustaining breast cancer metastasis potential 103.Overexpression of miR-7 in BCSCs decreases endothelial cell adhesion molecule (ESAM) expression by targeting RelA and inhibits tumorigenesis and distant lung metastasis 104."
OTUD7B affects neuronal cell death
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3
OTUD7B inhibits neuronal cell death.
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2
OTUD7B activates neuronal cell death.
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1
OTUD7B activates neuronal cell death. 1 / 1
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1
OTUD7B affects miR-500
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3
reach
"Importantly, the repressive effect of antagomiR-500 on NF-kappaB activity and BCL2L1, CCND1 expression were potently antagonised by individual silencing of CYLD, TAX1BP1, or OTUD7B (XREF_SUPPLEMENTARY), indicating that CYLD, TAX1BP1, and OTUD7B are functionally relevant effectors of miR-500 in NF-kappaB activation."
OTUD7B affects miR-1180
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3
OTUD7B affects ferroptosis
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3
OTUD7B inhibits ferroptosis.
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2
OTUD7B inhibits ferroptosis. 2 / 2
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2
OTUD7B activates ferroptosis.
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1
OTUD7B activates ferroptosis. 1 / 1
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1
OTUD7B affects cell death
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1
OTUD7B activates cell death. 1 / 3
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1
reach
"All these results suggested that Cezanne could act as a deubiquitination enzyme to deubiquitinate K48-linked ubiquitination and stabilize POLR2A, then promote the transcription of PIK3C2A in a POLR2A-dependent way.In our study, Cezanne colocalized with PIK3C3 and stabilized PIK3C3 by slowing down its ubiquitin-proteasome pathway degradation (Fig. 3), and we also found Cezanne promoted PIK3C2A transcription (Fig. 5)."
OTUD7B affects GβL
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3
OTUD7B affects DNA-templated transcription
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3
sparser
"Besides this, N4BP1 interacts with the deubiquitinase (DUB) Cezanne-1, which functions in the deubiquitination and stabilization of TRAF3 [ xref ] and subsequently modulates the activation of both the canonical [ xref ] and non-canonical NFkB [ xref ] by affecting the degradation of NIK and IkB, and the induction of c-REL ubiquitination and proteasome-mediated degradation [ xref ]."
reach
"Activation of HIF1α in response to dimethyloxallyl glycine, desferrioxamine or CoCl did not influence Cezanne expression (Online Fig. III) and silencing of HIF1α or HIF2α did not suppress Cezanne expression in hypoxic EC (Online Fig. IV), indicating that induction of Cezanne by hypoxia is HIF-independent."
Retinoic acid affects OTUD7B
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2
Retinoic acid increases the amount of OTUD7B. 2 / 2
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2
reach
"Others have shown retinoic acid (RA) treatment increases OTUD7B levels in HCC 24 while we observed that OTUD7B was subject to transcriptional repression by p53: the latter finding further suggests that p53 establishes negative feedback towards tuning the cellular levels of OTUD7B."
reach
"Others have shown retinoic acid (RA) treatment increases OTUD7B levels in HCC 24 while we observed that OTUD7B was subject to transcriptional repression by p53: the latter finding further suggests that p53 establishes negative feedback towards tuning the cellular levels of OTUD7B."
Phenylmercury acetate affects OTUD7B
2
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MiR-1180 affects OTUD7B
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2
reach
"Moreover, we reveal that the miR-1180 directly targets two negative regulators of the nuclear factor (NF)-kappaB signaling pathway (OTUD7B and TNIP2) XREF_BIBR XREF_BIBR XREF_BIBR, as well as the pro apoptotic Bcl-2 associated death promoter (BAD) protein, via post-transcriptional downregulation."
