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progression, as not only the classically studied pathways, such as PI3K/AKT and MAPK, appear to be involved in malignant TGFβ transformation, but also SMAD molecules might play a role in this event. Interleukins A large group of secreted proteins that bind to
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receptor complex with AMHRI. This complex phosphorylates AMHRI and activates serine/threonine protein kinase. Subsequently, intracellular Smad-proteins (R-SMads1/5/8) detach from the receptor complexes, allowing several proteins to enter the nucleus to
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)-1 and -2-containing complexes and Smad3 (a TGF-β signalling component) to promote transcription of target genes; it restricts Wnt pathway target genes transcription by blocking β-catenin from entering the nucleus; in the cytoplasm, menin binds to Akt
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. Therefore, in the present study, we investigated the effect of Dex on cell adhesion to ECM of two human ovarian cancer cell lines, HO-8910 and SKOV3, and examined the relationship between Dex's effect of enhancing adhesion and Dex-induced cell resistance to
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Division of Internal Medicine and Dermatology, Division of Biomedical Genetics, Division of Surgical Specialties, Department of Internal Medicine, University Medical Center Utrecht, Internal post number L.00.408, PO Box 85500, 3508 GA Utrecht, The Netherlands
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) Overexpressed Kaji et al . (2001) Menin–SMAD3 Cos7 (monkey kidney) Overexpressed Heppner et al . (2001) Menin–NFκB 293 (human embryonic kidney) Endogenous, overexpressed Sierra et al . (2006) Menin–β-catenin CRC (human colorectal cancer) Endogenous Dreijerink
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bovine serum (FBS). Primary cells were cultured from angiomyolipoma resections performed for therapeutic purposes. Excess material not required for clinical use was divided into small (∼3×3×3 mm) fragments, treated with type II collagenase and the
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suppresses TGFβ1‑induced human intestinal fibroblasts activities by regulating proliferation and apoptosis via the inhibition of the Smad and PI3K/AKT signaling pathway . Molecular Medicine Reports 18 3907 – 3913 . ( https://doi.org/10.3892/mmr.2018
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and cell death induced by certain growth factors. We have also checked the expression of proteins known to interact with menin in our tumour samples, such as JunD, Smad3 and NFκB factors, and none of these factors showed altered transcriptional
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Academic Unit of Clinical Oncology, Academic Unit of Pathology, Leeds Institute of Molecular Medicine, Cancer Research UK (CR‐UK), and Yorkshire Cancer Research (YCR) Sheffield Cancer Research Centre
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the first tumour reached 1 cm 3 . Microcomputed tomography imaging Analysis of bone volume was carried out using a Skyscan 1172 X-ray-computed microtomograph (Skyscan, Aartselaar, Belgium). Pixel size was set to 4.37 μm and scanning was initiated from
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regulatory function of microRNAs (miRNAs) on protein-coding gene expression through interacting with their 3′ UTR resulting in their posttranscriptional repression ( Djuranovic et al . 2011 ). Through this mechanism, miRNAs regulate various aspects of normal