IndraLab
Statements
USP8 is modified
27
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1
144
14
USP8 is phosphorylated.
27
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120
14
rlimsp
"Here, we demonstrate, in the context of a chimeric EGFR-ErbB2 receptor, that (i) EGF induces pY1091 Cbl binding site-dependent K63-polyubiquitination of EGFR-ErbB2, (ii) Cbl is tyrosine phosphorylated upon stimulation of EGFR-ErbB2 wt and Y1091F mutant receptor, (iii) EGF-induced activation of EGFR-ErbB2 induces Usp8 tyrosine phosphorylation, and (iv) ubiquitination of the EGFR-ErbB2 wt and Y1091F mutant is enhanced upon coexpression of catalytically inactive Usp8-C748A in the presence and absence of EGF."
rlimsp
"The phosphorylation of USP8 on the fourth serine (S718) of its 14-3-3 binding motif results in its binding with 14-3-3 proteins and catalytic inactivation. A structural study demonstrated that within the 14-3-3 binding motif, the amino acid preferences in each position are very similar, and the phosphorylation of serine at the fourth position is essential for its binding ability."
USP8 is ubiquitinated.
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15
sparser
"In the present study the linkage between PTEN loss, Akt activation, and USP8 levels and activity appeared to be somewhat different, and in our work Akt activation decreased, rather than enhanced, USP8 function by increasing USP8 ubiquitination and decreasing steady-state USP8 levels (data not shown)."
USP8 is dephosphorylated.
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9
USP8 is produced.
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1
USP8 deubiquitinates EGFR phosphorylated on Y1172, Y1110, K867, K737, K754, K929, Y1092, Y1016, Y1197, K970, and Y1069 on K716. 3 / 3
3
|
USP8 deubiquitinates EGFR phosphorylated on Y1172, Y1110, K737, K754, K929, Y1092, Y1016, K716, Y1197, K970, and Y1069 on K867. 3 / 3
3
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USP8 deubiquitinates EGFR phosphorylated on Y1172, Y1110, K867, K737, K754, K929, Y1092, Y1016, K716, Y1197, and Y1069 on K970. 3 / 3
3
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USP8 deubiquitinates EGFR phosphorylated on Y1172, Y1110, K867, K754, K929, Y1092, Y1016, K716, Y1197, K970, and Y1069 on K737. 3 / 3
3
|
USP8 deubiquitinates EGFR phosphorylated on Y1172, Y1110, K867, K737, K929, Y1092, Y1016, K716, Y1197, K970, and Y1069 on K754. 3 / 3
3
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USP8 deubiquitinates EGFR phosphorylated on Y1172, Y1110, K867, K737, K754, Y1092, Y1016, K716, Y1197, K970, and Y1069 on K929. 3 / 3
3
|
reach
"Whereas USP8 variants increase EGFR signaling in cultured cells, such an effect has not been consistently shown in vivo, suggesting that the effect is small or temporary or that other factors [XREF_BIBR] are involved in increased ACTH production and/or proliferation of USP8 mutation positive tumors."
reach
"As USP8 silencing significantly inhibited the PCa cell growth, proliferation, and metastasis and induced apoptosis and suppressed NF-kB signal activation by decreasing EGFR and PI3K, the USP8-specific inhibitor might be a novel therapeutic target to suppress PCa cell growth, proliferation, and metastasis."
reach
"Considering that activation of EGFR-MAPK signaling induces p27 (Kip1) degradation, and p27 (Kip1)-deficient mice develop corticotropinoma XREF_BIBR, XREF_BIBR, we speculate that through activating EGFR signaling USP8 mutation accelerates p27 (Kip1) degradation, representing an important molecular mechanism underlying ACTH hyperproduction (XREF_FIG)."
reach
"By the same mechanism, USP8 also directs the trafficking and lysosomal degradation of CXCR4 [XREF_BIBR], MET and epidermal growth factor receptor [XREF_BIBR, XREF_BIBR], implying that its loss consequent to increased RNF41 abundance would prolong and potentially amplify invasion signaling by these receptors."
reach
"USP8 has been shown to have opposing effects on EGF receptor degradation by either directly deubiquitinating receptors to prevent their degradation, or by deubiquitinating ESCRT complex proteins to stabilize them and thus promote EGF receptor degradation [XREF_BIBR, XREF_BIBR, XREF_BIBR - XREF_BIBR]."
reach
"Thereby, together with these data, it can be concluded that the elevated level of USP8 not only increases the expression of EGFR, PI3K, and P-Akt but also might increase the PI3K and P-Akt expression over EGFR silencing where the PI3K and P-Akt well established the downstream target of EGFR (
Figures 6C, D
)."
reach
"However, we found that UBPY decreases Smo ubiquitination regardless of the Hh signaling states and that the association between UBPY and Smo is not significantly affected by either Hh stimulation or Smo phosphorylation, suggesting that Smo deubiquitination by UBPY is unlikely to be a major mechanism by which Hh inhibits Smo ubiquitination, although we can not rule out the possibility that Hh regulates UBPY binding to Smo in a subtle way that escaped the detection by our coimmunoprecipitation assay."
reach
"However, we found that UBPY decreases Smo ubiquitination regardless of the Hh signaling states and that the association between UBPY and Smo is not significantly affected by either Hh stimulation or Smo phosphorylation, suggesting that Smo deubiquitination by UBPY is unlikely to be a major mechanism by which Hh inhibits Smo ubiquitination, although we can not rule out the possibility that Hh regulates UBPY binding to Smo in a subtle way that escaped the detection by our coimmunoprecipitation assay."
reach
"As shown in XREF_FIG, inactivation of USP8 in S2 cells by RNAi dramatically enhanced the levels of Smo ubiquitination (XREF_FIG, lane 4, compare to lane 2, top panel), whereas the reduction of other DUBs by RNAi did not, suggesting that the inhibition of Smo accumulation by USP8 RNAi in wing discs was due to the increase in Smo ubiquitination."
reach
"Furthermore, we observed that both Nrdp1 stability and ubiquitination were reduced in Min6 β-cells after palmitate treatment (Fig. 6D), thus demonstrating effects consistent with impact on the Clec16a pathway to maintain the upstream mitophagy complex.To determine whether glucolipotoxicity affects Clec16a to impact formation of the Clec16a-Nrdp1-USP8 complex, we overexpressed Clec16a in palmitate-treated Min6 β-cells."
reach
"Previous observations of defective mitochondrial integrity after glucolipotoxicity (7,36), coupled with our findings here of glucolipotoxicity-mediated destabilization of the Clec16a-Nrdp1-USP8 complex, could inspire future in vivo studies to evaluate the importance of dysfunctional mitophagy to β-cell failure in diabetes."
reach
"While the dynamics of the Clec16a-Nrdp1-USP8 complex are still a mystery, it is clear that Clec16a-mediated ubiquitination orchestrates mitophagic flux in β-cells.Our discovery of Clec16a as an E3 ligase, whose function is inhibited by lenalidomide, expands our insight into its functional role in mitophagy."
