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1. Full Text The role of TGF-β/SMAD4 signaling in cancer
by Zhao, Ming and Mishra, Lopa and Deng, Chu-Xia
International journal of biological sciences, ISSN 1449-2288, 01/2018, Volume 14, Issue 2, pp. 111 - 123
TGF-β | SMAD4 | Mouse model | Tumorigenesis | Prognosis | Biochemistry & Molecular Biology | Biology | Life Sciences & Biomedicine - Other Topics | Life Sciences & Biomedicine | Science & Technology | Neoplasms - metabolism | Signal Transduction | Smad4 Protein - physiology | Transforming Growth Factor beta - physiology | Models, Molecular | Epithelial-Mesenchymal Transition - genetics | Smad4 Protein - metabolism | Animals | Neoplasms - genetics | Smad4 Protein - genetics | DNA Repair | DNA Damage - genetics | Mice | Mutation | Transforming Growth Factor beta - metabolism | Adenocarcinoma | Deactivation | Stability | Transforming growth factor | DNA damage | Colorectal carcinoma | Inactivation | DNA repair | Smad4 protein | Biological activity | Skin cancer | Genomic instability | Adenomatous polyposis coli | Signal transduction | Signaling | Transcription activation | Skin | Pancreas | Cell migration | Deoxyribonucleic acid--DNA | Cancer | Tumors | Apoptosis | Index Medicus
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2. Full Text Iron regulates phosphorylation of Smad1/5/8 and gene expression of Bmp6, Smad7, Id1, and Atoh8 in the mouse liver
by Kautz, Léon and Meynard, Delphine and Monnier, Annabelle and Darnaud, Valérie and Bouvet, Régis and Wang, Rui-Hong and Deng, Chiuxia and Vaulont, Sophie and Mosser, Jean and Coppin, Hélène and Roth, Marie-Paule
Blood, ISSN 0006-4971, 08/2008, Volume 112, Issue 4, pp. 1503 - 1509
Life Sciences & Biomedicine | Hematology | Science & Technology | Bone Morphogenetic Protein 6 | Phosphorylation | Basic Helix-Loop-Helix Transcription Factors - genetics | Iron Overload - genetics | Signal Transduction | Liver - metabolism | Smad4 Protein - physiology | Male | Smad Proteins - genetics | Gene Expression Profiling | Mice, Knockout | Animals | Iron - physiology | Diet | Smad5 Protein - metabolism | Smad1 Protein - metabolism | Transcription, Genetic | Mice | Smad4 Protein - deficiency | Active Transport, Cell Nucleus | Smad8 Protein - metabolism | Smad7 Protein - genetics | Bone Morphogenetic Proteins - genetics | Smad Proteins - metabolism | Index Medicus | Abridged Index Medicus | Smad7 Protein | Liver | Smad4 Protein | Iron | Cellular Biology | Smad5 Protein | Life Sciences | Smad1 Protein | Smad Proteins | Bone Morphogenetic Proteins | Basic Helix-Loop-Helix Transcription Factors | Smad8 Protein | Iron Overload
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3. Full Text A SNAIL1-SMAD3/4 transcriptional repressor complex promotes TGF-β mediated epithelial-mesenchymal transition
by Pietras, Kristian and Philipson, Lennart and Neve, Etienne P. A and Albanell, Joan and Leopold, Philip L and Kukalev, Alexander and Pettersson, Ralf F and Virtanen, Ismo and Fuxe, Jonas and Johnson, Jill R and Crystal, Ronald G and de Herreros, Antonio Garcia and Vincent, Theresa and Moustakas, Aristidis and Rojo, Federico
Nature cell biology, ISSN 1465-7392, 08/2009, Volume 11, Issue 8, pp. 943 - 950
