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Our results show that SnoN, and SMAD heteromers can form a joint structural core for the binding of other transcription modulators.
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It is a critical negative regulator of TGF-beta1/Smad signal pathway, involving in tubule epithelial-mesenchymal transition (EMT), extracellular matrix (ECM) accumulation, and tubulointerstitial fibrosis.
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signal transducer and activator of transcription (Stat)3 represses Smad3 in synergy with the potent negative regulators of TGF-beta signaling, c-Ski and SnoN, whereby renders gefitinib-sensitive HCC827 cells resistant
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SnoN interacts with multiple components of the Hippo pathway to inhibit the binding of Lats2 to TAZ and the subsequent phosphorylation of TAZ, leading to TAZ stabilization.
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suggest that SnoN suppresses TGF-betainduced epithelial-mesenchymal transition and invasion of bladder cancer cells in a TIF1gammadependent manner
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the findings of this study demonstrate that the downregulation of SnoN expression in hRPTECs under high-glucose conditions is mediated by the increased expression of Smurf2 through the TGF-b1/Smad signaling pathway.
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RNAi-mediated downregulation of SnoN effectively inhibited proliferation and enhanced apoptosis of pancreatic cells.
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SKIL knockdown led to growth arrest in PC-3 and LNCaP cell line models of prostate cancer, and its overexpression led to increased invasiveness in RWPE-1 cells.
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Whole exome sequencing of the blood of the patient and both parents revealed a de novo germline SKIL mutation in the child that was not present in either parent
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Data indicate that tripartite motif containing 33 protein TIF1gamma promotes sumoylation of SKI-like proto-oncogene protein SnoN1 and regulates epithelial-mesenchymal transition (EMT).
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The results indicate that protein ubiquitination promotes megakaryopoiesis via degrading SnoN, an inhibitor of CD61 expression, strengths the roles of ubiquitination in cellular differentiation.
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SnoNspecific siRNA is capable of effectively inhibiting the expression of SnoN in human HepG2 cells, and the downregulation of SnoN expression induces growth inhibition and apoptosis
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these studies identify TLOC1 and SKIL as driver genes at 3q26 and more broadly suggest that cooperating genes may be coamplified in other regions with somatic copy number gain.
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High SnoN expression is associated with metastasis in breast cancer.
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Phospholipid Scramblase 1, an interferon-regulated gene located at 3q23, is regulated by SnoN/SkiL in ovarian cancer cells.
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These data strongly suggest that SnoN can function as a tumor suppressor at early stages of tumorigenesis in human cancer tissues.
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These results support our observation that cancer tissues have lower expression levels of SnoN, miR-720, and miR-1274A compared to adjacent normal tissues from esophageal squamous cell carcinoma patients.
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Data suggest that SKIL expression is modulated by antineoplastic agents and may be involved in drug resistance in ovarian carcinoma; up-regulation of SKIL expression by arsenic trioxide and reduction of apoptosis involves activation of PI3K pathway.
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SNON predominantly associates with SMAD2 at the promoters of primitive streak (PS) and early DE marker genes
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the SNON-SMAD4 complex negatively regulated basal SKIL gene expression through binding the promoter and recruiting histone deacetylases