IndraLab
Statements
sparser
"The key structural rearrangements include: (i) the presence of a neddylated SCF triggers the convergence of the N-terminal helical arms of CSN2 and CSN4 (hereafter CSN2 arm and CSN4 arm respectively), clamping CUL1 CTD and RBX1 RING , (ii) the flexible CUL1 WHB is repositioned against the stabilised RBX1 RING , aligning NEDD8 at the CSN active site and (iii) concurrent disruption of the CSN4-CSN6 interface enables flexibility and remodelling of the CSN5-CSN6 MPN domains, bringing the CSN5 active site closer to NEDD8 (Fig. xref )."
CSN7 subfamily binds COPS4 and COPS6. 1 / 1
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COPS6 affects Neoplasm Invasiveness
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COPS6 activates Neoplasm Invasiveness.
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COPS6 activates Neoplasm Invasiveness. 10 / 24
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"Also, WT CSN6 increased cell migration and invasion in a wound healing assay (p < 0.001, XREF_FIG) and in transwell migration and invasion assays (XREF_FIG), whereas CSN6 S148A lost such capability, demonstrating that the CSN6 promoted migration and invasion of colon cancer cells requires a phosphorylation event."
eidos
"CSN6 promotes GBM proliferation , migration , invasion , and tumorigenesis through upregulation of EGFR by blocking its ubiquitination ; this happens as a result of interactions with CHIP that cause its degradation , although CHIP auto-ubiquitination occurs through an unknown mechanism [ 91 ] ."
COPS6 inhibits Neoplasm Invasiveness.
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COPS6 affects cell population proliferation
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COPS6 activates cell population proliferation.
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COPS6 activates cell population proliferation. 10 / 28
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reach
"Through combinatorial effects on the MDM2-p53 signaling axis and now SKP2 mediated p57 Kip2 degradation, it is hypothesized that CSN6 overexpression can effectively promote cell proliferation by simultaneously relieving cell cycle restraints, apoptosis, senescence, and presumably p53 functions in DNA damage repair and cell metabolism, among other important tumor suppressive mechanisms."
COPS6 inhibits cell population proliferation.
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sparser
"As CSN6‐FOXO4 axis impacts on the expression of Glut1, biochemical assays that quantitates the glucose uptake (consumption) by assessing uptake of (2‐( N ‐(7‐nitrobenz‐2‐oxa‐1,3‐diazol‐4‐yl)amino)‐2‐deoxyglucose (2‐NBDG)), a green fluorescent glucose analog, additionally demonstrated that CSN6 knockdown inhibited 2‐NBDG uptake (Figure xref ), while FOXO4 knockdown increased 2‐NBDG uptake (Figure xref )."
COPS6 is modified
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reach
"These data imply that CSN6 possibly regulates the gene expression of SGOC genes and impacts SGOC amino acid metabolism through its negative impact on FOXO4 that transcriptionally suppresses the gene expression of SGOC genes.2.6
PKB/Akt-Mediated CSN6 Phosphorylation Enhances COP1-Regulated FOXO4 Ubiquitination and Subsequent Elevation of SGOC Genes."
sparser
"First, we have shown that S60 of CSN6 can be phosphorylated by PKB/Akt [ xref ] and that PKB/Akt enhances the steady‐state expression of CSN6. [ xref ] This S60 site is located in CSN6's MPN ( M pr1p and P ad1p N ‐terminal) domain, a domain found in the N‐terminus of yeast Mpr1 and Pad1 proteins. [ xref , xref , xref ] MPN domain contains polar residues that resemble the active site residues of metalloproteases [ xref ] and is involved in a proteasome‐associated deneddylation activity. [ xref ] Also the MPN domain is involved in heterodimerization between CSN6 and CSN5 to regulate Cullin neddylation. [ xref ] How S60 phosphorylation participates in any activity of the MPN domain remains to be identified."