Life Sciences & Biomedicine | Science & Technology | Cell Biology | Epithelial Cells - metabolism | Epithelial Cells - drug effects | Humans | Mesoderm - drug effects | Smad3 Protein - metabolism | Mammary Neoplasms, Experimental - metabolism | Promoter Regions, Genetic - genetics | Mammary Neoplasms, Experimental - genetics | Smad3 Protein - genetics | Cell Nucleus - metabolism | Chromatin Immunoprecipitation | Smad4 Protein - genetics | Mammary Neoplasms, Experimental - pathology | Tumor Cells, Cultured | Cadherins - genetics | Snail Family Transcription Factors | Intercellular Junctions - metabolism | Epithelial Cells - pathology | Transcription Factors - genetics | Reverse Transcriptase Polymerase Chain Reaction | Smad4 Protein - metabolism | Blotting, Western | Transcription Factors - metabolism | Transforming Growth Factor beta - pharmacology | Animals | Protein Binding | Mesoderm - metabolism | Mice | Mice, Inbred BALB C | Mesoderm - pathology | Cell Line, Transformed | Microscopy, Fluorescence | Index Medicus | Smad3 | Factor de creixement transformant beta | Smad4 | Metabolisme | Factors de transcripció | Medicin och hälsovetenskap
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4. Chemoresistance to doxorubicin induces epithelial-mesenchymal transition via upregulation of transforming growth factor β signaling in HCT116 colon cancer cells
by Li, Jinpeng and Liu, Hao and Yu, Jieping and Yu, Honggang
Molecular medicine reports, ISSN 1791-2997, 07/2015, Volume 12, Issue 1, pp. 192 - 198
Epithelial-mesenchymal transition | Transforming growth factor β/Smad4 signaling | Colon cancer | Doxorubicin chemoresistance | RNA interference | RNA, Small Interfering - genetics | Smad4 Protein - antagonists & inhibitors | Antibiotics, Antineoplastic - pharmacology | Cadherins - metabolism | Signal Transduction | Vimentin - metabolism | HCT116 Cells | Humans | Gene Expression Regulation, Neoplastic | Epithelial-Mesenchymal Transition - drug effects | Transcription Factors - genetics | Epithelial-Mesenchymal Transition - genetics | Smad4 Protein - metabolism | Transcription Factors - metabolism | Drug Resistance, Neoplasm - genetics | Transforming Growth Factor beta - genetics | Smad4 Protein - genetics | Vimentin - genetics | Cadherins - genetics | Snail Family Transcription Factors | Transforming Growth Factor beta - metabolism | Doxorubicin - pharmacology | Drug Resistance, Neoplasm - drug effects | RNA, Small Interfering - metabolism
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5. Full Text LncRNA AWPPH inhibits SMAD4 via EZH2 to regulate bladder cancer progression
by Zhu, Feng and Zhang, Xinjun and Yu, Qinnan and Han, Guangye and Diao, Fengxia and Wu, Chunlei and Zhang, Yan
Journal of cellular biochemistry, ISSN 0730-2312, 06/2018, Volume 119, Issue 6, pp. 4496 - 4505
cell proliferation and migration | SMAD4 | bladder cancer | lncRNA AWPPH | EZH2 | Biochemistry & Molecular Biology | Life Sciences & Biomedicine | Science & Technology | Cell Biology | Enhancer of Zeste Homolog 2 Protein - genetics | Enhancer of Zeste Homolog 2 Protein - metabolism | Cell Proliferation | Humans | RNA, Long Noncoding - genetics | Neoplasm Proteins - metabolism | Autophagy | RNA, Neoplasm - metabolism | Smad4 Protein - metabolism | Urinary Bladder Neoplasms - genetics | Smad4 Protein - genetics | Cell Line, Tumor | RNA, Neoplasm - genetics | Neoplasm Proteins - genetics | RNA, Long Noncoding - metabolism | Urinary Bladder Neoplasms - metabolism | Apoptosis | Cell Movement | Development and progression | Bladder cancer | Measuring instruments | Cell proliferation | Chromatin | Immunoprecipitation | Colonies | Epithelial cells | Bladder | Homology | Tissues | Assaying | Ribonucleic acid--RNA | Smad4 protein | Western blotting | Cell growth | Annexin V | Cell migration | Phagocytosis | Cancer | Index Medicus
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6. Full Text A reinforcing HNF4-SMAD4 feed-forward module stabilizes enterocyte identity
by Chen, Lei and Toke, Natalie H and Luo, Shirley and Vasoya, Roshan P and Fullem, Robert L and Parthasarathy, Aditya and Perekatt, Ansu O and Verzi, Michael P