E3_Ub_ligase binds USP8, RNF41, and CLEC16A. 1 / 1
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1
sparser
"There was evidence that Magel2 was involved in the leptin-POMC of the hypothalamus to maintain the energy balance of the body.[ xref ]Wijesuriya et al have found that MAGEL2 and Necdin connected leptin receptor (LepR) to the USP8-RNF41 ubiquitin complex through the LepR adapter protein, IRS4."
reach
"Furthermore, we observed that both Nrdp1 stability and ubiquitination were reduced in Min6 β-cells after palmitate treatment (Fig. 6D), thus demonstrating effects consistent with impact on the Clec16a pathway to maintain the upstream mitophagy complex.To determine whether glucolipotoxicity affects Clec16a to impact formation of the Clec16a-Nrdp1-USP8 complex, we overexpressed Clec16a in palmitate-treated Min6 β-cells."
reach
"Previous observations of defective mitochondrial integrity after glucolipotoxicity (7,36), coupled with our findings here of glucolipotoxicity-mediated destabilization of the Clec16a-Nrdp1-USP8 complex, could inspire future in vivo studies to evaluate the importance of dysfunctional mitophagy to β-cell failure in diabetes."
reach
"While the dynamics of the Clec16a-Nrdp1-USP8 complex are still a mystery, it is clear that Clec16a-mediated ubiquitination orchestrates mitophagic flux in β-cells.Our discovery of Clec16a as an E3 ligase, whose function is inhibited by lenalidomide, expands our insight into its functional role in mitophagy."
E3_Ub_ligase binds USP8, RNF41, and CLEC16A. 1 / 1
|
1
sparser
"There was evidence that Magel2 was involved in the leptin-POMC of the hypothalamus to maintain the energy balance of the body.[ xref ]Wijesuriya et al have found that MAGEL2 and Necdin connected leptin receptor (LepR) to the USP8-RNF41 ubiquitin complex through the LepR adapter protein, IRS4."
reach
"RNF41 also negatively regulates the stability of the ubiquitin isopeptidase USP8, a regulator of JAK2 associated cytokine receptor sorting and processing : elevated RNF41 destabilizes the endosomal-sorting-complexes-required-for-transport (ESCRT) -0 complex (Hrs and signal-transducing-and adapter-molecule (STAM) -1 or STAM2), which results in cargo arriving at sorting endosomes being routed to recycling endosomes rather than to lysosomes [XREF_BIBR]."
reach
"Although still a matter of debate, EGFR deubiquitination by the ESCRT-associated deubiquitinating (DUB) enzyme UBPY (ubiquitin-specific protease 8) appears to facilitate the transfer of activated EGFRs from early ubiquitin-binding ESCRT complexes (ESCRT-0, -I, -II) to ESCRT-III (Mizuno et al., 2005; Row et al., 2006; Alwan and van Leeuwen, 2007)."
reach
"However, we found that UBPY decreases Smo ubiquitination regardless of the Hh signaling states and that the association between UBPY and Smo is not significantly affected by either Hh stimulation or Smo phosphorylation, suggesting that Smo deubiquitination by UBPY is unlikely to be a major mechanism by which Hh inhibits Smo ubiquitination, although we can not rule out the possibility that Hh regulates UBPY binding to Smo in a subtle way that escaped the detection by our coimmunoprecipitation assay."
USP8 affects cell population proliferation
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37
1
USP8 inhibits cell population proliferation.
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18
1
USP8 activates cell population proliferation.
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19
USP8 activates cell population proliferation. 10 / 19
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19
reach
"As USP8 silencing significantly inhibited the PCa cell growth, proliferation, and metastasis and induced apoptosis and suppressed NF-kB signal activation by decreasing EGFR and PI3K, the USP8-specific inhibitor might be a novel therapeutic target to suppress PCa cell growth, proliferation, and metastasis."
reach
"Indeed, inhibition of USP8 either by its knockdown or synthetic small molecule led to attenuation of variety of receptor tyrosine kinase (RTK) activities, resulting in the inhibition of cell proliferation in gefitinib resistant and -sensitive non small cell lung cancer (NSCLC) cells [XREF_BIBR]."
USP8 affects apoptotic process
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7
27
1
USP8 inhibits apoptotic process.
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6
16
1
USP8 activates apoptotic process.
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1
11
USP8 activates apoptotic process. 10 / 12
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1
11
reach
"As USP8 silencing significantly inhibited the PCa cell growth, proliferation, and metastasis and induced apoptosis and suppressed NF-kB signal activation by decreasing EGFR and PI3K, the USP8-specific inhibitor might be a novel therapeutic target to suppress PCa cell growth, proliferation, and metastasis."
reach
"Furthermore, we observed that both Nrdp1 stability and ubiquitination were reduced in Min6 β-cells after palmitate treatment (Fig. 6D), thus demonstrating effects consistent with impact on the Clec16a pathway to maintain the upstream mitophagy complex.To determine whether glucolipotoxicity affects Clec16a to impact formation of the Clec16a-Nrdp1-USP8 complex, we overexpressed Clec16a in palmitate-treated Min6 β-cells."
reach
"Previous observations of defective mitochondrial integrity after glucolipotoxicity (7,36), coupled with our findings here of glucolipotoxicity-mediated destabilization of the Clec16a-Nrdp1-USP8 complex, could inspire future in vivo studies to evaluate the importance of dysfunctional mitophagy to β-cell failure in diabetes."
reach
"While the dynamics of the Clec16a-Nrdp1-USP8 complex are still a mystery, it is clear that Clec16a-mediated ubiquitination orchestrates mitophagic flux in β-cells.Our discovery of Clec16a as an E3 ligase, whose function is inhibited by lenalidomide, expands our insight into its functional role in mitophagy."
E3_Ub_ligase binds USP8, RNF41, and CLEC16A. 1 / 1
|
1
sparser
"Dithiothreitol, a reducing agent that reverses sulfhydration-mediated covalent modification, increased the ubiquitylation level of parkin, abolished the effects of exogenous H 2 S on USP8 deubiquitylation and suppressed the interaction of USP8 with parkin in neonatal rat cardiomyocytes treated with high glucose, oleate and palmitate."
reach
"Furthermore, we observed that both Nrdp1 stability and ubiquitination were reduced in Min6 β-cells after palmitate treatment (Fig. 6D), thus demonstrating effects consistent with impact on the Clec16a pathway to maintain the upstream mitophagy complex.To determine whether glucolipotoxicity affects Clec16a to impact formation of the Clec16a-Nrdp1-USP8 complex, we overexpressed Clec16a in palmitate-treated Min6 β-cells."
reach
"Previous observations of defective mitochondrial integrity after glucolipotoxicity (7,36), coupled with our findings here of glucolipotoxicity-mediated destabilization of the Clec16a-Nrdp1-USP8 complex, could inspire future in vivo studies to evaluate the importance of dysfunctional mitophagy to β-cell failure in diabetes."
reach
"While the dynamics of the Clec16a-Nrdp1-USP8 complex are still a mystery, it is clear that Clec16a-mediated ubiquitination orchestrates mitophagic flux in β-cells.Our discovery of Clec16a as an E3 ligase, whose function is inhibited by lenalidomide, expands our insight into its functional role in mitophagy."
