IndraLab
Statements
reach
"Both USP29 and TWIST1 are overexpressed in TNBC tumor specimens, but not in normal adult breast tissues, highlighting the potential of USP29 as a more druggable target toward TWIST1 stability in TNBC.It is also noteworthy that we can not rule out the possibility of additional mechanisms engaged in UPS29‐regulated tumor progression of TNBC since the ectopic expression of TWIST1 could not completely rescue functional alterations caused by the depletion of USP29 in TNBC cells."
reach
"As shown in Figure 3G–J and Figure S3O–R (Supporting Information), the knockdown of USP29 significantly decreased the expression of TWIST1, and increased cancer cellular sensitivity to these chemotherapeutic agents both in vitro and in vivo, which could be largely reversed by the reconstitution of TWIST1 in USP29‐depleted cells."
reach
"Of note, the depletion of USP29 in both MDA‐MB‐231 and BT549 cells significantly decreased the expression of TWIST1 and Vimentin, and increased the expression of epithelial marker E‐cadherin (Figure
3A; Figure S3C,D, Supporting Information), while the reconstitution of TWIST1 in USP29‐deficient cells could dramatically rescue such a change (Figure 3A)."
reach
"These observations imply the necessity of USP29 DUB activity in the regulation of Snail1, but the exact roles of USP29 mutations detected in cancer samples require further clarification.To evaluate the interaction between Snail1 and USP29, we carried out a series of co-immunoprecipitation experiments."
reach
"Further evidence showed that EMT might be the primary mechanism for the enhanced metastatic property in GC cells: USP13 and USP29 promoted TGF-β1-induced EMT through interacting with and deubiquitinating Snail, while USP3 facilitated this process by deubiquitinating SUZ12 (Wu et al. 2021; Zhang et al. 2022a, b; Qian et al. 2020)."
reach
"Results from endogenous immunoprecipitation assays suggested that USP29 constitutively interacted with cGAS in bone marrow derived macrophages (BMDMs), bone marrow derived dendritic cells (BMDCs), mouse embryonic fibroblasts (MEFs), mouse lung fibroblasts (MLFs) or human monocytic THP-1 cells and their association was potentiated after HSV-1 infection."
"Mechanistically, <span class="match term0">USP29</span> constitutively interacts with <span class="match term1">cGAS</span>, deconjugates K48-linked polyubiquitin chains from <span class="match term1">cGAS</span> and stabilizes <span class="match term1">cGAS</span> in uninfected cells or after HSV-1 infection"
sparser
"The overexpression of CDK1 has been detected in several types of human cancers and contributes to deregulated cell cycle, DNA damage response, protein synthesis, and other cell cycle independent functions. [ xref ] We next investigated whether CDK1 could phosphorylate USP29 and affect its tumor‐promoting function in TNBC."
sparser
"In this study, we reveal several unexpected tumor‐promoting functions and the clinical significance of the CDK1‐USP29 axis through stabilizing TWIST1 and provide preclinical evidence demonstrating that targeting CDK1‐USP29 axis is an appealing therapeutic strategy to conquer chemo‐resistance and metastasis in TNBC (Figure xref )."
sparser
"Taken together, the findings reveal a previously unrecognized tumor‐promoting function and clinical significance of the CDK1‐USP29 axis through stabilizing TWIST1 and provide the preclinical evidence that targeting this axis is an appealing therapeutic strategy to conquer chemo‐resistance and metastasis in TNBC."
USP29 is modified
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USP29 is phosphorylated.
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sparser
"As shown in Figure xref , Figure xref (Supporting Information), the phosphorylation of USP29 was detected in both MDA‐MB‐231 and BT549 cells by using phospho‐CDK substrate antibody and the genetic ablation or the pharmacological inhibition of CDK1 by RO‐3306 could significantly reduce this phosphorylation event (Figure xref , Figure xref , Supporting Information)."
USP29 is ubiquitinated.
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USP29 is sumoylated.
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USP29 is methylated.