reach
"These data imply that CSN6 possibly regulates the gene expression of SGOC genes and impacts SGOC amino acid metabolism through its negative impact on FOXO4 that transcriptionally suppresses the gene expression of SGOC genes.2.6
PKB/Akt-Mediated CSN6 Phosphorylation Enhances COP1-Regulated FOXO4 Ubiquitination and Subsequent Elevation of SGOC Genes."
reach
"Further, CSN6 KD tumors demonstrate decreased FASN protein levels based on immunohistochemistry (IHC) staining (Fig. 6i) and immunoblotting (Supplementary Fig. 4h), low BODIPY staining (Fig. 6j) and relatively low levels of tumor cell growth (as measured by Ki67 staining) (Fig. 6i), while CSN6-reexpressing tumors can restore the levels of FASN (Fig. 6i, Supplementary Fig. 4h), increase BODIPY staining (Fig. 6j), and elevate Ki67 staining concurrently (Fig. 6i)."
reach
"The significance of this interaction was demonstrated in that dox-induced CSN6 KD led to increased steady-state-expression of FBXW7β with concurrent decreased expression of FASN (Supplementary Fig. 3b), while CSN6 overexpression reduced FBXW7β and resulted in increased FASN level (Supplementary Fig. 3c)."
sparser
"Notably, studies have unveiled intriguing interactions, for instance, PKMYT1's physical interaction with β-catenin, which stabilizes β-catenin protein and activates Wnt signaling, bolstering non-small cell lung cancer CSC self-renewal. xref Additionally, the CSN6-TRIM21 axis has surfaced, spotlighting its role in driving cancer stemness during tumorigenesis."
sparser
"In addition, TRIM21’s function is associated with autoimmune diseases, such as systemic lupus erythematosus (SLE) and Sjögren’s syndrome. xref , xref Notably, patients with SLE or Sjögren’s syndrome have an increased risk for developing certain cancers, including non-Hodgkin’s lymphoma. xref In addition, TRIM21 interacts with endoglin, xref which is a prognostic marker in CRC xref and also act as a CSC marker in renal cell carcinoma. xref Future studies will need to address how the CSN6–TRIM21 axis may impact these signalling pathways to promote tumorigenesis."
reach
"Noticeably, reduced expression of Csn6 in Emicro-Myc background can also contribute to p53 stabilization in 33% of Emicro-Myc and Csn6 +/- lymphomas when compared with Emicro-Myc and Csn6 +/+, suggesting that both CSN6 mediated p53 downregulation and CSN6 mediated Myc elevation contribute to lymphomagenesis of this system (XREF_FIG)."
reach
"Compared with empty vector transfected control cells, cells transfected with CSN6 had a decelerated endogenous Myc turnover rate (XREF_FIG); the pulse chase analyses of over expressed Myc with CSN6 or with shRNA mediated CSN6 knockdown indicated that over expression of CSN6 stabilized Myc while shRNA-CSN6 increased Myc degradation (XREF_FIG)."
COPS6 affects Neoplasm Metastasis
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COPS6 activates Neoplasm Metastasis.
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COPS6 activates Neoplasm Metastasis. 10 / 20
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eidos
"CSN6 promotes tumor metastasis via up-regulating snail1 in xenograft model To identify the role of CSN6 in the metastatic potency of breast cancer cells in vivo , lentiviruses packed with CSN6-NC or CSN6 overexpression vectors were transfected into MDA-MB-231 cell lines , and the fluorescence intensity was detected by Olympus light microscope ( Figure 4A ) ."
COPS6 inhibits Neoplasm Metastasis.