E3_Ub_ligase binds USP8, RNF41, and CLEC16A. 1 / 1
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1
sparser
"It has been shown previously that a subset of SH3 domains bind ubiquitin ( xref , xref ), and a recent study using NMR titration experiments showed that the SH3 domain of STAM does in fact bind ubiquitin, and that this interaction can be competed off by USP8 binding to the SH3 domain of STAM ( xref )."
sparser
"The functional relevance of the interaction between USP8, AMSH, and STAM in the endocytic trafficking of activated growth factors is supported by other observations, including that catalytically inactive AMSH, a potential “substrate trap” mutant, resulted in the accumulation of ubiquitin on endosomes, an increased association with STAM, and the generation of a minor product consistent with ubiquitylated STAM ( xref )."
1
1
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9
12
sparser
"It has been shown previously that a subset of SH3 domains bind ubiquitin ( xref , xref ), and a recent study using NMR titration experiments showed that the SH3 domain of STAM does in fact bind ubiquitin, and that this interaction can be competed off by USP8 binding to the SH3 domain of STAM ( xref )."
sparser
"The functional relevance of the interaction between USP8, AMSH, and STAM in the endocytic trafficking of activated growth factors is supported by other observations, including that catalytically inactive AMSH, a potential “substrate trap” mutant, resulted in the accumulation of ubiquitin on endosomes, an increased association with STAM, and the generation of a minor product consistent with ubiquitylated STAM ( xref )."
reach
"Once deubiquitinated, BRIT1 is released from the BRUCE, USP8, and BRIT1 complex and targeted to DSBs by binding to gamma-H2AX at sites of DSB [XREF_BIBR], where BRIT1 recruits the SWI/SNF chromatin remodeling complex to facilitate relaxation of chromatin configuration for the access of repair factors to damaged chromatin [XREF_BIBR]."
sparser
"The putative substrate of BRUCE could be USP8 and if this is the case, ubiquitination of USP8 by BRUCE is expected to enhance its Dub activity over Ub-BRIT1, thereby facilitating removal of the Ub chains from K63-Ub-BRIT1 and promoting recruitment of de-ubiquitinated BRIT1 to sites of DNA damage."
reach
"The putative substrate of BRUCE could be USP8 and if this is the case, ubiquitination of USP8 by BRUCE is expected to enhance its Dub activity over Ub-BRIT1, thereby facilitating removal of the Ub chains from K63-Ub-BRIT1 and promoting recruitment of de-ubiquitinated BRIT1 to sites of DNA damage."
reach
"Once deubiquitinated, BRIT1 is released from the BRUCE, USP8, and BRIT1 complex and targeted to DSBs by binding to gamma-H2AX at sites of DSB [XREF_BIBR], where BRIT1 recruits the SWI/SNF chromatin remodeling complex to facilitate relaxation of chromatin configuration for the access of repair factors to damaged chromatin [XREF_BIBR]."
sparser
"As anticipated from earlier studies, a deletion of the MIM (Microtubule Interacting and Trafficking domain Interacting Motif) domain or mutation of two conserved leucine residues, L192 and L195, in this domain respectively abolished or strongly impeded the USP8::CHMP1B interaction."
sparser
"The function of USP8 at the endocytic pathway level partly relies on binding to and deubiquitination of the Endosomal Sorting Complex Required for Transport (ESCRT) protein CHMP1B. In the aim of finding chemical inhibitors of the USP8::CHMP1B interaction, we performed a high-throughput screening campaign using an HTRF® assay to monitor the interaction directly in lysates of cells co-expressing both partners."
reach
"The DUBs AMSH (associated molecule with the SH3 domain of STAM) XREF_BIBR and UBPY (ubiquitin isopeptidase Y/ubiquitin specific protease 8) XREF_BIBR, bind both the ESCRT-0 component STAM (signal transducing adaptor molecule) and ESCRT and III complex members XREF_BIBR, and are implicated in regulating EGFR sorting onto the degradative pathway."
sparser
"The functional relevance of the interaction between USP8, AMSH, and STAM in the endocytic trafficking of activated growth factors is supported by other observations, including that catalytically inactive AMSH, a potential “substrate trap” mutant, resulted in the accumulation of ubiquitin on endosomes, an increased association with STAM, and the generation of a minor product consistent with ubiquitylated STAM ( xref )."
USP8 affects docetaxel anhydrous
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2
13
USP8 inhibits docetaxel anhydrous.
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2
11
USP8 inhibits docetaxel anhydrous. 10 / 13
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2
11
reach
"Its overexpression increased the PCa cell migration and diminished the healing action of docetaxel in both cells.Similar to the wound healing assay, overexpression of USP8 resulted in the highest number of migrated cells for both Du145 and PC3 cells in the Transwell assay, which showed statistical significance compared to all other treatment group cells (
Figure 3B
)."
reach
"Notably, the combination treatment of docetaxel and SiUSP8 was found to have the lowest cell survival 65.1 ± 2.4% and 60.4 ± 2.1% in DU145 (
Figure 1C1
) and PC3 (
Figure 1C2
) cells, respectively, which were significant compared to control and individual treatments of SiUSP8 and docetaxel.On the other hand, compared to the control group, the USP8 overexpression eliminated the impact of docetaxel in PCa cells."
USP8 activates docetaxel anhydrous.
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2
USP8 affects Neoplasm Invasiveness
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1
14
USP8 activates Neoplasm Invasiveness.
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1
12
USP8 inhibits Neoplasm Invasiveness.
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2
USP8 inhibits Neoplasm Invasiveness. 2 / 2
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2
reach
"Moreover, Nrdp1 upregulation is accompanied by increased protein ubiquitylation and decreased protein levels of ubiquitin specific protease 8 (USP8) in OGD treated neurons, which led to a suppressed interaction between USP8 and HIF-1alpha and subsequently a reduction in HIF-1alpha protein accumulation in neurons under OGD conditions."
sparser
"Moreover, Nrdp1 upregulation is accompanied by increased protein ubiquitylation and decreased protein levels of ubiquitin-specific protease 8 (USP8) in OGD-treated neurons, which led to a suppressed interaction between USP8 and HIF-1α and subsequently a reduction in HIF-1α protein accumulation in neurons under OGD conditions."
sparser
"The major findings include: (1) Nrdp1 is significantly upregulated in the ischemic brain tissue and in OGD-treated neuronal cells; (2) overexpression or knockdown of Nrdp1 enhances or attenuates OGD-induced apoptosis in neurons, respectively, and these changes are accompanied by the downregulation or upregulation of Nrdp1’s substrate USP8; and (3) USP8 may directly interact with HIF-1α to prevent its degradation, and under OGD conditions, Nrdp1 may interfere with HIF-1α stabilization via promoting USP8 degradation."
reach
"In somatic cells, USP8 interacts with the ESCRT-0 machinery [i.e., STAM (signal transducing adaptor molecule) and HGS (hepatocyte growth factor regulated tyrosine kinase substrate)] and its deubiquitinating activity regulates the endosomal sorting of ubiquitinated cargo between the recycling pathway and the lysosomal degradation pathway [XREF_BIBR]."