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CGAS affects USP29
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sparser
"Interestingly, we found that TRIM38 constitutively interacts with cGAS but not with USP29, whereas USP29 constitutively interacts with cGAS but not with TRIM38 (Supplementary information, Fig. xref ), indicating that TRIM38 and USP29 independently interacts with and regulates cGAS."
sparser
"It has been proposed that three pools of cGAS exist in uninfected cells: unmodified, Lys217-sumoylated and constitutively Lys271-ubiquitinated cGAS. xref Sumoylation at Lys217 antagonizes K48-linked ubiquitination of Lys271 of cGAS, thereby inhibiting its proteasomal degradation. xref In our study, we found that USP29 constitutively interacted with cGAS and USP29 deficiency substantially potentiated basal K48-linked ubiquitination of cGAS and downregulated cGAS protein level without affecting its mRNA expression in uninfected cells, indicating that USP29 constitutively removes K48-linked ubiquitination of cGAS to maintain a relatively high level of cGAS under steady conditions."
USP29 binds cGAS. 1 / 1
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"With several substrates among proteins functioning in the DNA damage response, USP29 can be considered as one of the central ubiquitin hydrolases contributing to the maintenance of genome integrity.Our results show that the decreased levels of SETD8 in cells depleted of USP29 do not have an indirect effect on cell cycle progression and, moreover, demonstrate an interaction between USP29 and SETD8 in vivo."
reach
"Indeed, overexpression of wildtype USP29 diminished polyubiquitination of SETD8 in vivo, whereas the polyubiquitinated SETD8 was less affected by a co-expression of a catalytic inactive version of the ubiquitin hydrolase.We next demonstrated that the depletion of USP29 inhibited the accumulation of 53BP1 into foci after treating the cells with IR."
USP29 affects apoptotic process
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USP29 activates apoptotic process.
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USP29 activates apoptotic process. 10 / 11
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"Generally, our findings for the first time identify that USP29 upregulation during cerebral I/R may contribute to oxidative stress, neuronal apoptosis, and the progression of cerebral I/R injury and that inhibition of USP29 may help to develop novel therapeutic strategies to treat cerebral I/R injury.Multiple mechanisms are implicated in the pathogenesis of cerebral I/R injury, including oxidative stress and apoptosis."
reach
"Our findings for the first time identify that USP29 upregulation during cerebral I/R may contribute to oxidative stress, neuronal apoptosis, and the progression of cerebral I/R injury and that inhibition of USP29 may help to develop novel therapeutic strategies to treat cerebral I/R injury."
USP29 inhibits apoptotic process.
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"Results from endogenous immunoprecipitation assays suggested that USP29 constitutively interacted with cGAS in bone marrow derived macrophages (BMDMs), bone marrow derived dendritic cells (BMDCs), mouse embryonic fibroblasts (MEFs), mouse lung fibroblasts (MLFs) or human monocytic THP-1 cells and their association was potentiated after HSV-1 infection."
reach
"These observations imply the necessity of USP29 DUB activity in the regulation of Snail1, but the exact roles of USP29 mutations detected in cancer samples require further clarification.To evaluate the interaction between Snail1 and USP29, we carried out a series of co-immunoprecipitation experiments."
sparser
"To demonstrate proper verification of the insulin content in drug products, a quantitative analysis was performed on products containing recombinant hI, porcine insulin, and one hI analog, using the corresponding insulin-type-specific USP (USP29-NF24) and EP monographs appropriately validated for quantitation."
sparser
"In an initial screening assessment, all insulin products were tested with the chromatographic procedure described in the RP-HPLC identification method of the USP monograph (USP29-NF24), “Insulin.” Although this chromatographic procedure is only intended for use with human and porcine insulin products, we used this as a rapid preliminary assessment to screen qualitatively for potentially abnormal insulin traces in all products."
reach
"Such tumor-promoting effects of USP29 were experimentally validated through a series of in vitro and in vivo phenotypic assays, with several lines of evidence in support of the notion that USP29 expression positively correlated with the enhanced stemness of lung adenocarcinoma cells.It is intriguing that certain labile transcription factors can be stabilized by diverse DUBs, with p53 showing a leading example."
reach
"In our previous study, we revealed that USP29 promoted tumor cell aerobic glycolysis and glutamine anaplerosis by deubiquitinating and stabilizing the oncogenic MYC family and HIF1α, and systemic knockout of USP29 significantly suppressed tumor progression and prolonged the survival of tumor-bearing mice."