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COPS6 inhibits Neoplasm Metastasis. 1 / 1
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"Finally, to link CSN6 to the event, we showed that GSK3β (S9A)-enhanced FASN ubiquitination is attenuated by the expression of CSN6 (Fig. 4m), suggesting that CSN6 antagonized FBXW7β/GSK3β-mediated FASN ubiquitination.To determine the phenotypic effect of GSK3β in governing FBXW7β-mediated FASN degradation."
reach
"The significance of this interaction was demonstrated in that dox-induced CSN6 KD led to increased steady-state-expression of FBXW7β with concurrent decreased expression of FASN (Supplementary Fig. 3b), while CSN6 overexpression reduced FBXW7β and resulted in increased FASN level (Supplementary Fig. 3c)."
reach
"Mechanistic studies suggested that ERK2 directly binds to CSN6 Leu163/Val165 and phosphorylates COPS6 at Ser148, thereby regulating β-Trcp and stabilizing β-catenin expression, consequently blocking the ubiquitin-proteasome pathway and promoting CRC development.Programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) checkpoint blockade is an emerging immunotherapy modality in various tumors, while its regulatory mechanism remains uncertain."
reach
"Mechanistic studies suggested that ERK2 directly binds to CSN6 Leu163/Val165 and phosphorylates COPS6 at Ser148, thereby regulating β-Trcp and stabilizing β-catenin expression, consequently blocking the ubiquitin-proteasome pathway and promoting CRC development.Programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) checkpoint blockade is an emerging immunotherapy modality in various tumors, while its regulatory mechanism remains uncertain."
reach
"Mechanistic studies suggested that ERK2 directly binds to CSN6 Leu163/Val165 and phosphorylates COPS6 at Ser148, thereby regulating β-Trcp and stabilizing β-catenin expression, consequently blocking the ubiquitin-proteasome pathway and promoting CRC development.Programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) checkpoint blockade is an emerging immunotherapy modality in various tumors, while its regulatory mechanism remains uncertain."
reach
"For instance, Zhang et al[24] revealed that the COPS6-UBR5-CDK9 axis could control melanoma proliferation and metastasis, while Mao et al[25] found that COPS6 could promote migration and invasion of cervical cancer cells by regulating the expression level of cathepsin L through the autophagy-lysosomal system."
reach
"We also found that CSN6 overexpression in melanoma cells could prolong the half-life of CDK9 and that the decrease in CDK9 protein expression in CSN6-knockdown cells could be obviously rescued in the presence of MG132, indicating that CSN6 regulates CDK9 stability by reducing CDK9 ubiquitination."
reach
"In addition, to investigate whether CSN6 controls the ubiquitination and degradation of the E3 ligase UBR5 to stabilize CDK9, in vivo ubiquitination assays were performed and found that CSN6 increased UBR5 ubiquitination levels and decreased CDK9 ubiquitination levels in melanoma cells and 293FT cells."
sparser
"Notably, studies have unveiled intriguing interactions, for instance, PKMYT1's physical interaction with β-catenin, which stabilizes β-catenin protein and activates Wnt signaling, bolstering non-small cell lung cancer CSC self-renewal. xref Additionally, the CSN6-TRIM21 axis has surfaced, spotlighting its role in driving cancer stemness during tumorigenesis."
sparser
"In addition, TRIM21’s function is associated with autoimmune diseases, such as systemic lupus erythematosus (SLE) and Sjögren’s syndrome. xref , xref Notably, patients with SLE or Sjögren’s syndrome have an increased risk for developing certain cancers, including non-Hodgkin’s lymphoma. xref In addition, TRIM21 interacts with endoglin, xref which is a prognostic marker in CRC xref and also act as a CSC marker in renal cell carcinoma. xref Future studies will need to address how the CSN6–TRIM21 axis may impact these signalling pathways to promote tumorigenesis."
sparser
"NSC348884, a small‐molecule inhibitor targeting NPM1, disrupts its biological function via oligomerization interference (Figure xref , Supporting Information). [ xref , xref ] To assess the therapeutic potential of targeting the CSN6‐NPM1 axis for suppressing PDAC progression and overcoming gemcitabine resistance, we therefore treated PDAC cell lines with NSC348884."