reach
"Moreover, Nrdp1 upregulation is accompanied by increased protein ubiquitylation and decreased protein levels of ubiquitin specific protease 8 (USP8) in OGD treated neurons, which led to a suppressed interaction between USP8 and HIF-1alpha and subsequently a reduction in HIF-1alpha protein accumulation in neurons under OGD conditions."
sparser
"Moreover, Nrdp1 upregulation is accompanied by increased protein ubiquitylation and decreased protein levels of ubiquitin-specific protease 8 (USP8) in OGD-treated neurons, which led to a suppressed interaction between USP8 and HIF-1α and subsequently a reduction in HIF-1α protein accumulation in neurons under OGD conditions."
sparser
"The major findings include: (1) Nrdp1 is significantly upregulated in the ischemic brain tissue and in OGD-treated neuronal cells; (2) overexpression or knockdown of Nrdp1 enhances or attenuates OGD-induced apoptosis in neurons, respectively, and these changes are accompanied by the downregulation or upregulation of Nrdp1’s substrate USP8; and (3) USP8 may directly interact with HIF-1α to prevent its degradation, and under OGD conditions, Nrdp1 may interfere with HIF-1α stabilization via promoting USP8 degradation."
sparser
"As anticipated from earlier studies, a deletion of the MIM (Microtubule Interacting and Trafficking domain Interacting Motif) domain or mutation of two conserved leucine residues, L192 and L195, in this domain respectively abolished or strongly impeded the USP8::CHMP1B interaction."
sparser
"The function of USP8 at the endocytic pathway level partly relies on binding to and deubiquitination of the Endosomal Sorting Complex Required for Transport (ESCRT) protein CHMP1B. In the aim of finding chemical inhibitors of the USP8::CHMP1B interaction, we performed a high-throughput screening campaign using an HTRF® assay to monitor the interaction directly in lysates of cells co-expressing both partners."
USP8 affects cell growth
|
9
USP8 activates cell growth. 9 / 12
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9
reach
"As USP8 silencing significantly inhibited the PCa cell growth, proliferation, and metastasis and induced apoptosis and suppressed NF-kB signal activation by decreasing EGFR and PI3K, the USP8-specific inhibitor might be a novel therapeutic target to suppress PCa cell growth, proliferation, and metastasis."
sparser
"Interestingly, the crystal structure of USP8-Ubv complex shows a significantly different mode of binding than USP8-UB, suggesting phage selection using the Ubv library could find alternative binding modes with DUBs that maximize binding affinity. xref and xref also generated Ubvs for binding to DUBs of various families as well as viral DUBs."
E3_Ub_ligase binds Ubiquitin and USP8. 1 / 1
|
1
sparser
"There was evidence that Magel2 was involved in the leptin-POMC of the hypothalamus to maintain the energy balance of the body.[ xref ]Wijesuriya et al have found that MAGEL2 and Necdin connected leptin receptor (LepR) to the USP8-RNF41 ubiquitin complex through the LepR adapter protein, IRS4."
reach
"71 In contrast to PAR2, USP8 (or AMSH) does not impact CXCR4 ubiquitination but instead modulates the ubiquitin status of ESCRT-0 that is ubiquitinated by the E3 ligase AIP4, 23 reinforcing the idea that ubiquitination of the transport machinery represents an important regulatory event in GPCR trafficking."
USP8 affects BRIT1
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12
USP8 deubiquitinates BRIT1.
|
6
USP8 binds BRIT1.
|
6
reach
"Once deubiquitinated, BRIT1 is released from the BRUCE, USP8, and BRIT1 complex and targeted to DSBs by binding to gamma-H2AX at sites of DSB [XREF_BIBR], where BRIT1 recruits the SWI/SNF chromatin remodeling complex to facilitate relaxation of chromatin configuration for the access of repair factors to damaged chromatin [XREF_BIBR]."
sparser
"Dithiothreitol, a reducing agent that reverses sulfhydration-mediated covalent modification, increased the ubiquitylation level of parkin, abolished the effects of exogenous H 2 S on USP8 deubiquitylation and suppressed the interaction of USP8 with parkin in neonatal rat cardiomyocytes treated with high glucose, oleate and palmitate."
reach
"In somatic cells, USP8 interacts with the ESCRT-0 machinery [i.e., STAM (signal transducing adaptor molecule) and HGS (hepatocyte growth factor regulated tyrosine kinase substrate)] and its deubiquitinating activity regulates the endosomal sorting of ubiquitinated cargo between the recycling pathway and the lysosomal degradation pathway [XREF_BIBR]."
reach
"We will provide an overview of corticotroph tumorigenesis in the context of hypothalamic-pituitary-adrenal (HPA) axis regulation with an emphasis on the role of the glucocorticoid receptor in the resistance to the negative feedback of cortisol that occurs in CD, and we will explore the role of epidermal growth factor receptor (EGFR) signaling in ACTH hyper-secretion and corticotroph cell proliferation and the recent discovery of somatic ubiquitin specific peptidase 8 (USP8) mutations in a significant number of patients with sporadic CD with an emphasis on therapeutic implications."
USP8 affects Neoplasm Metastasis
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4
6
USP8 activates Neoplasm Metastasis.
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4
4
USP8 activates Neoplasm Metastasis. 8 / 8
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4
4
reach
"As USP8 silencing significantly inhibited the PCa cell growth, proliferation, and metastasis and induced apoptosis and suppressed NF-kB signal activation by decreasing EGFR and PI3K, the USP8-specific inhibitor might be a novel therapeutic target to suppress PCa cell growth, proliferation, and metastasis."
eidos
"USP8 regulates NF-kappaB activation through EGFR and PI3K stabilization to promote PCa cell proliferation and survival In multiple studies ( 29-32 ) , the EGFR is a substrate of USP8 deubiquitination , while USP8 has been shown to enhance gastric cancer cell proliferation and metastasis via the PI3K / AKT signaling pathway ( 30 ) ."
USP8 inhibits Neoplasm Metastasis.
|
2
reach
"Its overexpression increased the PCa cell migration and diminished the healing action of docetaxel in both cells.Similar to the wound healing assay, overexpression of USP8 resulted in the highest number of migrated cells for both Du145 and PC3 cells in the Transwell assay, which showed statistical significance compared to all other treatment group cells (
Figure 3B
)."
reach
"As USP8 silencing significantly inhibited the PCa cell growth, proliferation, and metastasis and induced apoptosis and suppressed NF-kB signal activation by decreasing EGFR and PI3K, the USP8-specific inhibitor might be a novel therapeutic target to suppress PCa cell growth, proliferation, and metastasis."
"The ubiquitin-conjugating enzyme UBE2E3 and ubiquitin-isopeptidase Y (UBPY) were identified, in a yeast two-hybrid screen, to interact with TDP-43 and this interaction is proposed to enhance the ubiquitination and accumulation of its insoluble high molecular weight aggregates (Hans et al., 2014)."
