Journal of Cell Science, ISSN 0021-9533, 09/2007, Volume 120, Issue 18, pp. 3163 - 3172
RASSF1A (Ras association domain family 1 isoform A) is a recently discovered tumor suppressor whose inactivation is implicated in the development of many human...
Epigenetic | Ras | RASSF1A | Tumor suppressor | ANAPHASE-PROMOTING COMPLEX | FREQUENT EPIGENETIC INACTIVATION | epigenetic | CPG ISLAND HYPERMETHYLATION | ASSOCIATION DOMAIN FAMILY-1 | tumor suppressor | MICROTUBULE-ASSOCIATED PROTEIN | CELL BIOLOGY | CELL LUNG-CANCER | K-RAS MUTATIONS | NASOPHARYNGEAL CARCINOMA | COLORECTAL-CANCER | HUMAN-CHROMOSOME 3P21.3 | Neoplasms - metabolism | ras Proteins - genetics | Protein Binding - genetics | Tumor Suppressor Proteins - metabolism | Signal Transduction | Epigenesis, Genetic | Humans | Gene Silencing | ras Proteins - metabolism | Protein Structure, Tertiary - genetics | Point Mutation | DNA Methylation | Animals | Cell Cycle | Neoplasms - genetics | Gene Deletion | Tumor Suppressor Proteins - genetics | Apoptosis
Epigenetic | Ras | RASSF1A | Tumor suppressor | ANAPHASE-PROMOTING COMPLEX | FREQUENT EPIGENETIC INACTIVATION | epigenetic | CPG ISLAND HYPERMETHYLATION | ASSOCIATION DOMAIN FAMILY-1 | tumor suppressor | MICROTUBULE-ASSOCIATED PROTEIN | CELL BIOLOGY | CELL LUNG-CANCER | K-RAS MUTATIONS | NASOPHARYNGEAL CARCINOMA | COLORECTAL-CANCER | HUMAN-CHROMOSOME 3P21.3 | Neoplasms - metabolism | ras Proteins - genetics | Protein Binding - genetics | Tumor Suppressor Proteins - metabolism | Signal Transduction | Epigenesis, Genetic | Humans | Gene Silencing | ras Proteins - metabolism | Protein Structure, Tertiary - genetics | Point Mutation | DNA Methylation | Animals | Cell Cycle | Neoplasms - genetics | Gene Deletion | Tumor Suppressor Proteins - genetics | Apoptosis
Journal Article
Nature Reviews Cancer, ISSN 1474-175X, 03/2017, Volume 17, Issue 3, pp. 145 - 159
The Notch signalling cascade is an evolutionarily conserved pathway that has a crucial role in regulating development and homeostasis in various tissues. The...
GAMMA-SECRETASE INHIBITION | CHROMOSOMAL TRANSLOCATIONS | STEM-CELLS | ONCOLOGY | NEGATIVE REGULATION | PANCREATIC-CANCER | SQUAMOUS-CELL CARCINOMA | MUTATIONAL LANDSCAPE | HUMAN-PAPILLOMAVIRUS | NF-KAPPA-B | NEUROENDOCRINE PHENOTYPE | Tumor Suppressor Proteins - physiology | Animals | Neoplasms - etiology | Humans | Receptors, Notch - physiology | Signal Transduction - physiology | Cell Differentiation | Tumor suppressor genes | Cellular signal transduction | Genetic aspects | Health aspects | Index Medicus
GAMMA-SECRETASE INHIBITION | CHROMOSOMAL TRANSLOCATIONS | STEM-CELLS | ONCOLOGY | NEGATIVE REGULATION | PANCREATIC-CANCER | SQUAMOUS-CELL CARCINOMA | MUTATIONAL LANDSCAPE | HUMAN-PAPILLOMAVIRUS | NF-KAPPA-B | NEUROENDOCRINE PHENOTYPE | Tumor Suppressor Proteins - physiology | Animals | Neoplasms - etiology | Humans | Receptors, Notch - physiology | Signal Transduction - physiology | Cell Differentiation | Tumor suppressor genes | Cellular signal transduction | Genetic aspects | Health aspects | Index Medicus
Journal Article
2003, Methods in molecular biology, ISBN 0896039862, Volume 222-223., xix, 657
Book
Oncogene, ISSN 0950-9232, 09/2008, Volume 27, Issue 38, pp. 5115 - 5123
Cancer development results from deregulated control of stem cell populations and alterations in their surrounding environment. Notch signaling is an important...