COPS6 affects Snail1
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sparser
"As CSN6‐FOXO4 axis impacts on the expression of Glut1, biochemical assays that quantitates the glucose uptake (consumption) by assessing uptake of (2‐( N ‐(7‐nitrobenz‐2‐oxa‐1,3‐diazol‐4‐yl)amino)‐2‐deoxyglucose (2‐NBDG)), a green fluorescent glucose analog, additionally demonstrated that CSN6 knockdown inhibited 2‐NBDG uptake (Figure xref ), while FOXO4 knockdown increased 2‐NBDG uptake (Figure xref )."
sparser
"NSC348884, a small‐molecule inhibitor targeting NPM1, disrupts its biological function via oligomerization interference (Figure xref , Supporting Information). [ xref , xref ] To assess the therapeutic potential of targeting the CSN6‐NPM1 axis for suppressing PDAC progression and overcoming gemcitabine resistance, we therefore treated PDAC cell lines with NSC348884."
reach
"Immunoblotting analysis showed that EGF treatment decreased the steady‐state expression of FOXO4 within 45 min (Figure
1A, Figure S1A, Supporting Information) and accelerated turnover rate of FOXO4 (Figure S1B, Supporting Information) in several CRC cell lines, whereas the EGF induced the expression of CSN6 and COP1, an E3 ligase, within that period of time (Figure 1A, Figure S1A, Supporting Information)."
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reach
"Through combinatorial effects on the MDM2-p53 signaling axis and now SKP2 mediated p57 Kip2 degradation, it is hypothesized that CSN6 overexpression can effectively promote cell proliferation by simultaneously relieving cell cycle restraints, apoptosis, senescence, and presumably p53 functions in DNA damage repair and cell metabolism, among other important tumor suppressive mechanisms."
reach
"Noticeably, reduced expression of Csn6 in Emicro-Myc background can also contribute to p53 stabilization in 33% of Emicro-Myc and Csn6 +/- lymphomas when compared with Emicro-Myc and Csn6 +/+, suggesting that both CSN6 mediated p53 downregulation and CSN6 mediated Myc elevation contribute to lymphomagenesis of this system (XREF_FIG)."
reach
"Under physiological condition, Csn6
liver cancer tissue demonstrated higher SPOP expression, less expression of MDM2, HMGCS1 and survivin (YAP1 target gene) when compared with Csn6
liver cancer tissue (Figure 6J,K), suggesting that CSN6‐MDM2 axis‐mediated SPOP ubiquitination and consequential HMGCS1 stabilization can be recapitulated in Csn6
mouse liver cancer.2.7
Targeting CSN6-HMGCS1 Axis to Suppress Tumor Growth in NAFLD Related HCC."
sparser
"In addition to demonstrating amplification of the CSN6 gene locus at 7q22.1 in human mammary tumors, xref they report that AKT phosphorylation at Ser60 stabilizes CSN6. xref Interestingly, by promoting 14–3-3σ degradation through stabilization of its E3-ligase COP1, CSN6 can activate AKT to create a self-propelling positive feedback loop xref ( xref )."
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COPS6 activates epithelial to mesenchymal transition.
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COPS6 increases the amount of epithelial to mesenchymal transition.
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reach
"Mechanistic studies suggested that ERK2 directly binds to CSN6 Leu163/Val165 and phosphorylates COPS6 at Ser148, thereby regulating β-Trcp and stabilizing β-catenin expression, consequently blocking the ubiquitin-proteasome pathway and promoting CRC development.Programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) checkpoint blockade is an emerging immunotherapy modality in various tumors, while its regulatory mechanism remains uncertain."
reach
"Mechanistic studies suggested that ERK2 directly binds to CSN6 Leu163/Val165 and phosphorylates COPS6 at Ser148, thereby regulating β-Trcp and stabilizing β-catenin expression, consequently blocking the ubiquitin-proteasome pathway and promoting CRC development.Programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) checkpoint blockade is an emerging immunotherapy modality in various tumors, while its regulatory mechanism remains uncertain."