"The ubiquitin-conjugating enzyme UBE2E3 and ubiquitin-isopeptidase Y (UBPY) were identified, in a yeast two-hybrid screen, to interact with TDP-43 and this interaction is proposed to enhance the ubiquitination and accumulation of its insoluble high molecular weight aggregates (Hans et al., 2014)."
sparser
"The proteasome has both ubiquitin ligases and DUBs that associate with it (Crosas et al., 2006) , and several DUB-ligase pairs interact directly, including BRCC36-BRCA1, BAP1-BRCA1, USP4-Ro52, USP7-MDM2, USP8-GRAIL, USP20-pVHL, USP33-pVHL and USP44-APC (Kee and Huibregtse, 2007; Marfany and Denuc, 2008; Ventii and Wilkinson, 2008) ."
sparser
"The proteasome has both ubiquitin ligases and DUBs that associate with it (Crosas et al., 2006) , and several DUB-ligase pairs interact directly, including BRCC36-BRCA1, BAP1-BRCA1, USP4-Ro52, USP7-MDM2, USP8-GRAIL, USP20-pVHL, USP33-pVHL and USP44-APC (Kee and Huibregtse, 2007; Marfany and Denuc, 2008; Ventii and Wilkinson, 2008) ."
reach
"As USP8 silencing significantly inhibited the PCa cell growth, proliferation, and metastasis and induced apoptosis and suppressed NF-kB signal activation by decreasing EGFR and PI3K, the USP8-specific inhibitor might be a novel therapeutic target to suppress PCa cell growth, proliferation, and metastasis."
eidos
"Thereby , together with these data , it can be concluded that the elevated level of USP8 not only increases the expression of EGFR , PI3K , and P-Akt but also might increase the PI3K and P-Akt expression over EGFR silencing where the PI3K and P-Akt well established the downstream target of EGFR ( Figures 6C , D ) ."
reach
"Thereby, together with these data, it can be concluded that the elevated level of USP8 not only increases the expression of EGFR, PI3K, and P-Akt but also might increase the PI3K and P-Akt expression over EGFR silencing where the PI3K and P-Akt well established the downstream target of EGFR (
Figures 6C, D
)."
reach
"Because PTEN dependent regulation of FLIP S stability is mediated by changes in FLIP S ubiquitination, we took the above USP8 modulated cells, transiently transfected a construct encoding HA tagged ubiquitin, and following FLIP S immunoprecipitation used Western blot analysis to monitor the effect of USP8 alteration on the extent of HA-ubiquitin incorporated into FLIP S."
USP8 affects Carcinogenesis
|
1
7
sparser
"Interestingly, the crystal structure of USP8-Ubv complex shows a significantly different mode of binding than USP8-UB, suggesting phage selection using the Ubv library could find alternative binding modes with DUBs that maximize binding affinity. xref and xref also generated Ubvs for binding to DUBs of various families as well as viral DUBs."
E3_Ub_ligase binds Ubiquitin and USP8. 1 / 1
|
1
sparser
"There was evidence that Magel2 was involved in the leptin-POMC of the hypothalamus to maintain the energy balance of the body.[ xref ]Wijesuriya et al have found that MAGEL2 and Necdin connected leptin receptor (LepR) to the USP8-RNF41 ubiquitin complex through the LepR adapter protein, IRS4."
USP8 affects cell migration
|
7
USP8 activates cell migration. 7 / 7
|
7
reach
"Its overexpression increased the PCa cell migration and diminished the healing action of docetaxel in both cells.Similar to the wound healing assay, overexpression of USP8 resulted in the highest number of migrated cells for both Du145 and PC3 cells in the Transwell assay, which showed statistical significance compared to all other treatment group cells (
Figure 3B
)."
USP8 affects cell cycle
|
2
5
USP8 activates cell cycle.
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1
4
USP8 inhibits cell cycle.
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1
1
USP8 affects GC
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7
sparser
"The functional relevance of the interaction between USP8, AMSH, and STAM in the endocytic trafficking of activated growth factors is supported by other observations, including that catalytically inactive AMSH, a potential “substrate trap” mutant, resulted in the accumulation of ubiquitin on endosomes, an increased association with STAM, and the generation of a minor product consistent with ubiquitylated STAM ( xref )."
"In addition, this study identifies USP8 as one of the best markers of Lewy bodies in human pigmented neurons in sporadic cases of Parkinson’s disease and demonstrates the ability of USP8 to hydrolyze K63-linked ubiquitin chains from α-synuclein in vitro"
"Another deubiquitinase, USP8, removes K63-linked ubiquitin chains of α-synuclein and prevents its lysosomal degradation."
BRIT1 affects USP8
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6
reach
"Once deubiquitinated, BRIT1 is released from the BRUCE, USP8, and BRIT1 complex and targeted to DSBs by binding to gamma-H2AX at sites of DSB [XREF_BIBR], where BRIT1 recruits the SWI/SNF chromatin remodeling complex to facilitate relaxation of chromatin configuration for the access of repair factors to damaged chromatin [XREF_BIBR]."
reach
"In the present study the linkage between PTEN loss, Akt activation, and USP8 levels and activity appeared to be somewhat different, and in our work Akt activation decreased, rather than enhanced, USP8 function by increasing USP8 ubiquitination and decreasing steady-state USP8 levels (data not shown)."
USP8 affects localization
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5
USP8 inhibits localization.
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3
USP8 inhibits localization. 3 / 3
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3
reach
"However, in the case of USP8, phosphorylation at Ser680 is also critical for its subcellular localization since mutation of Ser680 to Ala restricts its localization to the nucleus, whereas the wild type is predominantly localized into the cytosol essential for USP8 interaction with the protein 14-3-3ε [57]."
USP8 activates localization.
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2
USP8 affects inflammatory response
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5
USP8 inhibits inflammatory response.
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3
USP8 activates inflammatory response.
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2
reach
"In addition, studies have shown that USP8 knockdown or inhibitors can significantly reduce the viability of gefitinib-resistant and -sensitive NSCLC cells by reducing the expression of receptor tyrosine kinase (RTK).14,15Baykara et al find that the serum USP8 level in NSCLC patients was higher than in healthy individuals."
USP8 affects degradation
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5
sparser
"Although EGFR overexpression is not a consistent finding in USP8 mutation positive tumors, in vitro studies have proven that USP8 mutants inhibit the degradation of the ligand-bound EGFR in EGF-stimulated cells. xref , xref Expression of the somatostatin receptor type 5 (SSTR5) and O-6-methylguanine-DNA methyltransferase (MGMT) are increased in USP8 -mutated tumors, suggesting that such tumors might be responsive to the pharmacological treatment with pasireotide, but not with temozolomide. xref The frequency of USP8 mutations is higher in females in all the cohorts reported so far, but there are discrepancies among studies regarding other clinical and biochemical features. xref – xref , xref Interestingly, the frequency of USP8 mutations in a recently reported cohort of patients with Nelson’s syndrome (45%), was not higher than what has been reported for CD, although such mutations were associated with lower frequency of ACTH normalization after surgery. xref "
USP8 affects E3_Ub_ligase
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3
2
USP8 binds E3_Ub_ligase.
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1
2
E3_Ub_ligase binds Ubiquitin and USP8. 1 / 1
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1
E3_Ub_ligase binds USP8, RNF41, and CLEC16A. 1 / 1
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1
E3_Ub_ligase binds USP8. 1 / 1
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1
USP8 activates E3_Ub_ligase.