Epigenetics | Keratinocytes | Cancer stem cells | p63 | Rho signaling | p53 | SIGNALING PATHWAYS | RBP-J-KAPPA | HAIR FOLLICLE | BIOCHEMISTRY & MOLECULAR BIOLOGY | keratinocytes | BETA-CATENIN | P53 HOMOLOG | epigenetics | CELL BIOLOGY | ONCOLOGY | GROWTH ARREST | CERVICAL-CANCER CELLS | GENETICS & HEREDITY | NEGATIVE TRANSCRIPTIONAL REGULATOR | KERATINOCYTE STEM-CELLS | cancer stem cells | NF-KAPPA-B | Species Specificity | Keratinocytes - radiation effects | Humans | Receptors, Notch - genetics | Tumor Suppressor Protein p53 - physiology | Neoplasms - virology | Neoplasms - genetics | Cell Transformation, Neoplastic - genetics | Tumor Virus Infections - physiopathology | Tumor Suppressor Proteins - genetics | Female | Neoplasms - physiopathology | Cell Differentiation - physiology | Genes, Tumor Suppressor | Oncogene Proteins, Viral - physiology | Receptors, Notch - physiology | Uterine Cervical Neoplasms - physiopathology | Uterine Cervical Neoplasms - genetics | Ultraviolet Rays - adverse effects | Tumor Suppressor Proteins - physiology | Keratinocytes - pathology | Animals | Uterine Cervical Neoplasms - virology | Signal Transduction - physiology | Mice | Apoptosis - physiology | DNA Damage | Receptor, Notch1 - genetics | Receptor, Notch1 - physiology | Care and treatment | Tumor suppressor genes | Cellular signal transduction | Genetic aspects | Research | Health aspects | Risk factors | Cancer | Signal transduction | Gene expression | Stem cells | Cell cycle | cancer therapy | carcinogenesis
Epigenetics | Keratinocytes | Cancer stem cells | p63 | Rho signaling | p53 | SIGNALING PATHWAYS | RBP-J-KAPPA | HAIR FOLLICLE | BIOCHEMISTRY & MOLECULAR BIOLOGY | keratinocytes | BETA-CATENIN | P53 HOMOLOG | epigenetics | CELL BIOLOGY | ONCOLOGY | GROWTH ARREST | CERVICAL-CANCER CELLS | GENETICS & HEREDITY | NEGATIVE TRANSCRIPTIONAL REGULATOR | KERATINOCYTE STEM-CELLS | cancer stem cells | NF-KAPPA-B | Species Specificity | Keratinocytes - radiation effects | Humans | Receptors, Notch - genetics | Tumor Suppressor Protein p53 - physiology | Neoplasms - virology | Neoplasms - genetics | Cell Transformation, Neoplastic - genetics | Tumor Virus Infections - physiopathology | Tumor Suppressor Proteins - genetics | Female | Neoplasms - physiopathology | Cell Differentiation - physiology | Genes, Tumor Suppressor | Oncogene Proteins, Viral - physiology | Receptors, Notch - physiology | Uterine Cervical Neoplasms - physiopathology | Uterine Cervical Neoplasms - genetics | Ultraviolet Rays - adverse effects | Tumor Suppressor Proteins - physiology | Keratinocytes - pathology | Animals | Uterine Cervical Neoplasms - virology | Signal Transduction - physiology | Mice | Apoptosis - physiology | DNA Damage | Receptor, Notch1 - genetics | Receptor, Notch1 - physiology | Care and treatment | Tumor suppressor genes | Cellular signal transduction | Genetic aspects | Research | Health aspects | Risk factors | Cancer | Signal transduction | Gene expression | Stem cells | Cell cycle | cancer therapy | carcinogenesis
Journal Article
1990, Immunology series, ISBN 9780824782184, Volume 51., viii, 273
Book
Nucleic Acids Research, ISSN 0305-1048, 05/2013, Volume 41, Issue 9, pp. 4976 - 4987
Protein-coding genes account for only a small part of the human genome, whereas the vast majority of transcripts make up the non-coding RNAs including long...