Nature genetics, ISSN 1061-4036, 05/2019, Volume 51, Issue 5, pp. 777 - 785
Life Sciences & Biomedicine | Genetics & Heredity | Science & Technology | Caco-2 Cells | Hepatocyte Nuclear Factor 4 - metabolism | Signal Transduction | Enterocytes - cytology | Enterocytes - metabolism | Humans | Hepatocyte Nuclear Factor 4 - genetics | Binding Sites - genetics | Smad4 Protein - metabolism | Mice, Knockout | Cell Differentiation - genetics | Animals | Enhancer Elements, Genetic | Smad4 Protein - genetics | Hepatocyte Nuclear Factor 4 - deficiency | Mice | Smad4 Protein - deficiency | Cell Differentiation - physiology | Transcription factors | Developmental genetics | Intestines | Physiological aspects | Bone morphogenetic proteins | Genetic aspects | Research | Transforming growth factors | Smad protein | Chromatin | Ontology | Modules | Genomics | Homeostasis | Genomes | Regulatory sequences | Gene expression | Epithelium | Smad4 protein | Signaling | Intestine | Stem cells | Hepatocyte nuclear factor 4 | Disruption | Differentiation | Feedforward | Bioinformatics | Binding sites | Deoxyribonucleic acid--DNA | Plastic foam | Index Medicus
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7. Full Text SMAD4 gene mutation renders pancreatic cancer resistance to radiotherapy through promotion of autophagy
by Wang, Feng and Xia, Xiaojun and Yang, Chunying and Shen, Jianliang and Mai, Junhua and Kim, Han-Cheon and Kirui, Dickson and Kang, Ya'an and Fleming, Jason B and Koay, Eugene J and Mitra, Sankar and Ferrari, Mauro and Shen, Haifa
Clinical cancer research, ISSN 1078-0432, 07/2018, Volume 24, Issue 13, pp. 3176 - 3185
Life Sciences & Biomedicine | Oncology | Science & Technology | Immunohistochemistry | Genomic Instability | Cell Proliferation | Pancreatic Neoplasms - metabolism | Reactive Oxygen Species - metabolism | Apoptosis - radiation effects | Autophagy - radiation effects | Humans | Cell Survival - genetics | Apoptosis - genetics | Biomarkers, Tumor | Gene Knockdown Techniques | Smad4 Protein - genetics | Antineoplastic Agents - pharmacology | Autophagy - genetics | Disease Models, Animal | Pancreatic Neoplasms - radiotherapy | Radiation Tolerance - genetics | Pancreatic Neoplasms - genetics | Cell Survival - radiation effects | Smad4 Protein - metabolism | Animals | Cell Line, Tumor | Mice | DNA Damage | Mutation | Flow cytometry | Radiation effects | Cell survival | Radiosensitivity | Chloroquine | Radiation | Radioresistance | siRNA | Radiation therapy | Assaying | Survival | Autophagy | Smad4 protein | Proteins | Depletion | Inhibitors | Experimental design | Pancreatic cancer | Point mutation | N-Acetyl-L-cysteine | Phagocytosis | Cancer | Tumors | Index Medicus | radiotherapy | pancreatic cancer | SMAD4 | autophagy | reactive oxygen species
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8. Full Text MicroRNA-20a-5p promotes colorectal cancer invasion and metastasis by downregulating Smad4
by Cheng, Dantong and Zhao, Senlin and Tang, Huamei and Zhang, Dongyuan and Sun, Hongcheng and Yu, Fudong and Jiang, Weiliang and Yue, Ben and Wang, Jingtao and Zhang, Meng and Yu, Yang and Liu, Xisheng and Sun, Xiaofeng and Zhou, Zongguang and Qin, Xuebin and Zhang, Xin and Yan, Dongwang and Wen, Yugang and Peng, Zhihai
Oncotarget, ISSN 1949-2553, 2016, Volume 7, Issue 29, pp. 45199 - 45213
Prognosis | Smad4 | Metastasis | miR-20a-5p | Colorectal cancer | Oncology | Life Sciences & Biomedicine | Science & Technology | Cell Biology | Colorectal Neoplasms - mortality | Smad4 Protein - antagonists & inhibitors | Neoplasm Invasiveness | Down-Regulation | Humans | Middle Aged | Proportional Hazards Models | Male | Neoplasm Metastasis | Animals | Smad4 Protein - genetics | Colorectal Neoplasms - drug therapy | Epithelial-Mesenchymal Transition | Cell Line, Tumor | Adult | Female | Aged | Mice | Mice, Inbred BALB C | MicroRNAs - physiology | 3' Untranslated Regions | Colorectal Neoplasms - pathology | Index Medicus