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2
"The ubiquitin-conjugating enzyme UBE2E3 and ubiquitin-isopeptidase Y (UBPY) were identified, in a yeast two-hybrid screen, to interact with TDP-43 and this interaction is proposed to enhance the ubiquitination and accumulation of its insoluble high molecular weight aggregates (Hans et al., 2014)."
"The ubiquitin-conjugating enzyme UBE2E3 and ubiquitin-isopeptidase Y (UBPY) were identified, in a yeast two-hybrid screen, to interact with TDP-43 and this interaction is proposed to enhance the ubiquitination and accumulation of its insoluble high molecular weight aggregates (Hans et al., 2014)."
sparser
"The functional relevance of the interaction between USP8, AMSH, and STAM in the endocytic trafficking of activated growth factors is supported by other observations, including that catalytically inactive AMSH, a potential “substrate trap” mutant, resulted in the accumulation of ubiquitin on endosomes, an increased association with STAM, and the generation of a minor product consistent with ubiquitylated STAM ( xref )."
E3_Ub_ligase affects USP8
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3
2
E3_Ub_ligase binds USP8.
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1
2
E3_Ub_ligase binds Ubiquitin and USP8. 1 / 1
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1
E3_Ub_ligase binds USP8, RNF41, and CLEC16A. 1 / 1
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1
E3_Ub_ligase binds USP8. 1 / 1
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1
E3_Ub_ligase ubiquitinates USP8.
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2
USP8 affects trichoplein
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4
USP8 affects signal transduction
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4
USP8 inhibits signal transduction.
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2
USP8 activates signal transduction.
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2
USP8 affects cilium assembly
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1
3
USP8 inhibits cilium assembly.
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1
1
USP8 activates cilium assembly.
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2
reach
"As USP8 silencing significantly inhibited the PCa cell growth, proliferation, and metastasis and induced apoptosis and suppressed NF-kB signal activation by decreasing EGFR and PI3K, the USP8-specific inhibitor might be a novel therapeutic target to suppress PCa cell growth, proliferation, and metastasis."
USP8 affects ESCRT-III
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4
USP8 activates ESCRT-III.
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3
reach
"Deubiquitinating enzymes (DUBs) AMSH and UBPY targeting ESCRT-III play an important role in ESCRT regulated processes [XREF_BIBR, XREF_BIBR, XREF_BIBR] and many ESCRT-III interaction partners recognize sequence motifs located within the C-terminus of ESCRT-III family members [XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR]."
USP8 binds ESCRT-III.
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1
Trichoplein affects USP8
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3
reach
"The putative substrate of BRUCE could be USP8 and if this is the case, ubiquitination of USP8 by BRUCE is expected to enhance its Dub activity over Ub-BRIT1, thereby facilitating removal of the Ub chains from K63-Ub-BRIT1 and promoting recruitment of de-ubiquitinated BRIT1 to sites of DNA damage."
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3
USP8 activates epithelial to mesenchymal transition. 3 / 3
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3
reach
"Here in this study, we found that knocking down USP8 significantly inhibited the PCa cell migration by suppressing the EMT process through the increased E-cadherin and decreased N-cadherin, whereas USP8 overexpression promoted the EMT process through the decreased E-cadherin and increased N-cadherin and so thereby increased the migration of both DU145 and PC3 cells.Knocking down USP8 downregulated the NF-κB signal by decreasing its intermediatory proteins (IKK, P-IKB, p65, and P-p65), whereas USP8 overexpression promoted the NF-κB signal by increasing its intermediatory proteins."
USP8 increases the amount of USP8.
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2
reach
"PTEN deficient cells, which have low levels of USP8 and high levels of FLIP S, were relatively TRAIL resistant, and as previously noted, introduction of WT USP8 (but not blank vector or catalytically inactive USP8) increased USP8 levels and significantly increased the extent of TRAIL induced apoptosis (XREF_FIG)."
USP8 phosphorylates USP8.
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1
sparser
"The impact of METTL3 on m 6 A methylation of MALAT1 was examined by methylated RNA immunoprecipitation (RIP), the interaction between PTBP1 and MALAT1 or USP8 mRNA by combining RNA pull-down, RIP, and RNA stability assays, and the crosstalk between USP8 and TAK1 by co-immunoprecipitation and protein degradation assays."
sparser
"(ii) Ubiquitin-mediated negative effect on the host immune response leading to a positive effect on viral replication, e.g., Zika virus (ZIKV) NS1 interacts with USP8 (Ubiquitin Specific Peptidase 8) and causes the deubiquitination of Caspase 1 and prevents its proteasomal degradation."
sparser
"Anti-viral PARP 13 PB2, PA (IAV) ADP ribosylation of the PB2, PA proteins promotes recognition by E3 ubiquitin ligase and subsequent degradation [41] Pro-viral PARP1 Type I Interferon Receptor (IFNAR1) ADP ribosylation by PARP1promotes proteasomal degradation of IFNAR1 during IAV infection [42] (ii) Ubiquitin-mediated negative effect on the host immune response leading to a positive effect on viral replication, e.g., Zika virus (ZIKV) NS1 interacts with USP8 (Ubiquitin Specific Peptidase 8) and causes the deubiquitination of Caspase 1 and prevents its proteasomal degradation."
USP8 affects Cell Survival
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3
SJB3-019A affects USP8
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1
2
sparser
"The impact of METTL3 on m 6 A methylation of MALAT1 was examined by methylated RNA immunoprecipitation (RIP), the interaction between PTBP1 and MALAT1 or USP8 mRNA by combining RNA pull-down, RIP, and RNA stability assays, and the crosstalk between USP8 and TAK1 by co-immunoprecipitation and protein degradation assays."
sparser
"(ii) Ubiquitin-mediated negative effect on the host immune response leading to a positive effect on viral replication, e.g., Zika virus (ZIKV) NS1 interacts with USP8 (Ubiquitin Specific Peptidase 8) and causes the deubiquitination of Caspase 1 and prevents its proteasomal degradation."
sparser
"Anti-viral PARP 13 PB2, PA (IAV) ADP ribosylation of the PB2, PA proteins promotes recognition by E3 ubiquitin ligase and subsequent degradation [41] Pro-viral PARP1 Type I Interferon Receptor (IFNAR1) ADP ribosylation by PARP1promotes proteasomal degradation of IFNAR1 during IAV infection [42] (ii) Ubiquitin-mediated negative effect on the host immune response leading to a positive effect on viral replication, e.g., Zika virus (ZIKV) NS1 interacts with USP8 (Ubiquitin Specific Peptidase 8) and causes the deubiquitination of Caspase 1 and prevents its proteasomal degradation."
Sulforaphane affects USP8
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2
Sodium arsenate affects USP8
2
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Sodium arsenate increases the amount of USP8.
1
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Sodium arsenate decreases the amount of USP8.
1
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Phenethyl caffeate affects USP8
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2
MiR-302a-3p affects USP8
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1
1
Iridium atom affects USP8
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2
Iridium atom binds USP8. 2 / 2
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2
sparser
"Other NCIs such as C-H···π between the substrate and the catalyst, C-H···O involving the substrate C-H and the oxygen of the B 2 pin 2 ligand and C-H···N between the substrate and the N atom of the Ir-bound ubpy confirm the significance of such interactions in providing the desirable differential energies between the competing TSs that form the basis of the extent of regioselectivity."