Hsa-mir-4533 affects OTUD7B
2
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Hsa-mir-4516 affects OTUD7B
2
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Hsa-mir-4475 affects OTUD7B
2
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Hsa-mir-4434 affects OTUD7B
2
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Hsa-miR-95-5p affects OTUD7B
2
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Hsa-miR-7846-3p affects OTUD7B
2
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Hsa-miR-6892-5p affects OTUD7B
2
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Hsa-miR-6878-5p affects OTUD7B
2
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Hsa-miR-6760-5p affects OTUD7B
2
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Hsa-miR-6134 affects OTUD7B
2
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Hsa-miR-6079 affects OTUD7B
2
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Hsa-miR-5703 affects OTUD7B
2
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Hsa-miR-4799-5p affects OTUD7B
2
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Hsa-miR-154-5p affects OTUD7B
2
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Hsa-miR-103a-3p affects OTUD7B
2
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Entinostat affects OTUD7B
2
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Cadmium dichloride affects OTUD7B
2
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Benzo[a]pyrene affects OTUD7B
2
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All-trans-retinoic acid affects OTUD7B
1
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1
All-trans-retinoic acid increases the amount of OTUD7B. 2 / 2
1
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1
Sal-miR-1 and 3 affects OTUD7B
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2
OTUD7B affects localization
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2
OTUD7B affects immune response
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2
OTUD7B affects cell migration
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2
OTUD7B affects activation
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2
OTUD7B affects Wnt signaling pathway
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1
OTUD7B affects Ventricular Remodeling
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OTUD7B inhibits Ventricular Remodeling. 2 / 2
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2
OTUD7B affects Sal-miR-1
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2
OTUD7B affects Proteasome
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OTUD7B inhibits Proteasome. 1 / 2
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1
OTUD7B affects Pancreatic Neoplasms
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2
OTUD7B activates Pancreatic Neoplasms. 2 / 2
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2
OTUD7B affects NMHC IIA
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2
sparser
"Besides this, N4BP1 interacts with the deubiquitinase (DUB) Cezanne-1, which functions in the deubiquitination and stabilization of TRAF3 [ xref ] and subsequently modulates the activation of both the canonical [ xref ] and non-canonical NFkB [ xref ] by affecting the degradation of NIK and IkB, and the induction of c-REL ubiquitination and proteasome-mediated degradation [ xref ]."
OTUD7B affects LCL161-induced lung cancer cell invasion
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2
OTUD7B affects LCL161-induced lung cancer cell intrapulmonary metastasis
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2
OTUD7B affects LCL161-induced invasion
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2
OTUD7B affects H3K4me2
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2
reach
"The fact that many of these gene hits are linked to cell cycle likely explains the result that the primary functions of OTUD7B or LSD1 in coordinating cell cycle progression.The above ChIP‐seq and RNA‐seq datasets were aligned to explore the potential correlations between OTUD7B‐induced H3K4me2 and LSD1 occupancy changes and changes in gene transcription."
OTUD7B affects FAO genes
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2
OTUD7B affects Akt-pS473
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2
6-propyl-2-thiouracil affects OTUD7B
2
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4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide increases the amount of OTUD7B.
1
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4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide decreases the amount of OTUD7B.
1
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sparser
"Multiple DUBs from the human ovarian tumor (OTU) DUB family that display various degrees of specificities towards different ubiquitin linkage types have been identified and can be used for UbiCRest: For instance, OTUB1 specifically cleaves K48-, OTUD1 K63-, Cezanne K11-, and OTULIN M1-linked ubiquitylation, whereas OTUD3 displays specificity towards K6- and K11-linked ubiquitylation ( xref )."
Sulfadimethoxine affects OTUD7B
1
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Sodium arsenite affects OTUD7B
1
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Reactive oxygen species affects OTUD7B
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1
Reactive oxygen species activates OTUD7B. 1 / 1
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1
Pyrimidifen affects OTUD7B
1
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Pyrachlostrobin affects OTUD7B
1
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1
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Pirinixic acid affects OTUD7B
1
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PcDNA3.1-OTUD7B affects OTUD7B
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1
Monoubiquitin affects OTUD7B
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1
reach
"The monoubiquitin-bound OTUD7B crystal structure 5LRW (after removal of the monoubiquitin), which had also served as the homology template for our previous work on OTUD7A, was chosen for the virtual screen, with the binding site located between residues W234, Q237, Q238, T239, Q241, N242, S245, G246, L247, Y249, W254, E257, W258, E260, L261, L264, L294, E295, E296, F297, H298, P330, F331, H390, and F391."