reach
"In our previous study, we revealed that USP29 promoted tumor cell aerobic glycolysis and glutamine anaplerosis by deubiquitinating and stabilizing the oncogenic MYC family and HIF1α, and systemic knockout of USP29 significantly suppressed tumor progression and prolonged the survival of tumor-bearing mice."
sparser
"To examine which kind of polyubiquitin chains USP29 removes from AURKB, we co-transfected 293T cells with Flag-AURKB, Myc-USP29 and HA-tagged ubiquitin mutants retaining a single lysine residue, and uncovered that USP29 specifically deconjugated the K48-linked polyubiquitin chains (Fig. xref G), a well-established destruction signal to trigger 26 S proteasome-mediated proteolysis [ xref ]."
sparser
"In this study, we reveal several unexpected tumor‐promoting functions and the clinical significance of the CDK1‐USP29 axis through stabilizing TWIST1 and provide preclinical evidence demonstrating that targeting CDK1‐USP29 axis is an appealing therapeutic strategy to conquer chemo‐resistance and metastasis in TNBC (Figure xref )."
sparser
"Taken together, the findings reveal a previously unrecognized tumor‐promoting function and clinical significance of the CDK1‐USP29 axis through stabilizing TWIST1 and provide the preclinical evidence that targeting this axis is an appealing therapeutic strategy to conquer chemo‐resistance and metastasis in TNBC."
reach
"With several substrates among proteins functioning in the DNA damage response, USP29 can be considered as one of the central ubiquitin hydrolases contributing to the maintenance of genome integrity.Our results show that the decreased levels of SETD8 in cells depleted of USP29 do not have an indirect effect on cell cycle progression and, moreover, demonstrate an interaction between USP29 and SETD8 in vivo."
sparser
"To assess the potential role of USP29 in regulating AURKB ubiquitination, we co-expressed HA-AURKB, Myc-Ub, and Flag-USP29 in 293T cells, and revealed thatUSP29 markedly impaired the polyubiquitination of AURKB, which requires the DUB activity of USP29, as the catalytic-inactive C294S (substitution of cysteine 294 to serine) mutant that was reported to display a similar substrate-binding capacity [ xref ], failed to reduce AURKB polyubiquitination (Fig. xref F)."
sparser
"We examined the cell activity after the H/R challenge with a CCK-8 assay and found that the cell viability of the Flag-USP29 group was significantly higher than that of control cells ( xref ), which indicates that USP29 overexpression enhanced the cells’ tolerance to the H/R challenge."
sparser
"The proteomic data revealed 81 and 39 putative binding proteins (with coverage > 30%) in control and Flag-USP29 immunoprecipitates, respectively (Supplementary Fig. xref A), and AURKB, a well-established oncogenic driver, was specifically immunoprecipitated by USP29 (Fig. xref B and Supplementary Fig. xref B)."
sparser
"To assess the potential role of USP29 in regulating AURKB ubiquitination, we co-expressed HA-AURKB, Myc-Ub, and Flag-USP29 in 293T cells, and revealed thatUSP29 markedly impaired the polyubiquitination of AURKB, which requires the DUB activity of USP29, as the catalytic-inactive C294S (substitution of cysteine 294 to serine) mutant that was reported to display a similar substrate-binding capacity [ xref ], failed to reduce AURKB polyubiquitination (Fig. xref F)."
sparser
"We examined the cell activity after the H/R challenge with a CCK-8 assay and found that the cell viability of the Flag-USP29 group was significantly higher than that of control cells ( xref ), which indicates that USP29 overexpression enhanced the cells’ tolerance to the H/R challenge."
sparser
"The proteomic data revealed 81 and 39 putative binding proteins (with coverage > 30%) in control and Flag-USP29 immunoprecipitates, respectively (Supplementary Fig. xref A), and AURKB, a well-established oncogenic driver, was specifically immunoprecipitated by USP29 (Fig. xref B and Supplementary Fig. xref B)."
USP29 affects inflammatory response
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USP29 inhibits inflammatory response.
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USP29 inhibits inflammatory response. 8 / 8
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"Thus, our results suggest that USP29 attenuates hepatic I/R injury by inhibiting the inflammatory response and apoptosis.We performed an RNA-sequencing (RNA-Seq) analysis of liver tissues from USP29 knockout mice and controls with I/R injury after 3h, and the results of the KEGG signaling pathway enrichment analysis showed that the MAPK signaling pathway was the most affected after USP29 knockout."