COPS6 affects Carcinogenesis
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COPS6 activates Carcinogenesis. 7 / 8
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eidos
"CSN6 promotes GBM proliferation , migration , invasion , and tumorigenesis through upregulation of EGFR by blocking its ubiquitination ; this happens as a result of interactions with CHIP that cause its degradation , although CHIP auto-ubiquitination occurs through an unknown mechanism [ 91 ] ."
reach
"29
The latest research showed that constitutive photomorphogenic 9 signalosome complex subunit 6 (CSN6) and plant homeodomain finger protein 19 (PHF19) exacerbate the pathological myocardial hypertrophy induced by Ang II by inhibiting the expression of SIRT2, and the overexpression of SIRT2 can reduce the effect of CSN6 in promoting myocardial hypertrophy."
COPS6 affects cell migration
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COPS6 activates cell migration. 7 / 7
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reach
"Also, WT CSN6 increased cell migration and invasion in a wound healing assay (p < 0.001, XREF_FIG) and in transwell migration and invasion assays (XREF_FIG), whereas CSN6 S148A lost such capability, demonstrating that the CSN6 promoted migration and invasion of colon cancer cells requires a phosphorylation event."
reach
"Under physiological condition, Csn6
liver cancer tissue demonstrated higher SPOP expression, less expression of MDM2, HMGCS1 and survivin (YAP1 target gene) when compared with Csn6
liver cancer tissue (Figure 6J,K), suggesting that CSN6‐MDM2 axis‐mediated SPOP ubiquitination and consequential HMGCS1 stabilization can be recapitulated in Csn6
mouse liver cancer.2.7
Targeting CSN6-HMGCS1 Axis to Suppress Tumor Growth in NAFLD Related HCC."
COPS6 affects cell cycle
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COPS6 activates cell cycle.
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COPS6 activates cell cycle. 4 / 4
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"This study revealed that CSN6 knockdown in melanoma cells inhibited cell proliferation in vitro and tumorigenicity in mice by inducing cell cycle arrest and that the anti-proliferative effect could be rescued by overexpressing CSN6 in CSN6-knockdown melanoma cells, suggesting that CSN6 has critical roles in triggering melanoma initiation and progression."
COPS6 inhibits cell cycle.
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COPS6 inhibits cell cycle. 2 / 2
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"Through combinatorial effects on the MDM2-p53 signaling axis and now SKP2 mediated p57 Kip2 degradation, it is hypothesized that CSN6 overexpression can effectively promote cell proliferation by simultaneously relieving cell cycle restraints, apoptosis, senescence, and presumably p53 functions in DNA damage repair and cell metabolism, among other important tumor suppressive mechanisms."
COPS6 affects E3_Ub_ligase
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COPS6 binds E3_Ub_ligase.
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COPS6 activates E3_Ub_ligase.
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reach
"In another study, quercetin inhibited the viability of HT29 cells, caused cell shrinkage, chromatin condensation, and nuclear collapse, lessened the protein expression levels of phosphorylated-Akt, and augmented the protein degradation of constitutive photomorphogenesis 6 signalosome (CSN6) (Yang et al., 2016)."
sparser
"These results show that the CSN complex bear only one copy of Csn6, either a full-length or a truncated form (S6CD); while the MPN − domain fragment of Csn6, when expressed without the S6CD and incapable of integrating into the CSN complex, can still interact with over-stoichiometric amounts of Flag-Csn6 ( xref , xref , xref )."
COPS6 affects cell growth
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sparser
"These results show that the CSN complex bear only one copy of Csn6, either a full-length or a truncated form (S6CD); while the MPN − domain fragment of Csn6, when expressed without the S6CD and incapable of integrating into the CSN complex, can still interact with over-stoichiometric amounts of Flag-Csn6 ( xref , xref , xref )."