Indometacin affects USP8
2
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Hsa-miR-95-5p affects USP8
2
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Hsa-miR-4789-3p affects USP8
2
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Hsa-miR-466 affects USP8
2
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Hsa-miR-4643 affects USP8
2
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Hsa-miR-19b-3p affects USP8
2
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Hsa-miR-19a-3p affects USP8
2
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Bisphenol A affects USP8
2
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USP8 affects ubiquitination TrkB
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2
USP8 affects sulforaphane
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2
USP8 affects removal
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2
USP8 affects lipopolysaccharide
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2
USP8 affects iridium atom
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2
Iridium atom binds USP8. 2 / 2
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2
sparser
"Other NCIs such as C-H···π between the substrate and the catalyst, C-H···O involving the substrate C-H and the oxygen of the B 2 pin 2 ligand and C-H···N between the substrate and the N atom of the Ir-bound ubpy confirm the significance of such interactions in providing the desirable differential energies between the competing TSs that form the basis of the extent of regioselectivity."
USP8 affects ferroptosis
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1
1
USP8 affects endocytosis
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2
USP8 affects cell differentiation
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2
Mutated USP8 inhibits cell differentiation. 1 / 1
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1
USP8-C748A inhibits cell differentiation. 1 / 1
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1
USP8 affects TrkB-dependent neuronal differentiation
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2
reach
"Moreover, USP8 downregulated several pro inflammatory cytokines [nitric oxide (NO), tumor necrosis factor alpha (TNF-alpha), prostaglandin E 2 (PGE 2), and interleukin-1beta (IL-1beta)] in the serum and brain, and the relevant protein factors [inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2)] in the brain."
reach
"The protein levels of cell membrane protein marker E-cadherin (XREF_FIG, bottom panel) and cell total protein marker beta-actin (XREF_FIG, bottom panel) were not affected under these conditions, thereby indicating that the change in hOAT1 expression induced by USP8 wild type transfection was not due to the general perturbation of membrane and cellular proteins."
USP8 affects SAIT301
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2
USP8 affects Pituitary ACTH Hypersecretion
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1
USP8 activates Pituitary ACTH Hypersecretion. 1 / 2
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1
reach
"Notable examples include: the UCH family member BRCA1-associated protein 1 (BAP1), mutated in melanoma, mesothelioma and renal cell carcinoma ; USP6, translocated in aneurysmal bone cysts ; USP7, mutated in neurological disorders ; USP8, whose mutations cause Cushing disease ; USP9X, whose mutations cause developmental disorders and whose expression is dysregulated in cancer ; USP15, amplified in certain glioblastoma, breast and ovarian cancers ; and CYLD, commonly mutated in cylindromatosis ."
USP8 affects POMC promoter
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2
reach
"Moreover, USP8 downregulated several pro inflammatory cytokines [nitric oxide (NO), tumor necrosis factor alpha (TNF-alpha), prostaglandin E 2 (PGE 2), and interleukin-1beta (IL-1beta)] in the serum and brain, and the relevant protein factors [inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2)] in the brain."
USP8 affects ESCRT-III subunits
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2
USP8 affects ESCRT
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2
USP8 affects Carcinoma, Non-Small-Cell Lung
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1
USP8 activates Carcinoma, Non-Small-Cell Lung. 1 / 2
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1
reach
"Indeed, inhibition of USP8 either by its knockdown or synthetic small molecule led to attenuation of variety of receptor tyrosine kinase (RTK) activities, resulting in the inhibition of cell proliferation in gefitinib-resistant and -sensitive non-small cell lung cancer (NSCLC) cells [47] ."
USP8 affects CHMP proteins
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2
USP8 affects Ala-Gly-Ser
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2
reach
"Thereby, together with these data, it can be concluded that the elevated level of USP8 not only increases the expression of EGFR, PI3K, and P-Akt but also might increase the PI3K and P-Akt expression over EGFR silencing where the PI3K and P-Akt well established the downstream target of EGFR (
Figures 6C, D
)."
USP8 affects AIP4
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2
SAIT301 affects USP8
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2
RNAi affects USP8
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2
RA-9 affects USP8
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2
ESCRT-III subunits affects USP8
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2
ESCRT affects USP8
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2
CHMP proteins affects USP8
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2
AIP4 affects USP8
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2
Titanium dioxide affects USP8
1
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SiRNA2 affects USP8
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1
SiRNA USP8 affects USP8
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1
PCMV3-USP8 affects USP8
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1
Nocodazole affects USP8
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1
Nocodazole activates USP8. 1 / 1
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1
Hsa-miR-4753-5p affects USP8
1
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Hsa-miR-132-3p affects USP8
1
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Doxorubicin affects USP8
1
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Dexamethasone affects USP8
1
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Artonin F affects USP8
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1
[1,2-b]pyrazine-2,3-dicarbonitrile affects USP8
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1
WP1130 affects USP8
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1
eidos
"For example , 8-mercapto-N - ( ( tetrahydro-3-furanyl ) methyl ) -4 - quinoline carboxamide , LND-57444 , VLX1570 , ML323 , ( ADC-01 , ADC-03 , HBX41108 , HBX19818 , P5091 , P22077 ) , 9 - ( ethoxyimino ) -9 H-indeno ( 1,2 - b ) pyrazine-2 ,3 - dicarbonitrile , WP1130 , Mitoxantrone and GSK2643943A are able to inhibit PSMD14 , UCHL1 , UCHL5 and USP14 , USP1 , USP7 , USP8 , USP9X , USP11 and USP20 , respectively ."
Vehicle Emissions affects USP8
1
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sparser
"There was evidence that Magel2 was involved in the leptin-POMC of the hypothalamus to maintain the energy balance of the body.[ xref ]Wijesuriya et al have found that MAGEL2 and Necdin connected leptin receptor (LepR) to the USP8-RNF41 ubiquitin complex through the LepR adapter protein, IRS4."
Ubiquitin affects E3_Ub_ligase
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1
USP8 affects α-syn
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1
USP8 affects transcription, DNA-templated
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1
Mutated USP8 activates transcription, DNA-templated. 1 / 1
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1
USP8 affects proteolysis
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1
USP8 inhibits proteolysis. 1 / 1
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1
USP8 affects protein stability ID1
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1
USP8 affects protein kinase B signaling
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1
USP8 inhibits protein kinase B signaling. 1 / 1
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1
USP8 affects procollagen IV
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1
USP8 affects poly-ubiquitin chains
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1
reach
"Stefan et al. discovered and structurally identified the first covalent inhibitor of NEDD4-1, which switches the mechanism of NEDD4-1 from processive to distributive, following which NEDD4-1 synthesizes the attachment of poly-ubiquitin chains to the substrate in the presence of the deubiquitinating enzyme USP8 ."
USP8 affects pathway
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1
USP8 affects osteogenic differentiation
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1
USP8 affects neuregulin receptor
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1
USP8 affects morphology
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1
USP8 affects migration
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1
USP8 affects melanoma cell growth
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1
USP8 affects linked chains
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1
USP8 affects inhibitory therapeutic drugs
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1
USP8 affects inhibitive miR-302a-3p ossification
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1
USP8 affects hormonogenesis ..