USP29 activates inflammatory response.
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USP29 activates inflammatory response. 1 / 1
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USP29 affects Reperfusion Injury
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USP29 activates Reperfusion Injury.
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USP29 inhibits Reperfusion Injury.
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USP29 inhibits Reperfusion Injury. 3 / 3
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reach
"Thus, our results suggest that USP29 attenuates hepatic I/R injury by inhibiting the inflammatory response and apoptosis.We performed an RNA-sequencing (RNA-Seq) analysis of liver tissues from USP29 knockout mice and controls with I/R injury after 3h, and the results of the KEGG signaling pathway enrichment analysis showed that the MAPK signaling pathway was the most affected after USP29 knockout."
reach
"In our previous study, we revealed that USP29 promoted tumor cell aerobic glycolysis and glutamine anaplerosis by deubiquitinating and stabilizing the oncogenic MYC family and HIF1α, and systemic knockout of USP29 significantly suppressed tumor progression and prolonged the survival of tumor-bearing mice."
USP29 affects E7
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sparser
"The Gaussia princeps luciferase protein complementation assay shows that USP15 interacts with the key oncoprotein human papillomavirus (HPV) E6, while USP29 and USP33 bind to E7 protein, suggesting that cellular DUBs impact HPV tumorigenesis by regulating the stability of the viral proteins [ xref ]."
USP29 affects cell population proliferation
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USP29 activates cell population proliferation. 7 / 7
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reach
"These data support the notion that USP29 promotes gastric cancer proliferation primarily through stabilization of AURKB.As deregulation of AURKB is observed in different tumors [4], to test whether USP29 is a global regulator of AURKB, we analyzed AURKB protein expression in neuroblastoma SKN-BE2, lung cancer A549 and colorectal cancer HCT116 cells with or without USP29 depletion."
USP29 affects cell migration
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reach
"In primary mouse hepatocyte injury induced by H/R in vitro, USP29 deficiency promoted phosphorylation of JNK and p38 compared to control cells (Figure 6A), whereas USP29 overexpression inhibited phosphorylation of JNK and p38, ERK phosphorylation was not affected by the USP29 expression (Figure 6B)."
reach
"In primary mouse hepatocyte injury induced by H/R in vitro, USP29 deficiency promoted phosphorylation of JNK and p38 compared to control cells (Figure 6A), whereas USP29 overexpression inhibited phosphorylation of JNK and p38, ERK phosphorylation was not affected by the USP29 expression (Figure 6B)."
USP29 affects glycolytic process
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USP29 activates glycolytic process.
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USP29 activates glycolytic process. 4 / 4
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reach
"USP29 was reported to promote tumor cell glycolysis in normoxia or hypoxia by stabilizing HIF1α, and thus, we proposed that USP29 may also regulate de novo nucleotide synthesis under hypoxia.To assess this hypothesis, we depleted endogenous USP29 in SK-N-BE2 cells and then analyzed nucleotide synthesis in cells cultured under hypoxic conditions (1% O ) using C glucose as a tracer."
USP29 inhibits glycolytic process.
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USP29 inhibits glycolytic process. 1 / 1
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reach
"34 However, previous studies have reported that Usp29 can enhance SARS-CoV-2 virulence by preventing the proteasomal degradation of ORF9b, and the level of the USP29 mRNA in the peripheral blood mononuclear cells of SARS-CoV-2 patients was higher than that in healthy individuals.35 Interestingly, the change in the USP mRNA levels in human peripheral blood mononuclear cells did not correspond with those in the USP protein levels in the mouse cerebral cortexes."
USP29 affects SARS-CoV-2
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USP29 activates SARS-CoV-2. 5 / 5
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reach
"34 However, previous studies have reported that Usp29 can enhance SARS-CoV-2 virulence by preventing the proteasomal degradation of ORF9b, and the level of the USP29 mRNA in the peripheral blood mononuclear cells of SARS-CoV-2 patients was higher than that in healthy individuals.35 Interestingly, the change in the USP mRNA levels in human peripheral blood mononuclear cells did not correspond with those in the USP protein levels in the mouse cerebral cortexes."