COPS6 affects Aldh1a1 mRNA
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Pirinixic acid affects COPS6
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sparser
"Given that CSN6 is a potential Tespa1 interacting factor by protein-protein interaction analysis using STRING database (Supplementary Fig. xref ), we first conducted an in situ proximity ligation assay and found that Tespa1 could interact with CSN6 in HSCs upon 5-FU and IR treatment (Supplementary Fig. xref )."
sparser
"By plotting the mean intensity of the fluorescent signal for EGFP and EGFP-CSN6, and curve fitted using a non-linear regression and the exponential one-phase association model, it was found that CSN6 has a larger immobile fraction than EGFP ( xref )); a result consistent with a strong association with substructures within the midbody such as the contractile ring."
CSN3 affects COPS6
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COPS6 affects nucleotide metabolic process
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sparser
"Given that CSN6 is a potential Tespa1 interacting factor by protein-protein interaction analysis using STRING database (Supplementary Fig. xref ), we first conducted an in situ proximity ligation assay and found that Tespa1 could interact with CSN6 in HSCs upon 5-FU and IR treatment (Supplementary Fig. xref )."
sparser
"By plotting the mean intensity of the fluorescent signal for EGFP and EGFP-CSN6, and curve fitted using a non-linear regression and the exponential one-phase association model, it was found that CSN6 has a larger immobile fraction than EGFP ( xref )); a result consistent with a strong association with substructures within the midbody such as the contractile ring."
COPS6 affects CSN3
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Snail1 affects COPS6
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E3_Ub_ligase affects COPS6
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CSN3 affects COPS5
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COPS6 affects migration
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eidos
"CSN6 promotes GBM proliferation , migration , invasion , and tumorigenesis through upregulation of EGFR by blocking its ubiquitination ; this happens as a result of interactions with CHIP that cause its degradation , although CHIP auto-ubiquitination occurs through an unknown mechanism [ 91 ] ."
COPS6 affects lipid biosynthetic process
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COPS6 affects interleukin-6 production
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COPS6 affects apoptotic process
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COPS6 inhibits apoptotic process. 3 / 3
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reach
"Through combinatorial effects on the MDM2-p53 signaling axis and now SKP2 mediated p57 Kip2 degradation, it is hypothesized that CSN6 overexpression can effectively promote cell proliferation by simultaneously relieving cell cycle restraints, apoptosis, senescence, and presumably p53 functions in DNA damage repair and cell metabolism, among other important tumor suppressive mechanisms."
COPS6 affects Snail1 protein
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COPS6 affects Hypertrophy
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COPS6 affects A0A288CFT1
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COPS5 affects CSN3
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Angiotensin-2 affects COPS6
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A0A288CFT1 affects COPS6
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P57 affects COPS6
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Cobalt dichloride affects COPS6
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Caspase recruitment domain affects COPS6
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Bisphenol A affects COPS6
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Ser148 affects MAPK1
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reach
"Mechanistic studies suggested that ERK2 directly binds to CSN6 Leu163/Val165 and phosphorylates COPS6 at Ser148, thereby regulating β-Trcp and stabilizing β-catenin expression, consequently blocking the ubiquitin-proteasome pathway and promoting CRC development.Programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) checkpoint blockade is an emerging immunotherapy modality in various tumors, while its regulatory mechanism remains uncertain."
MPN domain affects COPS6
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MAPK1 affects Ser148
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reach
"Mechanistic studies suggested that ERK2 directly binds to CSN6 Leu163/Val165 and phosphorylates COPS6 at Ser148, thereby regulating β-Trcp and stabilizing β-catenin expression, consequently blocking the ubiquitin-proteasome pathway and promoting CRC development.Programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) checkpoint blockade is an emerging immunotherapy modality in various tumors, while its regulatory mechanism remains uncertain."
MAPK1 affects Leu163
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reach
"Mechanistic studies suggested that ERK2 directly binds to CSN6 Leu163/Val165 and phosphorylates COPS6 at Ser148, thereby regulating β-Trcp and stabilizing β-catenin expression, consequently blocking the ubiquitin-proteasome pathway and promoting CRC development.Programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) checkpoint blockade is an emerging immunotherapy modality in various tumors, while its regulatory mechanism remains uncertain."