HOST GENE | ACTIVATION | MELANOMA | LONG NONCODING RNA | CHROMATIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | GENE-EXPRESSION | DIFFERENTIATION | CANCER | MICRORNA | Colonic Neoplasms - genetics | Cell Proliferation | Response Elements | Down-Regulation | Humans | Tumor Suppressor Protein p53 - metabolism | MicroRNAs - metabolism | RNA, Long Noncoding - genetics | Colonic Neoplasms - metabolism | Animals | RNA, Long Noncoding - biosynthesis | Cell Line, Tumor | Neoplasms - pathology | Genes, Tumor Suppressor | RNA, Long Noncoding - metabolism | Molecular Biology
HOST GENE | ACTIVATION | MELANOMA | LONG NONCODING RNA | CHROMATIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | GENE-EXPRESSION | DIFFERENTIATION | CANCER | MICRORNA | Colonic Neoplasms - genetics | Cell Proliferation | Response Elements | Down-Regulation | Humans | Tumor Suppressor Protein p53 - metabolism | MicroRNAs - metabolism | RNA, Long Noncoding - genetics | Colonic Neoplasms - metabolism | Animals | RNA, Long Noncoding - biosynthesis | Cell Line, Tumor | Neoplasms - pathology | Genes, Tumor Suppressor | RNA, Long Noncoding - metabolism | Molecular Biology
Journal Article
Journal of Molecular Endocrinology, ISSN 0952-5041, 06/2012, Volume 48, Issue 3, pp. R45 - R53
Maternally expressed gene 3 (MEG3) is an imprinted gene belonging to the imprinted DLK1-MEG3 locus located at chromosome 14q32.3 in humans. Its mouse ortholog,...
ORIGIN | DLK1-GTL2 IMPRINTED DOMAIN | GROWTH | ENDOCRINOLOGY & METABOLISM | GENE-EXPRESSION | PROMOTER REGION | NONFUNCTIONING PITUITARY-ADENOMAS | CANCER | LOCUS | GTL2 GENE | P53 | Gene Expression | Cell Proliferation | RNA, Untranslated - metabolism | Neovascularization, Physiologic - genetics | Pituitary Neoplasms - genetics | Humans | Gene Silencing | Tumor Suppressor Protein p53 - metabolism | RNA, Untranslated - genetics | Tumor Suppressor Protein p53 - genetics | DNA Methylation | Animals | Neoplasms - genetics | Gene Deletion | Mice | Genes, Tumor Suppressor
ORIGIN | DLK1-GTL2 IMPRINTED DOMAIN | GROWTH | ENDOCRINOLOGY & METABOLISM | GENE-EXPRESSION | PROMOTER REGION | NONFUNCTIONING PITUITARY-ADENOMAS | CANCER | LOCUS | GTL2 GENE | P53 | Gene Expression | Cell Proliferation | RNA, Untranslated - metabolism | Neovascularization, Physiologic - genetics | Pituitary Neoplasms - genetics | Humans | Gene Silencing | Tumor Suppressor Protein p53 - metabolism | RNA, Untranslated - genetics | Tumor Suppressor Protein p53 - genetics | DNA Methylation | Animals | Neoplasms - genetics | Gene Deletion | Mice | Genes, Tumor Suppressor
Journal Article
Nature, ISSN 0028-0836, 05/2019, Volume 569, Issue 7756, pp. 1 - 2
Writing in Nature, Walter et at.1 report their analysis of the role of the tumour-suppressor protein retinoblastoma (Rb), using an experimental system that...