Midostaurin affects OTUD7B
1
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Methimazole affects OTUD7B
1
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Methidathion affects OTUD7B
1
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Methapyrilene affects OTUD7B
1
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Linc00976 affects OTUD7B
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1
Hsa-mir-548s affects OTUD7B
1
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Hsa-mir-4739 affects OTUD7B
1
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Hsa-mir-4698 affects OTUD7B
1
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Hsa-mir-4663 affects OTUD7B
1
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Hsa-mir-4537 affects OTUD7B
1
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Hsa-mir-4457 affects OTUD7B
1
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Hsa-mir-4284 affects OTUD7B
1
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Hsa-mir-4282 affects OTUD7B
1
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Hsa-miR-92b-3p affects OTUD7B
1
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Hsa-miR-877-5p affects OTUD7B
1
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Hsa-miR-8063 affects OTUD7B
1
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Hsa-miR-7977 affects OTUD7B
1
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Hsa-miR-7850-5p affects OTUD7B
1
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Hsa-miR-766-3p affects OTUD7B
1
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Hsa-miR-6851-5p affects OTUD7B
1
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Hsa-miR-6849-3p affects OTUD7B
1
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Hsa-miR-6847-3p affects OTUD7B
1
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Hsa-miR-6721-5p affects OTUD7B
1
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Hsa-miR-6720-5p affects OTUD7B
1
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Hsa-miR-6516-5p affects OTUD7B
1
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Hsa-miR-6514-3p affects OTUD7B
1
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Hsa-miR-6500-5p affects OTUD7B
1
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Hsa-miR-6499-3p affects OTUD7B
1
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Hsa-miR-616-5p affects OTUD7B
1
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Hsa-miR-5189-5p affects OTUD7B
1
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Hsa-miR-513a-3p affects OTUD7B
1
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Hsa-miR-508-5p affects OTUD7B
1
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Hsa-miR-500a-3p affects OTUD7B
1
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Hsa-miR-4756-5p affects OTUD7B
1
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Hsa-miR-4419b affects OTUD7B
1
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Hsa-miR-373-5p affects OTUD7B
1
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Hsa-miR-371b-5p affects OTUD7B
1
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Hsa-miR-3689d affects OTUD7B
1
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Hsa-miR-367-3p affects OTUD7B
1
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Hsa-miR-363-3p affects OTUD7B
1
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Hsa-miR-3606-3p affects OTUD7B
1
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Hsa-miR-339-5p affects OTUD7B
1
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Hsa-miR-3202 affects OTUD7B
1
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Hsa-miR-32-5p affects OTUD7B
1
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Hsa-miR-3190-5p affects OTUD7B
1
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Hsa-miR-24-3p affects OTUD7B
1
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Hsa-miR-214-5p affects OTUD7B
1
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Hsa-miR-19a-3p affects OTUD7B
1
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Hsa-miR-1292-3p affects OTUD7B
1
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Hsa-miR-125b-2-3p affects OTUD7B
1
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Hsa-miR-1229-3p affects OTUD7B
1
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Fulvestrant affects OTUD7B
1
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Doxorubicin affects OTUD7B
1
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Dorsomorphin affects OTUD7B
1
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Diethylstilbestrol affects OTUD7B
1
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Deoxynivalenol affects OTUD7B
1
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Decabromodiphenyl ether affects OTUD7B
1
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Cadmium atom affects OTUD7B
1
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Benzo[e]pyrene affects OTUD7B
1
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Asparaginyl β-hydroxylase factor affects OTUD7B
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1
Anti-LTbetaR affects OTUD7B
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1
Aflatoxin B1 affects OTUD7B
1
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UBA domain affects OTUD7B
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1
TNF receptor affects OTUD7B
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1
Sal-miR1 affects OTUD7B
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1
Sal-miR-3 affects OTUD7B
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1
1
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Rap80/Abraxas/BRCA1 affects OTUD7B
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1
reach
"Thus, Cezanne2 facilitates Cezanne in regulating Rap80/Abraxas/BRCA1 and Rad18 recruitment.Whereas knockdown of either Cezanne or Cezanne2 alone did not result in much change in 53BP1 IRIF (Fig. 7B; Supplemental Fig. S8), depletion of both genes by siRNAs, however, led to a significant decrease in 53BP1 IRIF (Fig. 7B)."