Leu163 affects MAPK1
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reach
"Mechanistic studies suggested that ERK2 directly binds to CSN6 Leu163/Val165 and phosphorylates COPS6 at Ser148, thereby regulating β-Trcp and stabilizing β-catenin expression, consequently blocking the ubiquitin-proteasome pathway and promoting CRC development.Programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) checkpoint blockade is an emerging immunotherapy modality in various tumors, while its regulatory mechanism remains uncertain."
FBXW7β affects COPS6
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CUL affects CSN2
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COPS6 affects v-myc avian myelocytomatosis viral oncogene homolog
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COPS6 affects turnover OCT1
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COPS6 affects steady-state TRIM21
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eidos
"Tripartite motif ( TRIM ) protein family members ( numbering > 70 ) have been implicated in various cellular functions , including cell proliferation , differentiation , development , apoptosis , antiviral activity , autophagy and oncogenesis.44 TRIM21 plays a pivotal role in immune activation during pathogen infection , but its cellular function remains unclear.45 Interestingly , CSN6 is able to decrease the steady-state expression of TRIM21 by enhancing TRIM21 ubiquitination , thereby promoting cancer stemness ."
COPS6 affects pyrimidine
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COPS6 affects pathway
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COPS6 affects p57
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COPS6 affects caspase recruitment domain
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COPS6 affects biosynthetic process
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COPS6 affects Wounds and Injuries
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COPS6 inhibits Wounds and Injuries. 2 / 2
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eidos
"HVIPs have been reported to reduce both trauma and criminal justice recidivism ( Cooper et al ., 2006 ; Shibru et al ., 2007 ) ; however , there is limited and mixed evidence to support their effectiveness ( Affinati et al ., 2016 ; Chong et al ., 2015 ; Cooper et al ., 2006 ; Dicker , 2016 ; Juillard et al ., 2016 ; Purtle et al ., 2013 ; Smith et al ., 2013 ) ."
COPS6 affects Stomach Neoplasms
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COPS6 affects Snail1 stability
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COPS6 affects Ser148
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reach
"Mechanistic studies suggested that ERK2 directly binds to CSN6 Leu163/Val165 and phosphorylates COPS6 at Ser148, thereby regulating β-Trcp and stabilizing β-catenin expression, consequently blocking the ubiquitin-proteasome pathway and promoting CRC development.Programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) checkpoint blockade is an emerging immunotherapy modality in various tumors, while its regulatory mechanism remains uncertain."
COPS6 affects MPN domain
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reach
"Mechanistic studies suggested that ERK2 directly binds to CSN6 Leu163/Val165 and phosphorylates COPS6 at Ser148, thereby regulating β-Trcp and stabilizing β-catenin expression, consequently blocking the ubiquitin-proteasome pathway and promoting CRC development.Programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) checkpoint blockade is an emerging immunotherapy modality in various tumors, while its regulatory mechanism remains uncertain."
reach
"Mechanistic studies suggested that ERK2 directly binds to CSN6 Leu163/Val165 and phosphorylates COPS6 at Ser148, thereby regulating β-Trcp and stabilizing β-catenin expression, consequently blocking the ubiquitin-proteasome pathway and promoting CRC development.Programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) checkpoint blockade is an emerging immunotherapy modality in various tumors, while its regulatory mechanism remains uncertain."
COPS6 affects LC3-II
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COPS6 affects FBXW7β
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COPS6 affects DNA-templated transcription
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COPS6 inhibits DNA-templated transcription.
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COPS6 inhibits DNA-templated transcription. 1 / 1
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COPS6 activates DNA-templated transcription.
