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findings reveal that Akt activity determines the phosphorylation status of TBC1D7 at the phospho-switch Ser-124, which governs binding to either 14-3-3 or beta-TrCP2, resulting in increased or decreased stability of TBC1D7, respectively.
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Study found that the F-box protein bTrCP binds a DSGmotif located within the N-terminus of STIL, and that mutation of this degron leads to STIL stabilization and consequent centriole overduplication.
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Reciprocal regulation between betaTrCP and Smurf1 has been found to inhibit proliferative capacity of liver cancer cells.
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a phosphorylation mutant form of Mxi1 (Mxi1-S160A), which cannot be degraded by S6K1 and beta-Trcp, is much more stable and efficient in suppressing the transcriptional activity of Myc and radioresistance in lung cancer cells.
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beta-TrCP was identified as a novel interacting partner of ASK1 that is capable of ubiquitinating and degrading ASK1 through the ubiquitin-proteasome system. These findings suggest that beta-TrCP is capable of suppressing oxidative stress-induced caspase 3-dependent apoptosis through suppression of ASK1.
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The primary role of the S(52,56) residues of Vpu in antagonism of CD4, GaLV Env, and BST-2/tetherin is to recruit the SCF/betaTrCP ubiquitin ligase.
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TSPAN15 interacts with BTRC to promote oesophageal squamous cell carcinoma metastasis via activating NF-kappaB signaling.
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BTrCP-FBXW2-SKP2 axis forms an oncogene-tumour suppressor-oncogene cascade to control cancer cell growth with FBXW2 acting as a tumour suppressor by promoting SKP2 degradation.
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Data show that the SCF(beta-TrCP) ubiquitin E3 ligase complex responsible for regulating the active protein kinase C-associated kinase (RIPK4) level.
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SAG/RBX2 E3 ligase complexes with UBCH10 and UBE2S ubiquitin-conjugating enzymes to ubiquitylate beta-TrCP1 via K11-linkage for degradation.
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Data indicate the role of tyrosine kinase c-Src (Src) in rescuing Taz (transcriptional coactivator with PDZ-binding motif) from E3 ligase SCF(beta-TrCP)-mediated degradation.
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SCFbeta-TRCP negatively regulates the FLCN complex by promoting FNIP2 degradation in Birt-Hogg-Dube syndrome-associated renal cancer.
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beta-TRCP depletion in HepG2 hepatocellular carcinoma cells resulted in increased Lipin1 protein abundance.
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It demonstrates that degradation of Lipin-1 is regulated by BTRC in the cytoplasm and on membranes
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we identified two independent SNPs (i.e., WNT2B rs1175649 G>T and BTRC rs61873997 G>A) that showed a predictive role in CM-specific survival, with an effect-allele-attributed hazards ratio (adjusted hazards ratio) of 1.99 (95% confidence interval = 1.41-2.81, P = 8.10 x 10(-5)) and 0.61 (0.46-0.80, 3.12x10(-4)), respectively.
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It has been proposed that CENP-W may function as a booster of beta-TrCP1 nuclear import to increase the oncogenicity of beta-TrCP1.
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oncogenic effect of miR-182 and its reversal by beta-TrCP2 were confirmed in vivo This study suggests that beta-TrCP and miR-182 may be possible biomarkers and targets for early detection and treatment of pancreatic cancer
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Beta-TrCP controls ubiquitination and degradation of liver-enriched transcription factor CREB-H.
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Phosphorylated VEGFR-2 was reduced by hyperglycemia while total VEGFR-2 was almost unaltered. However, VEGFR-2 was reduced when directly exposed to reactive oxygen species, with resultant co-location of beta-TrCP and VEGFR-2.
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Low GAS7C increases cancer cell motility by promoting N-WASP/FAK/F-actin cytoskeleton dynamics. It also enhances beta-catenin stability via hnRNP U/beta-TrCP complex formation.