OTUD7B affects signaling
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1
OTUD7B affects required VHL
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1
OTUD7B affects phenylephrine
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1
OTUD7B inhibits phenylephrine. 1 / 1
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1
OTUD7B affects p53.Finally
|
1
reach
"Together these findings establish that OTUD7B functions to de-ubiquitinate wildtype and mutant forms of p53.Finally, to ascertain the type of ubiquitin modification present in p53 removed by OTUD7B, we repeated the ubiquitination assay after transfecting a series of ubiquitin mutants (K6, K11, K27, K29, K33, K48 and K63) where all but one lysine had not been mutated (Figure 4G)."
OTUD7B affects noncanonical NF-kappaB
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1
OTUD7B affects monoubiquitin
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1
reach
"The monoubiquitin-bound OTUD7B crystal structure 5LRW (after removal of the monoubiquitin), which had also served as the homology template for our previous work on OTUD7A, was chosen for the virtual screen, with the binding site located between residues W234, Q237, Q238, T239, Q241, N242, S245, G246, L247, Y249, W254, E257, W258, E260, L261, L264, L294, E295, E296, F297, H298, P330, F331, H390, and F391."
OTUD7B affects mRFP-GFP-LC3
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1
OTUD7B affects glutathione
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1
OTUD7B decreases the amount of glutathione. 1 / 1
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1
OTUD7B affects deubiquitinase enzyme
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1
OTUD7B affects angiogenesis
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1
OTUD7B activates angiogenesis. 1 / 1
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1
OTUD7B affects UBA domain
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1
OTUD7B affects TOPflash
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1
OTUD7B affects TNF receptor
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1
OTUD7B affects Sal-miR-1 3-induced upregulation SMC-specific contractile proteins
|
1
OTUD7B affects Reactive Oxygen Species
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1
OTUD7B decreases the amount of Reactive Oxygen Species. 1 / 1
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1
OTUD7B affects PIK3 C3
|
1
eidos
"Mechanistically , we demonstrated that STAMBP / AMSH ( STAM-binding protein ) promotes the stabilization of ULK1 by removing its lysine 48 ( K48 ) - linked ubiquitination , whereas OTUD7B mediates the degradation of PIK3 C3 by enhancing its K48-linked ubiquitination , thus positively or negatively affects autophagy flux , respectively ."
OTUD7B affects PI3K/AKT/mTOR
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1
OTUD7B affects PHD-mediated HIF-1alpha hydroxylation
|
1
OTUD7B affects NIK processing p100
|
1
OTUD7B affects NF-kappaB-Lin28
|
1
OTUD7B affects NF-kappaB pathway liver cancer
|
1
reach
"OTU deubiquitinase 7B (OTUD7B) deubiquitinates lysine-specific demethylase 1 (LSD1) to decrease histone H3 lysine 4 (H3K4)/H3K9 methylation, thereby sustaining breast cancer metastasis potential 103.Overexpression of miR-7 in BCSCs decreases endothelial cell adhesion molecule (ESAM) expression by targeting RelA and inhibits tumorigenesis and distant lung metastasis 104."