Deactivation | Lung cancer | Cyclin-dependent kinases | Retinoblastoma protein | Activation | Metastasis | Kinases | Gene expression | Inactivation | Cancer therapies | Success | Cyclin-dependent kinase 4 | Suppressors | Cyclin-dependent kinase 2 | Proteins | DNA-binding protein | Genetic engineering | Children | Retinoblastoma | Deoxyribonucleic acid--DNA | Tumors
Deactivation | Lung cancer | Cyclin-dependent kinases | Retinoblastoma protein | Activation | Metastasis | Kinases | Gene expression | Inactivation | Cancer therapies | Success | Cyclin-dependent kinase 4 | Suppressors | Cyclin-dependent kinase 2 | Proteins | DNA-binding protein | Genetic engineering | Children | Retinoblastoma | Deoxyribonucleic acid--DNA | Tumors
Journal Article
International Journal of Cancer, ISSN 0020-7136, 04/2012, Volume 130, Issue 8, pp. 1715 - 1725
Cellular senescence is an irreversible arrest of cell growth. Biochemical and morphological changes occur during cellular senescence, including the formation...
senescence | tumor suppressor gene p16 | HISTONE METHYLTRANSFERASE ACTIVITY | P16(INK4A) EXPRESSION | TRANSCRIPTIONAL REPRESSION | SELF-RENEWAL | FACTOR-KAPPA-B | HETEROCHROMATIN FOCI | POLYCOMB GROUP PROTEINS | PREMATURE SENESCENCE | ONCOLOGY | IN-VIVO | LYSINE 9 | Cellular Senescence - genetics | Gene Expression - drug effects | Humans | Cellular Senescence - drug effects | Cellular Senescence - physiology | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Neoplasms - prevention & control | Cyclin-Dependent Kinase Inhibitor p16 - physiology | Tumor Suppressor Protein p53 - genetics | Tumor Suppressor Protein p53 - physiology | Cell Cycle Checkpoints | Telomere Shortening | Neoplasms - genetics | Retinoblastoma Protein - genetics | Antineoplastic Agents - pharmacology | Neoplasms - physiopathology | Retinoblastoma Protein - physiology | Transcription factors | Senescence | Kinases | Cell cycle | Tumor suppressor gene p16
senescence | tumor suppressor gene p16 | HISTONE METHYLTRANSFERASE ACTIVITY | P16(INK4A) EXPRESSION | TRANSCRIPTIONAL REPRESSION | SELF-RENEWAL | FACTOR-KAPPA-B | HETEROCHROMATIN FOCI | POLYCOMB GROUP PROTEINS | PREMATURE SENESCENCE | ONCOLOGY | IN-VIVO | LYSINE 9 | Cellular Senescence - genetics | Gene Expression - drug effects | Humans | Cellular Senescence - drug effects | Cellular Senescence - physiology | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Neoplasms - prevention & control | Cyclin-Dependent Kinase Inhibitor p16 - physiology | Tumor Suppressor Protein p53 - genetics | Tumor Suppressor Protein p53 - physiology | Cell Cycle Checkpoints | Telomere Shortening | Neoplasms - genetics | Retinoblastoma Protein - genetics | Antineoplastic Agents - pharmacology | Neoplasms - physiopathology | Retinoblastoma Protein - physiology | Transcription factors | Senescence | Kinases | Cell cycle | Tumor suppressor gene p16
Journal Article
Genes and Development, ISSN 0890-9369, 12/2009, Volume 23, Issue 23, pp. 2700 - 2704
While the global down-regulation of microRNAs ( miRNAs) is a common feature of human tumors, its genetic basis is largely undefined. To explore this question,...