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COPS6 activates DNA-templated transcription. 1 / 1
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COPS6 affects CRC PDOs
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COPS6 affects ALV-J
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COPS6 affects 14-3-3sigma
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COPS6 affects 3',5'-cyclic AMP
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COPS5 affects MPN domain
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17alpha-ethynylestradiol affects COPS6
2
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Tert-Butylhydroperoxide affects COPS6
1
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Hsa-miR-328-3p affects COPS6
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Benzo[a]pyrene affects COPS6
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Aristolochic acid A affects COPS6
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Apoptotic process affects COPS6
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Apoptotic process activates COPS6. 1 / 1
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UBR5 affects A375
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RING-box protein 1 affects CUL
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LOC100128400 affects COPS6
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IGHV3OR15-7 affects COPS6
1
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EGFR-ERK affects COPS6
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CUL affects RING-box protein 1
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CSN7 subfamily affects COPS6
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CSN2 affects csn
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CSN2 affects RING-box protein 1
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CSN2 affects RBX1
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COPS6 affects ubiquitination degradation cancer associated proteins
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COPS6 affects ubiquitin proteasome system-mediated Nkx2.2 protein
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COPS6 affects tumour-formation diluted
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COPS6 affects tumour growth
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COPS6 affects spheres enriched
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COPS6 affects soft agar colony
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COPS6 affects proteasome complex disassembly
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COPS6 activates proteasome complex disassembly. 1 / 1
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COPS6 affects photomorphogenesis
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COPS6 inhibits photomorphogenesis. 1 / 1
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reach
"In another study, quercetin inhibited the viability of HT29 cells, caused cell shrinkage, chromatin condensation, and nuclear collapse, lessened the protein expression levels of phosphorylated-Akt, and augmented the protein degradation of constitutive photomorphogenesis 6 signalosome (CSN6) (Yang et al., 2016)."
COPS6 affects metastasis potential breast cancer cells
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COPS6 affects lactate fructose-1
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COPS6 affects growth migration invasion melanoma cells
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COPS6 affects decelerated turnover TRIM21
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COPS6 affects cycloheximide
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COPS6 inhibits cycloheximide. 1 / 1
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COPS6 affects cullin E3 ligases
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COPS6 affects cellular senescence
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COPS6 inhibits cellular senescence. 1 / 1
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reach
"Through combinatorial effects on the MDM2-p53 signaling axis and now SKP2 mediated p57 Kip2 degradation, it is hypothesized that CSN6 overexpression can effectively promote cell proliferation by simultaneously relieving cell cycle restraints, apoptosis, senescence, and presumably p53 functions in DNA damage repair and cell metabolism, among other important tumor suppressive mechanisms."
COPS6 affects cancer stemness
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COPS6 affects breast cancer cells
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COPS6 affects activity
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COPS6 affects Ubiquitination
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COPS6 activates Ubiquitination. 1 / 1
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COPS6 affects RING-box protein 1
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1
reach
"Further, CSN6 KD tumors demonstrate decreased FASN protein levels based on immunohistochemistry (IHC) staining (Fig. 6i) and immunoblotting (Supplementary Fig. 4h), low BODIPY staining (Fig. 6j) and relatively low levels of tumor cell growth (as measured by Ki67 staining) (Fig. 6i), while CSN6-reexpressing tumors can restore the levels of FASN (Fig. 6i, Supplementary Fig. 4h), increase BODIPY staining (Fig. 6j), and elevate Ki67 staining concurrently (Fig. 6i)."
COPS6 affects LOC100128400
1
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COPS6 affects IGHV3OR15-7
1
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COPS6 affects FBXW7beta
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1
COPS6 affects EGFR-interacting E3 ligase CHIP
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1
COPS6 affects CSN7 subfamily
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1
COPS6 affects CSN6-CSN5 hetreodimer
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1
COPS6 affects CD8-Positive T-Lymphocytes
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1
COPS6 inhibits CD8-Positive T-Lymphocytes. 1 / 1
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1
COPS6 affects A375
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1
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1
COPS4 affects CSN7 subfamily
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1
CHX affects COPS6
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1
Akt inhibitor affects COPS6
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1
A375 affects UBR5
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1
1
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