USP29 affects Carcinogenesis
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sparser
"To examine which kind of polyubiquitin chains USP29 removes from AURKB, we co-transfected 293T cells with Flag-AURKB, Myc-USP29 and HA-tagged ubiquitin mutants retaining a single lysine residue, and uncovered that USP29 specifically deconjugated the K48-linked polyubiquitin chains (Fig. xref G), a well-established destruction signal to trigger 26 S proteasome-mediated proteolysis [ xref ]."
Cadmium dichloride affects USP29
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Cadmium dichloride increases the amount of USP29.
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Cadmium dichloride decreases the amount of USP29.
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USP29 affects cellular antiviral responses
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USP29 affects K48
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K48 affects USP29
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Pirinixic acid affects USP29
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Pirinixic acid decreases the amount of USP29.
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Pirinixic acid activates USP29.
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USP29 affects nucleotide biosynthetic process
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USP29 activates nucleotide biosynthetic process. 3 / 3
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USP29 affects malonaldehyde
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USP29 activates malonaldehyde.
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USP29 inhibits malonaldehyde.
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USP29 inhibits malonaldehyde. 1 / 1
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USP29 affects cerebral R injury
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eidos
"Our findings for the first time identify that USP29 upregulation during cerebral I / R may contribute to oxidative stress , neuronal apoptosis , and the progression of cerebral I / R injury and that inhibition of USP29 may help to develop novel therapeutic strategies to treat cerebral I / R injury ."
eidos
"Generally , our findings for the first time identify that USP29 upregulation during cerebral I / R may contribute to oxidative stress , neuronal apoptosis , and the progression of cerebral I / R injury and that inhibition of USP29 may help to develop novel therapeutic strategies to treat cerebral I / R injury ."
reach
"Of note, the depletion of USP29 in both MDA‐MB‐231 and BT549 cells significantly decreased the expression of TWIST1 and Vimentin, and increased the expression of epithelial marker E‐cadherin (Figure
3A; Figure S3C,D, Supporting Information), while the reconstitution of TWIST1 in USP29‐deficient cells could dramatically rescue such a change (Figure 3A)."
reach
"As shown in Figure S6G,H (Supporting Information), the stable overexpression of USP29 in luminal breast cancer cell MCF‐7 decreased the level of epithelial marker E‐cadherin and increased the expression of mesenchymal marker Vimentin, whereas the 3A mutant failed to induce such phenotypes."
USP29 affects TAK1-JNK
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USP29 affects Neoplasm Invasiveness
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USP29 activates Neoplasm Invasiveness.
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USP29 inhibits Neoplasm Invasiveness.
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USP29 inhibits Neoplasm Invasiveness. 1 / 1
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K48 affects CGAS
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2,3,7,8-tetrachlorodibenzodioxine decreases the amount of USP29.
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2,3,7,8-tetrachlorodibenzodioxine increases the amount of USP29.
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Cadmium atom affects USP29
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Cadmium atom increases the amount of USP29.
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Cadmium atom decreases the amount of USP29.
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Bisphenol F affects USP29
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Bisphenol F increases the amount of USP29.
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Bisphenol F demethylates USP29.
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Bisphenol A affects USP29
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USP29 affects proteasome complex disassembly
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USP29 inhibits proteasome complex disassembly. 2 / 2
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USP29 affects polyubiquitin chains
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USP29 affects pathways
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USP29 affects neuronal apoptosis
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eidos
"Generally , our findings for the first time identify that USP29 upregulation during cerebral I / R may contribute to oxidative stress , neuronal apoptosis , and the progression of cerebral I / R injury and that inhibition of USP29 may help to develop novel therapeutic strategies to treat cerebral I / R injury ."
eidos
"Our findings for the first time identify that USP29 upregulation during cerebral I / R may contribute to oxidative stress , neuronal apoptosis , and the progression of cerebral I / R injury and that inhibition of USP29 may help to develop novel therapeutic strategies to treat cerebral I / R injury ."
USP29 affects immune response
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USP29 activates immune response. 2 / 2
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reach
"46 In this study, we demonstrated that USP29 deconjugated K48 linked polyubiquitin chains from K271 of cGAS in resting cells or after HSV-1 infection, which stabilized cGAS to produce cGAMP and activate MITA mediated antiviral immunity as well as autoimmunity (Supplementary information, FigS7e)."