Dicer | Mouse models | Tumor suppressor | MicroRNAs | Cancer | Haploinsufficiency | mouse models | TRANSFORMATION | RNAS | tumor suppressor | LET-7 | DEVELOPMENTAL BIOLOGY | CELL BIOLOGY | haploinsufficiency | BIOGENESIS | REPRESSION | GENETICS & HEREDITY | cancer | MUTATIONS | EXPRESSION | Lung Neoplasms - genetics | Tumor Suppressor Proteins - metabolism | Ribonuclease III - genetics | Ribonuclease III - metabolism | Lung Neoplasms - mortality | Humans | Mice, Inbred C57BL | MicroRNAs - metabolism | Lung Neoplasms - physiopathology | Mutation - genetics | Animals | Gene Deletion | Tumor Suppressor Proteins - genetics | Sarcoma - mortality | Survival Analysis | Cell Line, Tumor | Sarcoma - physiopathology | Mice | Sarcoma - genetics | Disease Models, Animal | Human genome | Analysis | Tumor suppressor genes | Genetic aspects | Research | Gene expression | Research Communication
Dicer | Mouse models | Tumor suppressor | MicroRNAs | Cancer | Haploinsufficiency | mouse models | TRANSFORMATION | RNAS | tumor suppressor | LET-7 | DEVELOPMENTAL BIOLOGY | CELL BIOLOGY | haploinsufficiency | BIOGENESIS | REPRESSION | GENETICS & HEREDITY | cancer | MUTATIONS | EXPRESSION | Lung Neoplasms - genetics | Tumor Suppressor Proteins - metabolism | Ribonuclease III - genetics | Ribonuclease III - metabolism | Lung Neoplasms - mortality | Humans | Mice, Inbred C57BL | MicroRNAs - metabolism | Lung Neoplasms - physiopathology | Mutation - genetics | Animals | Gene Deletion | Tumor Suppressor Proteins - genetics | Sarcoma - mortality | Survival Analysis | Cell Line, Tumor | Sarcoma - physiopathology | Mice | Sarcoma - genetics | Disease Models, Animal | Human genome | Analysis | Tumor suppressor genes | Genetic aspects | Research | Gene expression | Research Communication
Journal Article
Nature Reviews Molecular Cell Biology, ISSN 1471-0072, 05/2012, Volume 13, Issue 5, pp. 283 - 296
The importance of the physiological function of phosphatase and tensin homologue (PTEN) is illustrated by its frequent disruption in cancer. By suppressing the...
PATHWAY ACTIVATION | SOMA SIZE | NUCLEAR PTEN | GENETIC DISSECTION | UBIQUITIN LIGASE | NEGATIVE REGULATION | HEMATOPOIETIC STEM-CELLS | PROSTATE-CANCER | MOUSE MODEL | TENSIN-HOMOLOG PTEN | CELL BIOLOGY | PTEN Phosphohydrolase - genetics | Tumor Suppressor Proteins - metabolism | Signal Transduction | Humans | PTEN Phosphohydrolase - physiology | Gene Expression Regulation | Neoplasms - enzymology | PTEN Phosphohydrolase - metabolism | Cell Nucleus - enzymology | Tumor Suppressor Proteins - physiology | Animals | Tumor Suppressor Proteins - genetics | Protein Conformation | Mutation | Neoplasms - pathology | Neoplastic Stem Cells - enzymology | Neoplastic Stem Cells - physiology | Phosphatases | Physiological aspects
PATHWAY ACTIVATION | SOMA SIZE | NUCLEAR PTEN | GENETIC DISSECTION | UBIQUITIN LIGASE | NEGATIVE REGULATION | HEMATOPOIETIC STEM-CELLS | PROSTATE-CANCER | MOUSE MODEL | TENSIN-HOMOLOG PTEN | CELL BIOLOGY | PTEN Phosphohydrolase - genetics | Tumor Suppressor Proteins - metabolism | Signal Transduction | Humans | PTEN Phosphohydrolase - physiology | Gene Expression Regulation | Neoplasms - enzymology | PTEN Phosphohydrolase - metabolism | Cell Nucleus - enzymology | Tumor Suppressor Proteins - physiology | Animals | Tumor Suppressor Proteins - genetics | Protein Conformation | Mutation | Neoplasms - pathology | Neoplastic Stem Cells - enzymology | Neoplastic Stem Cells - physiology | Phosphatases | Physiological aspects