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1
USP8 affects gene expression
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1
USP8 activates gene expression. 1 / 1
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1
USP8 affects gastric cancer cell
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1
eidos
"USP8 regulates NF-kappaB activation through EGFR and PI3K stabilization to promote PCa cell proliferation and survival In multiple studies ( 29-32 ) , the EGFR is a substrate of USP8 deubiquitination , while USP8 has been shown to enhance gastric cancer cell proliferation and metastasis via the PI3K / AKT signaling pathway ( 30 ) ."
USP8 affects gain-of-function USP8 protein
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1
USP8 affects extracellular vesicle-mediated CD8
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1
USP8 affects ethylenediamine
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1
USP8 decreases the amount of ethylenediamine. 1 / 1
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1
USP8 affects dpp-lacZ
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1
USP8 affects dominant negative mutant protein
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1
USP8 affects distinct protein targets
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1
USP8 affects circulating extracellular vesicles
|
1
USP8 affects chains
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1
USP8 affects cell cycle arrest
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1
USP8 inhibits cell cycle arrest. 1 / 1
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1
USP8 affects assess synergism proteasome
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1
USP8 affects alpha-syn SH-SY5Y human cells
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1
USP8 affects activity
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1
USP8 affects activation NF-kappaB pro-inflammatory cytokines
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1
USP8 affects accumulation Cx43
|
1
eidos
"Thus , we propose that , in the absence of AMSH , ubiquitinated Cx43 is mainly directed to degradation , while lack of USP8 results in the accumulation of Cx43 , likely at late endosomes / MVBs , modified with ubiquitin chains that favor its sorting into ILVs that will be subsequently secreted as EVs ( Bejarano et al , 2012 ; Martins-Marques et al , 2015c ) ."
USP8 affects abundance cell surface receptors
|
1
USP8 affects abnormalities caused mutant HTT
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1
USP8 affects Wnt receptor
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1
USP8 affects USP8 inhibitor
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1
USP8 affects TGF-beta SMAD-induced epithelial-mesenchymal transition EMT invasion metastasis tumor cells
|
1
USP8 affects SH3 domain
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1
USP8 affects RP23-78H4.1
1
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USP8 affects Maintenance
|
1
USP8 activates Maintenance. 1 / 1
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1
sparser
"The impact of METTL3 on m 6 A methylation of MALAT1 was examined by methylated RNA immunoprecipitation (RIP), the interaction between PTBP1 and MALAT1 or USP8 mRNA by combining RNA pull-down, RIP, and RNA stability assays, and the crosstalk between USP8 and TAK1 by co-immunoprecipitation and protein degradation assays."
USP8 affects K63-Ub-BRIT1
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1
USP8 affects K6-linked Parkin ubiquitination
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1
USP8 affects K6 ubiquitination
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1
USP8 affects ID1-TXNIP
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1
USP8 affects HRS
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1
USP8 affects GST14-3-3
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1
USP8 affects Fzd receptors
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1
USP8 affects ESCRT-III complex
|
1
USP8 affects ESCRT-0
|
1
reach
"71 In contrast to PAR2, USP8 (or AMSH) does not impact CXCR4 ubiquitination but instead modulates the ubiquitin status of ESCRT-0 that is ubiquitinated by the E3 ligase AIP4, 23 reinforcing the idea that ubiquitination of the transport machinery represents an important regulatory event in GPCR trafficking."
USP8 affects Cushing Syndrome
|
1
USP8 activates Cushing Syndrome. 1 / 1
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1
USP1 inhibitors affects USP8
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1
Src-family kinases affects USP8
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1
STAMBP affects HRS
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1
STAM affects SH3 domain
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1
STAM affects HRS
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1
SH3 domain affects USP8
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1
RP23-78H4.1 affects USP8
1
|
sparser
"There was evidence that Magel2 was involved in the leptin-POMC of the hypothalamus to maintain the energy balance of the body.[ xref ]Wijesuriya et al have found that MAGEL2 and Necdin connected leptin receptor (LepR) to the USP8-RNF41 ubiquitin complex through the LepR adapter protein, IRS4."
RNF41 affects E3_Ub_ligase
|
1
Particulate Matter affects USP8
1
|
sparser
"The impact of METTL3 on m 6 A methylation of MALAT1 was examined by methylated RNA immunoprecipitation (RIP), the interaction between PTBP1 and MALAT1 or USP8 mRNA by combining RNA pull-down, RIP, and RNA stability assays, and the crosstalk between USP8 and TAK1 by co-immunoprecipitation and protein degradation assays."
sparser
"In RPE1 cells, EGFR knockdown is sufficient to repress the USP8-trichoplein-Aurora A axis and induce ciliogenesis, however, we do not exclude the involvement of other RTKs in other cell types since USP8 is also activated by PDGFRs and FGFR1-mediated phosphorylation in vitro (Supplementary Fig. xref )."
NMDAR affects USP8
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1
ML364 affects USP8
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1
sparser
"The impact of METTL3 on m 6 A methylation of MALAT1 was examined by methylated RNA immunoprecipitation (RIP), the interaction between PTBP1 and MALAT1 or USP8 mRNA by combining RNA pull-down, RIP, and RNA stability assays, and the crosstalk between USP8 and TAK1 by co-immunoprecipitation and protein degradation assays."
HRS affects USP8
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1
HER-3 affects USP8
|
1
HER-3 increases the amount of USP8. 1 / 1
|
1
GST14-3-3 affects USP8
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1
GSK2643943A affects USP8
|
1
eidos
"For example , 8-mercapto-N - ( ( tetrahydro-3-furanyl ) methyl ) -4 - quinoline carboxamide , LND-57444 , VLX1570 , ML323 , ( ADC-01 , ADC-03 , HBX41108 , HBX19818 , P5091 , P22077 ) , 9 - ( ethoxyimino ) -9 H-indeno ( 1,2 - b ) pyrazine-2 ,3 - dicarbonitrile , WP1130 , Mitoxantrone and GSK2643943A are able to inhibit PSMD14 , UCHL1 , UCHL5 and USP14 , USP1 , USP7 , USP8 , USP9X , USP11 and USP20 , respectively ."
reach
"Together, the results indicate that the blockade of the FGF/FGFR system by extracellular or intracellular inhibitors exerts a significant impact on the primary cilium in TRAMP-C2 cells.Activation of different tyrosine kinase receptors suppresses ciliogenesis in retinal epithelial cells by stabilizing the trichoplein-Aurora A complex following phosphorylation of the deubiquitinase USP8 [39]."
ESCRT-III affects USP8
|
1
ESCRT-III complex affects USP8
|
1
EGFR-ErbB2 chimera affects USP8
|
1
EGFR-ERBB4 CYT-1 affects USP8
|
1
E3_Ub_ligase affects Ubiquitin
|
1
E3_Ub_ligase affects RNF41
|
1
E3-DUB affects USP8
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1
DUB-specifi c affects USP8
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1
CLEC16A affects E3_Ub_ligase, RNF41, and USP8
|
1
Aroclor 1254 affects USP8
1
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1
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