USP29 affects fatty acid catabolic process
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USP29 affects colony
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USP29 affects VSV-eGFP
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USP29 affects TNBC
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USP29 affects Oxidative Stress
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USP29 activates Oxidative Stress. 2 / 2
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eidos
"Our findings for the first time identify that USP29 upregulation during cerebral I / R may contribute to oxidative stress , neuronal apoptosis , and the progression of cerebral I / R injury and that inhibition of USP29 may help to develop novel therapeutic strategies to treat cerebral I / R injury ."
eidos
"Generally , our findings for the first time identify that USP29 upregulation during cerebral I / R may contribute to oxidative stress , neuronal apoptosis , and the progression of cerebral I / R injury and that inhibition of USP29 may help to develop novel therapeutic strategies to treat cerebral I / R injury ."
USP29 affects OGD/R
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reach
"In primary mouse hepatocyte injury induced by H/R in vitro, USP29 deficiency promoted phosphorylation of JNK and p38 compared to control cells (Figure 6A), whereas USP29 overexpression inhibited phosphorylation of JNK and p38, ERK phosphorylation was not affected by the USP29 expression (Figure 6B)."
reach
"In primary mouse hepatocyte injury induced by H/R in vitro, USP29 deficiency promoted phosphorylation of JNK and p38 compared to control cells (Figure 6A), whereas USP29 overexpression inhibited phosphorylation of JNK and p38, ERK phosphorylation was not affected by the USP29 expression (Figure 6B)."
USP29 affects Interferon
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USP29 inhibits Interferon.
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USP29 inhibits Interferon. 1 / 1
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USP29 activates Interferon.
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USP29 activates Interferon. 1 / 1
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reach
"USP29 was reported to promote tumor cell glycolysis in normoxia or hypoxia by stabilizing HIF1α, and thus, we proposed that USP29 may also regulate de novo nucleotide synthesis under hypoxia.To assess this hypothesis, we depleted endogenous USP29 in SK-N-BE2 cells and then analyzed nucleotide synthesis in cells cultured under hypoxic conditions (1% O ) using C glucose as a tracer."
TAK1 inhibitors affects USP29
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TAK1 inhibitors inhibits USP29.
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TAK1 inhibitors activates USP29.
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reach
"Moreover, TAK1 inhibitors abrogated the protective effect of USP29 on hepatic I/R injury, suggesting that the regulation of hepatic I/R injury by USP29 is dependent on the TAK1-JNK/p38 pathway.We used USP29 full knockout mice rather than hepatocyte-specific knockout mice, which may contain confounding effects of USP29 function in hepatic inflammatory cells."
SIRT1 knockout affects USP29
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Oxidative Stress affects USP29
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Infections affects USP29
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Infections activates USP29. 2 / 2
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eidos
"Sequence analysis of USP29 promoter ( -5000 bp ~ +100 bp ) failed to identify any recognizable IRF , NF-kappaB , or STAT binding sites , indicating that the transcriptional regulation of USP29 by viral infection is different from that of OTUD4 , USP25 or INKIT previously reported.37 ,40,41 In this context , it has been shown that transcription factors JTV1 and FBP co-activate USP29 transcription in response to oxidative stress and that one of the evolutionarily conserved sequence elements ( CSE1 ) on Usp29 promoter suppresses its transcription.39 ,42 USP29 promotes HSV-1-triggered innate antiviral signaling in THP-1 cells Because USP29 interacted with cGAS and was upregulated by HSV-1 infection , we investigated its role in regulating HSV-1 - or cytoplasmic DNA-triggered innate immune signaling ."
