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Genes & development, ISSN 0890-9369, 05/2013, Volume 27, Issue 10, pp. 1101 - 1114
.... Mule deficiency resulted in increased penetrance, number, and severity of skin tumors, which could be reversed by concomitant genetic knockout of c-Myc but not by knockout of p53 or p19Arf... 
Huwe1 | c-Myc | Mule | Ras | p21 | Miz1 | Genetics & Heredity | Life Sciences & Biomedicine | Developmental Biology | Science & Technology | Cell Biology | Protein Inhibitors of Activated STAT - deficiency | Tetradecanoylphorbol Acetate - pharmacology | 9,10-Dimethyl-1,2-benzanthracene - pharmacology | Male | Protein Inhibitors of Activated STAT - metabolism | Cyclin-Dependent Kinase Inhibitor p15 - biosynthesis | Oncogene Protein p21(ras) - metabolism | Cyclin-Dependent Kinase Inhibitor p16 | Oncogene Protein p21(ras) - antagonists & inhibitors | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cell Transformation, Neoplastic - genetics | Cyclin-Dependent Kinase Inhibitor p15 - genetics | Nuclear Proteins - deficiency | Protein Inhibitors of Activated STAT - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Nuclear Proteins - genetics | Protein Inhibitors of Activated STAT - antagonists & inhibitors | Skin Neoplasms - pathology | Cyclin-Dependent Kinase Inhibitor p21 - biosynthesis | Signal Transduction | Down-Regulation | Cells, Cultured | Ubiquitin-Protein Ligases - metabolism | Nuclear Proteins - metabolism | Skin Neoplasms - chemically induced | Proto-Oncogene Proteins c-myc - metabolism | Mice, Knockout | Skin Neoplasms - metabolism | Keratinocytes - pathology | Animals | Tumor Suppressor Protein p53 | Keratinocytes - drug effects | Keratinocytes - metabolism | Nuclear Proteins - antagonists & inhibitors | Proto-Oncogene Proteins c-myc - deficiency | Skin Neoplasms - genetics | Proto-Oncogene Proteins c-myc - antagonists & inhibitors | Ubiquitin-Protein Ligases - deficiency | Mice | Proto-Oncogene Proteins c-myc - genetics | Cyclin-Dependent Kinase Inhibitor p15 - metabolism | Genes, ras | Ubiquitin-Protein Ligases - genetics | Oncogene Protein p21(ras) - genetics | Carcinogenesis | Ras genes | Analysis | Index Medicus | Research Paper
Journal Article
The Journal of experimental medicine, ISSN 0022-1007, 2014, Volume 211, Issue 7, pp. 1379 - 1391
Journal Article
Nature (London), ISSN 1476-4687, 02/2010, Volume 464, Issue 7287, pp. 409 - 412
Journal Article
Journal Article
PLoS genetics, ISSN 1553-7404, 03/2017, Volume 13, Issue 3, pp. e1006682 - e1006682
.... Embryonic stem cells (ESCs) present a fast cell cycle with a short G1 phase. This is due to the lack of expression of cell cycle inhibitors, which ultimately determines naive pluripotency by holding back differentiation... 
Life Sciences & Biomedicine | Genetics & Heredity | Science & Technology | Cell Cycle - genetics | Cell Proliferation - genetics | Hepatocyte Nuclear Factor 1-alpha - genetics | Humans | Cells, Cultured | Gene Expression Regulation | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Mice, Transgenic | Hepatocyte Nuclear Factor 1-alpha - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Promoter Regions, Genetic - genetics | Blotting, Western | Mouse Embryonic Stem Cells - metabolism | Gene Knockdown Techniques | Animals | Wnt Signaling Pathway - genetics | Cyclin-Dependent Kinase Inhibitor p15 - genetics | Base Sequence | HEK293 Cells | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Mice | Cyclin-Dependent Kinase Inhibitor p15 - metabolism | Research | Embryonic stem cells | Wnt proteins | Gene expression | Cell cycle | Cell culture | Transcription factors | High resolution | Target recognition | Genomics | Diapause | Embryo cells | c-Myc protein | Mimicry | Proteins | Signal transduction | Cell activation | Deoxyribonucleic acid--DNA | Data acquisition | Melanoma | RNA polymerase | Nucleic acids | Ablation | Adenomatous polyposis coli | Gene silencing | Antigen-presenting cells | Stem cells | Fruit flies | Ligands | Nuclei (cytology) | Cell proliferation | Destruction | Laboratories | Genes | Homeostasis | Antibodies | Genomes | Malignancy | CCAAT/enhancer-binding protein | Kinases | Regeneration (physiology) | Adipogenesis | Deactivation | Decision analysis | Urban regeneration | Effectors | Tumor suppressor genes | β-Catenin | Differentiation | Pluripotency | Tumors | Cancer | Index Medicus | Cloning | Cell cycle inhibitors | Cell division | Cell staining | Gene expression regulation | G1 phase | Activation | Deoxyribonucleic acid | DNA
Journal Article
Cell death & disease, ISSN 2041-4889, 03/2017, Volume 8, Issue 3, pp. e2665 - e2665
..., both in vitro and in vivo. Mechanistic investigations demonstrated that BLACAT1 had a key role in G1/G0 arrest, and showed that BLACAT1 can repress p15 expression by binding to EZH2, thus contributing to the regulation of CRC cell cycle and proliferation. Our results suggest that BLACAT1, as a cell cycle regulator, may serve as a potential target for colon cancer prevention and treatment in human CRC. 
Life Sciences & Biomedicine | Science & Technology | Cell Biology | Cell Proliferation - genetics | Enhancer of Zeste Homolog 2 Protein - genetics | Prognosis | Colorectal Neoplasms - genetics | Humans | Carcinogenesis - genetics | Gene Expression Regulation, Neoplastic | Gene Silencing | Apoptosis - genetics | RNA, Long Noncoding - genetics | Xenograft Model Antitumor Assays | Animals | Cyclin-Dependent Kinase Inhibitor p15 - genetics | Epigenesis, Genetic - genetics | Cell Line, Tumor | Protein Binding | Mice | Colorectal Neoplasms - pathology | Epigenetics | Ribonucleic acid--RNA | Medical diagnosis | Colorectal cancer | Cell adhesion & migration | Index Medicus | Original
Journal Article