OTUD7B affects LEF1/β-catenin
|
1
OTUD7B affects LC3B-II
|
1
OTUD7B affects LC3B-I
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1
OTUD7B affects KLF4 protein clarify
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1
eidos
"OTUD7B downregulation by Sal-miR-1 and 3 attenuates KLF4 protein levels To clarify which substrate is regulated and deubiquitinated by OTUD7B in the context of VSMC migration and adhesion , we used 3 protein-protein interaction prediction databases ( Cytoscape : http://apps.cytoscape.org/apps/agilentliteraturesearch; inBio-Map : https://www.intomics.com/inbio/map.html#search; Genemania : http://genemania.org ) to search for putative proteins interacting with OTUD7B ."
OTUD7B affects K63-polyubiquitin chains
|
1
OTUD7B affects K63-,
|
1
reach
"Additionally, in vitro differentiated Otud7b -/- Th1 cells produced less IFNgamma, a result that was substantiated by in vivo experiments showing that Otud7b -/- mice generated fewer Th1 cells in response to bacterial infection or during myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis."
OTUD7B affects Histone_H3
|
1
OTUD7B leads to the demethylation of Histone_H3 on lysine. 1 / 1
|
1
reach
"OTU deubiquitinase 7B (OTUD7B) deubiquitinates lysine-specific demethylase 1 (LSD1) to decrease histone H3 lysine 4 (H3K4)/H3K9 methylation, thereby sustaining breast cancer metastasis potential 103.Overexpression of miR-7 in BCSCs decreases endothelial cell adhesion molecule (ESAM) expression by targeting RelA and inhibits tumorigenesis and distant lung metastasis 104."
OTUD7B affects HMG domain
|
1
OTUD7B affects HIF-1alpha VHL dependent manner independent PHD-mediated prolyl hydroxylation
|
1
OTUD7B affects HIF-1alpha HIF-2alpha
|
1
OTUD7B affects H3K9me2
|
1
OTUD7B affects H3K9
|
1
OTUD7B affects GbetaL
|
1
OTUD7B affects FAO-related genes
|
1
OTUD7B affects EFGR
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1
OTUD7B affects DiUb
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1
OTUD7B affects DNA Damage
|
1
OTUD7B activates DNA Damage. 1 / 1
|
1
reach
"In cells microirradiated with a laser, GFP-tagged Cezanne accumulated at laser-induced DNA damage, and lack of the UBA domain (ΔUBA mutant) abolished the recruitment of Cezanne to DNA damage sites, indicating that Cezanne localization to DNA damage sites depends on the UBA domain (Fig. 6A)."
OTUD7B affects Carcinoma, Hepatocellular
|
1
OTUD7B activates Carcinoma, Hepatocellular. 1 / 1
|
1
OTUD7B affects Autoimmune Diseases
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1
OTUD7B inhibits Autoimmune Diseases. 1 / 1
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1
OTUD7B inhibitor affects OTUD7B
|
1
Notch signaling pathway affects OTUD7B
|
1
Notch signaling pathway activates OTUD7B. 1 / 1
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1
reach
"In addition, both the RHBDL2-SA and RHBDL2 plus OTUD7B-silencing groups significantly reversed the increased expression levels of the Notch signaling pathway downstream target genes (HES1, HEY1, ZEB1, MMP9, SNAIL1, and TWIST1) and cleaved Notch1 (Fig. 7F, G), as well as the enhanced luciferase reporter activity (Fig. 7H) mediated by the RHBDL2."
LEF1/β-catenin affects OTUD7B
|
1
LEF1 affects HMG domain
|
1
K63-, affects UBA domain
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1
HMG domain affects OTUD7B
|
1
FIH affects OTUD7B
|
1
Endothelial Cells affects OTUD7B
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1
Endothelial Cells activates OTUD7B. 1 / 1
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1
DiUb affects SHBG
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1
Bulk RNA-seq data affects OTUD7B
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1
1
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1,4-dithiothreitol affects OTUD7B
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1
1,4-dithiothreitol activates OTUD7B. 1 / 1
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1
% oxygen affects OTUD7B
|
1
2,2',5,5'-tetrachlorobiphenyl affects OTUD7B
1
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