Valproic acid affects USP29
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Treatment IFNs affects USP29
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Transfection dsDNA Poly affects USP29
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Thioacetamide affects USP29
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Thimerosal affects USP29
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Promoter affects USP29
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Polyubiquitin affects USP29
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Polyubiquitin chain affects USP29
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Permethrin affects USP29
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Perfluorohexanesulfonic acid affects USP29
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Paclitaxel affects USP29
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Paclitaxel deubiquitinates USP29. 1 / 1
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Oncoprotein affects USP29
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USP29 binds oncoprotein and HR. 1 / 1
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Nuclear factor-like 2 affects USP29
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Methylmercury chloride affects USP29
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Methimazole affects USP29
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Metastatic-inducing affects USP29
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Hsa-miR-335-5p affects USP29
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Element binding protein affects USP29
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Deltamethrin affects USP29
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Crocidolite asbestos affects USP29
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CGAS affects USP25
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CGAS affects TRIM38
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Benzo[a]pyrene affects USP29
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sparser
"The Gaussia princeps luciferase protein complementation assay shows that USP15 interacts with the key oncoprotein human papillomavirus (HPV) E6, while USP29 and USP33 bind to E7 protein, suggesting that cellular DUBs impact HPV tumorigenesis by regulating the stability of the viral proteins [ xref ]."
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USP29 affects viral process
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USP29 activates viral process. 1 / 1
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USP29 affects ubiquitination cGAS K464R cGAS
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USP29 affects type I IFNs
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USP29 affects tumorigenesis in vitro
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USP29 affects tumor mouse xenograft models
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USP29 affects sub-G1 population
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USP29 affects signal transduction
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USP29 activates signal transduction. 1 / 1
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USP29 affects response to xenobiotic stimulus
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USP29 activates response to xenobiotic stimulus. 1 / 1
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USP29 affects response to oxidative stress
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USP29 activates response to oxidative stress. 1 / 1
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USP29 affects regulation of cell cycle
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USP29 inhibits regulation of cell cycle. 1 / 1
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USP29 affects proteasome inhibitor
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USP29 activates proteasome inhibitor. 1 / 1
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USP29 affects proteasomal cGAS
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USP29 affects proliferative behavior colon cancer cells
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USP29 affects polyubiquitination protein
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USP29 affects polyubiquitin
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USP29 affects polyubiquitin chain
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USP29 affects phenylephrine
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USP29 activates phenylephrine. 1 / 1
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USP29 affects oncoprotein
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USP29 binds oncoprotein and HR. 1 / 1
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USP29 affects nuclear factor-like 2
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USP29 affects interaction Snail SCP1
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USP29 affects innate antiviral responses
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USP29 affects gene expression
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USP29 activates gene expression. 1 / 1
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USP29 affects focus 53BP1
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USP29 affects downstream targets
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USP29 affects cleaved caspase-3
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USP29 affects cerebral R-induced caspase-3 activation
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USP29 affects cerebral R-induced SIRT1
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USP29 affects cerebral R-caused brain edema
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USP29 affects cerebral R injury mice
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USP29 affects cellular sensitivity irradiation
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USP29 affects cell division cycle
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USP29 affects cell cycle
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USP29 activates cell cycle. 1 / 1
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USP29 affects cell apoptosis
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USP29 affects benefits
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USP29 affects autoimmunity Cyclic GMP-AMP synthase
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USP29 affects autoimmunity Correction
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USP29 affects apoptosis HCT116 cells
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USP29 affects Zim1
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reach
"For the genes at the Peg3 imprinted region, decreased expression of Zim1 and increased expression of Usp29, Peg3, and Peg3os were similarly observed comparing female M−Z− embryos with female M+Z+ embryos or comparing male M−Z− embryos with male M+Z+ embryos (Table 2, Supplementary Figure S10A-S10A')."
sparser
"The Gaussia princeps luciferase protein complementation assay shows that USP15 interacts with the key oncoprotein human papillomavirus (HPV) E6, while USP29 and USP33 bind to E7 protein, suggesting that cellular DUBs impact HPV tumorigenesis by regulating the stability of the viral proteins [ xref ]."