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9. Full Text Genistein downregulates onco-miR-1260b and upregulates sFRP1 and Smad4 via demethylation and histone modification in prostate cancer cells
by Hirata, H and Hinoda, Y and Shahryari, V and Deng, G and Tanaka, Y and Tabatabai, Z.L and Dahiya, R
British journal of cancer, ISSN 0007-0920, 03/2014, Volume 110, Issue 6, pp. 1645 - 1654
miR-1260b | apoptosis | Smad4 | genistein | sFRP1 | Life Sciences & Biomedicine | Oncology | Science & Technology | Tumors of the urinary system | Urinary tract. Prostate gland | Nephrology. Urinary tract diseases | Biological and medical sciences | Multiple tumors. Solid tumors. Tumors in childhood (general aspects) | Medical sciences | Tumors | Prostatic Neoplasms - metabolism | Prostatic Neoplasms - pathology | Ataxia Telangiectasia Mutated Proteins - metabolism | Tissue Array Analysis | Down-Regulation | Humans | In Situ Hybridization, Fluorescence | Male | MicroRNAs - metabolism | Smad4 Protein - metabolism | Up-Regulation - drug effects | Histones - genetics | Prostatic Neoplasms - genetics | Smad4 Protein - genetics | Ataxia Telangiectasia Mutated Proteins - biosynthesis | Genistein - pharmacology | MicroRNAs - genetics | Gene Expression Regulation, Neoplastic - drug effects | Histones - metabolism | Ataxia Telangiectasia Mutated Proteins - genetics | Smad4 Protein - biosynthesis | Anticarcinogenic Agents - pharmacology | DNA Methylation - drug effects | Prostatic Neoplasms - drug therapy | Index Medicus | Molecular Diagnostics
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10. Full Text SMAD4-mediated WNT signaling controls the fate of cranial neural crest cells during tooth morphogenesis
by Li, Jingyuan and Huang, Xiaofeng and Xu, Xun and Mayo, Julie and Bringas Jr, Pablo and Jiang, Rulang and Wang, Songling and Chai, Yang
Development (Cambridge), ISSN 0950-1991, 05/2011, Volume 138, Issue 10, pp. 1977 - 1989
SMAD4 | Bone formation | Mouse | Canonical WNT signaling | WNT inhibitor | Odontoblast | TGFβ/BMP | Life Sciences & Biomedicine | Developmental Biology | Science & Technology | Male | Odontogenesis - genetics | Neural Crest - metabolism | Ameloblasts - metabolism | Cell Differentiation - genetics | Intercellular Signaling Peptides and Proteins - metabolism | Smad4 Protein - genetics | Gene Expression Regulation, Developmental | Tooth - embryology | Tooth - cytology | Female | Membrane Proteins - metabolism | Odontoblasts - cytology | Cell Differentiation - physiology | Cell Lineage - genetics | Neural Crest - cytology | Odontoblasts - metabolism | Signal Transduction | Ameloblasts - cytology | Smad4 Protein - physiology | Intercellular Signaling Peptides and Proteins - genetics | Dentin - embryology | Mice, Transgenic | Dental Enamel - embryology | Cell Lineage - physiology | Mice, Knockout | Pregnancy | Animals | Neural Crest - embryology | Mice | Odontogenesis - physiology | Smad4 Protein - deficiency | Wnt Proteins - physiology | Tooth - metabolism | Index Medicus | Dentin | Mesenchyme | Wnt protein | catenin | Frizzled-related protein 1 | Teeth | Transforming growth factor- beta | Neural crest | Osteoblasts | Smad4 protein | Morphogenesis | Signal transduction | Dental enamel | Cell fate | Odontoblasts | Bone morphogenetic proteins | Skull | Differentiation | Dkk1 protein | s | BMP | TGFβ
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