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Nature (London), ISSN 1476-4687, 02/2011, Volume 470, Issue 7334, pp. 409 - 413
The mature gut renews continuously and rapidly throughout adult life, often in a damage-inflicting micro-environment. The major driving force for self-renewal... 
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Intestinal Mucosa - metabolism | Cell Proliferation | Adenoma - genetics | Colorectal Neoplasms - genetics | Homeodomain Proteins - metabolism | Humans | Casein Kinase Ialpha - genetics | Male | Loss of Heterozygosity | Wnt Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - deficiency | Tumor Suppressor Protein p53 - genetics | Adenoma - metabolism | Genes, APC | Adenoma - enzymology | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cellular Senescence | Neoplasm Invasiveness - pathology | Tumor Suppressor Proteins - deficiency | Intestinal Mucosa - enzymology | Tumor Suppressor Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Fibroblasts | Female | Genes, Tumor Suppressor | Colorectal Neoplasms - metabolism | Cell Line | Colorectal Neoplasms - enzymology | Tumor Suppressor Proteins - metabolism | Signal Transduction | Casein Kinase Ialpha - deficiency | Tumor Suppressor Protein p53 - metabolism | Tumor Suppressor Protein p53 - deficiency | beta Catenin - metabolism | Disease Progression | Homeodomain Proteins - genetics | Mice, Knockout | Animals | Cell Transformation, Neoplastic | Adenoma - pathology | Cell Line, Tumor | Mice | DNA Damage | Colorectal Neoplasms - pathology | Casein Kinase Ialpha - metabolism | Intestinal Mucosa - pathology | Index Medicus
Journal Article
Nature communications, ISSN 2041-1723, 11/2018, Volume 9, Issue 1, pp. 5110 - 13
.... Here we propose that miR-224/-520c-dependent TUSC3 deficiency enhances the metastatic potential of NSCLC through the alteration of three unfolded protein response pathways and HRD1-dependent ERAD... 
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Endoribonucleases - genetics | Humans | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | MicroRNAs - metabolism | Activating Transcription Factor 6 - genetics | Tumor Suppressor Protein p53 - genetics | In Situ Hybridization | Tumor Suppressor Proteins - genetics | Membrane Proteins - metabolism | Gene Expression Regulation, Neoplastic - physiology | Gene Expression Regulation, Neoplastic - genetics | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Cell Proliferation - genetics | Tumor Suppressor Proteins - metabolism | Endoribonucleases - metabolism | Unfolded Protein Response - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Membrane Proteins - genetics | Endoplasmic Reticulum-Associated Degradation - genetics | Carcinoma, Non-Small-Cell Lung - metabolism | Cell Proliferation - physiology | Tumor Suppressor Protein p53 - metabolism | Ubiquitin-Protein Ligases - metabolism | Signal Transduction - genetics | Reverse Transcriptase Polymerase Chain Reaction | Xenograft Model Antitumor Assays | Activating Transcription Factor 6 - metabolism | Animals | Endoplasmic Reticulum-Associated Degradation - physiology | Cell Line, Tumor | Signal Transduction - physiology | Mice | Ubiquitin-Protein Ligases - genetics | Unfolded Protein Response - physiology | Small cell lung carcinoma | p53 Protein | Lung cancer | Non-small cell lung carcinoma | Lung carcinoma | Metastasis | Substrates | Metastases | Proteins | Protein folding | Chromosome 8 | Tumor suppressor genes | miRNA | Solid tumors | Tumors | Cancer | Index Medicus
Journal Article
Nature (London), ISSN 1476-4687, 03/2011, Volume 471, Issue 7336, pp. 119 - 123
...). Defects in DNA damage response factors such as ataxia telangiectasia mutated (ATM) protein and combined deficiencies in classical non-homologous end joining and p53 predispose to RAG-initiated genomic rearrangements and lymphomagenesis(2-11... 
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Genomic Instability | Protein-Serine-Threonine Kinases - deficiency | Gene Rearrangement, T-Lymphocyte - genetics | Chromosomes, Mammalian - genetics | DNA-Binding Proteins - deficiency | DNA-Binding Proteins - metabolism | Tumor Suppressor Proteins - deficiency | Tumor Suppressor Proteins - chemistry | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Recombination, Genetic - genetics | Lymphoma - pathology | Chromosome Deletion | Tumor Suppressor Proteins - metabolism | Kaplan-Meier Estimate | Protein-Serine-Threonine Kinases - genetics | Thymus Gland - cytology | Lymphoma - genetics | In Situ Hybridization, Fluorescence | Ataxia Telangiectasia Mutated Proteins | Genes, p53 - genetics | DNA-Binding Proteins - genetics | DNA-Binding Proteins - chemistry | Disease Progression | Animals | Genes, Immunoglobulin Heavy Chain - genetics | Mice | Receptors, Antigen, T-Cell - genetics | Translocation, Genetic - genetics | Causes of | Tumor suppressor genes | Lymphomas | Genetic aspects | Abnormalities | Software | Chromosomes | Deoxyribonucleic acid--DNA | Cell cycle | Apoptosis | Tumors | Index Medicus | Thymus Gland | Translocation, Genetic | Protein-Serine-Threonine Kinases | Gene Rearrangement, T-Lymphocyte | Receptors, Antigen, T-Cell | Lymphoma | Chromosomes, Mammalian | Genes, Immunoglobulin Heavy Chain | Life Sciences | Genes, p53 | Immunology | Recombination, Genetic | Cell Cycle Proteins | Tumor Suppressor Proteins | DNA-Binding Proteins
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 05/2005, Volume 102, Issue 23, pp. 8204 - 8209
Journal Article
Genes & development, ISSN 0890-9369, 07/2009, Volume 23, Issue 16, pp. 1895 - 1909
Journal Article
Nature (London), ISSN 1476-4687, 03/2010, Volume 464, Issue 7287, pp. 374 - 379
.... Senescence induced by oncogenes or by loss of tumour suppressor genes is thought to critically depend on induction of the p19(Arf)-p53 pathway... 
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Proto-Oncogene Proteins p21(ras) - genetics | Cellular Senescence - drug effects | Male | Prostate - metabolism | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | S-Phase Kinase-Associated Proteins - antagonists & inhibitors | Adenovirus E1A Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Fibroblasts | Prostatic Neoplasms - prevention & control | Prostatic Neoplasms - drug therapy | Proto-Oncogene Proteins p21(ras) - metabolism | PTEN Phosphohydrolase - genetics | Prostatic Neoplasms - pathology | Cyclin-Dependent Kinase Inhibitor p16 - deficiency | PTEN Phosphohydrolase - deficiency | Cells, Cultured | Tumor Suppressor Protein p53 - metabolism | Cyclin-Dependent Kinase Inhibitor p16 - genetics | PTEN Phosphohydrolase - metabolism | SKP Cullin F-Box Protein Ligases - metabolism | S-Phase Kinase-Associated Proteins - metabolism | Tumor Suppressor Protein p53 - deficiency | Animals | Activating Transcription Factor 4 - metabolism | Adenovirus E1A Proteins - genetics | Prostate - cytology | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | S-Phase Kinase-Associated Proteins - genetics | Mice | Cell Transformation, Neoplastic - drug effects | Prevention | Care and treatment | Physiological aspects | Aging | Tumor suppressor genes | Genetic aspects | Research | Cells | Tumors | Cell cycle | Apoptosis | Index Medicus
Journal Article