USP29 affects Thr578
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USP29 affects SETD8 protein
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USP29 affects OGD R-induced caspase-3
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USP29 affects Nuclear erythroid 2-related factor 2
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USP29 affects Neuroblastoma
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USP29 activates Neuroblastoma. 1 / 1
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USP29 affects Neoplastic Stem Cells
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USP29 activates Neoplastic Stem Cells. 1 / 1
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USP29 affects Neoplasm Metastasis
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USP29 activates Neoplasm Metastasis. 1 / 1
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USP29 affects NF-kappaB activation
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USP29 affects MASLD
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USP29 affects MASH
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USP29 affects Ki67 colon cancer cells
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USP29 affects K48-linked ubiquitination degradation cGAS
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USP29 affects IFNs
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USP29 affects IFN-beta IFN-alpha IL-6 TNF
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USP29 affects IFN-1
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USP29 affects Hypertrophy
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1
USP29 inhibits Hypertrophy. 1 / 1
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1
USP29 affects HSV-1-triggered downstream
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1
USP29 affects HSV-1-triggered downstream investigate USP29 regulating antiviral signaling
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1
USP29 affects HR
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1
USP29 binds oncoprotein and HR. 1 / 1
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1
USP29 affects HCT116
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1
USP29 affects H4K20me1
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1
USP29 affects H4K20
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1
USP29 affects H4K20 monomethylation
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1
USP29 affects Fig. S4A-B
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1
USP29 affects FAO-related
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1
USP29 affects DNA-templated transcription
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1
USP29 activates DNA-templated transcription. 1 / 1
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1
USP29 affects DNA Delays Cell-Cycle Progression investigate
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1
USP29 affects Colon Cancer Growth
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1
USP29 affects Cerebral R Injury
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1
USP29 affects Cerebral Oxidative Stress Apoptosis free radicals contribute cerebral R injury neuronal apoptosis
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1
USP29 affects Cell Previous researchers reported functions USP29 regulate cancer-related proteins
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1
USP29 affects Cell Hypoxia
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1
USP29 inhibits Cell Hypoxia. 1 / 1
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1
USP29 affects Carcinoma, Non-Small-Cell Lung
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1
USP29 activates Carcinoma, Non-Small-Cell Lung. 1 / 1
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1
USP29 affects Brain Edema
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1
USP29 activates Brain Edema. 1 / 1
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1
USP29 affects Autoimmunity
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1
USP29 inhibits Autoimmunity. 1 / 1
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1
eidos
"USP29 deficiency alleviates autoimmunity in Trex1 - / - mice Consistent with the results obtained with USP29 knockout cells , we found that the protein levels of cGAS were substantially lower in various organs such as heart , liver , kidney and spleen from Usp29m / m mice than in those from Usp29 + / + mice ( Fig. 7a ) ."
USP29 affects adenosine 5'-monophosphate
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1
USP29 activates adenosine 5'-monophosphate. 1 / 1
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1
USP25 affects cGAS
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1
Thr578 affects USP29
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1
TRIM38 affects cGAS
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1
TGF‐β affects USP29
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1
Suppl affects USP29
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1
SeV infection affects USP29
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1
SIRT1 silence affects USP29
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1
Peg3-DMR affects USP29
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1
PFT-α affects USP29
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1
NeoR affects USP29
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1
N-nitrosomorpholine affects USP29
1
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MKI67 affects HCT116
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1
MIMT1 allele affects USP29
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1
K48 affects ACSL5
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1
Il12p40 affects USP29
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1
ICR affects USP29
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1
HR affects oncoprotein
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1
USP29 binds oncoprotein and HR. 1 / 1
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1
HCT116 affects USP29
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1
Glyphosate affects USP29
1
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Gentamicins affects USP29
1
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FUBP1-USP29-AURKB affects USP29
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1
ECR18 affects USP29
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1
sparser
"The Gaussia princeps luciferase protein complementation assay shows that USP15 interacts with the key oncoprotein human papillomavirus (HPV) E6, while USP29 and USP33 bind to E7 protein, suggesting that cellular DUBs impact HPV tumorigenesis by regulating the stability of the viral proteins [ xref ]."
CRISPR affects USP29
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1
Adenoviridae Infections affects USP29
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1
Adenoviridae Infections activates USP29. 1 / 1
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1
reach
"To investigate the effect of USP29 on hepatocyte apoptosis and inflammatory response in response to H/R stimulation in vitro, we overexpressed USP29 in primary hepatocytes by adenovirus infection and obtained USP29 knockout primary hepatocytes by isolating the livers of USP29-KO mice."
6-propyl-2-thiouracil affects USP29
1
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2-palmitoylglycerol affects USP29
1
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4,4'-sulfonyldiphenol affects USP29
1
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2,3',4,4',5-pentachlorobiphenyl affects USP29
1
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1
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