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Cell Death and Differentiation, ISSN 1350-9047, 11/2017, Volume 24, Issue 11, pp. 1948 - 1962
High Mobility Group A1 (HMGA1) is an architectural chromatin protein whose overexpression is a feature of malignant neoplasias with a causal role in cancer... 
TRANSFORMATION | HMGA PROTEINS | GENE | BIOCHEMISTRY & MOLECULAR BIOLOGY | RESISTANCE | REQUIRES | DEATH | TRANSCRIPTIONAL REGULATION | EXPRESSION | MTOR | TRANSGENIC MICE | CELL BIOLOGY | Neoplasms - metabolism | Skin Neoplasms - pathology | Green Fluorescent Proteins - metabolism | Cell Proliferation | Cell Survival | Microtubule-Associated Proteins - metabolism | Humans | Gene Silencing | Protein-Serine-Threonine Kinases - genetics | Autophagy-Related Protein-1 Homolog - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | HMGA1a Protein - metabolism | Autophagy | Gene Knockdown Techniques | Skin Neoplasms - metabolism | Animals | Autophagy-Related Protein 5 - metabolism | Transcription, Genetic | Mice | HeLa Cells | Neoplasms - pathology | Autophagy-Related Protein-1 Homolog - genetics | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | TOR protein | Cell proliferation | Chromatin | Deregulation | Transcription | Mobility | Phagosomes | A1 protein | Kinases | DNA repair | Skin cancer | Proteins | Cell growth | Protein folding | Deoxyribonucleic acid--DNA | Cell survival | Stability | Organelles | Survival | High mobility group proteins | Depletion | Cell death | Tumor suppressor genes | Viability | Phagocytosis | Cancer | Apoptosis | Original Paper
Journal Article
Gastroenterology, ISSN 0016-5085, 2013, Volume 144, Issue 3, pp. 624 - 635.e4
Journal Article
Cell Biochemistry and Function, ISSN 0263-6484, 10/2017, Volume 35, Issue 7, pp. 464 - 471
High Mobility Group AT‐hook 1 (HMGA1) was identified as a target of miR‐214 in human cervical and colorectal cancers (CaCx and CRC) in a previous study. While... 
gene expression regulation | microRNA‐214 | human colorectal cancer | signal transduction | tumour suppressor | human cervical cancer | oncogene | High Mobility Group AT‐hook 1 | High Mobility Group AT-hook 1 | microRNA-214 | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSDUCER | KAPPA-B | BETA-CATENIN | HMGA1 EXPRESSION | CELL BIOLOGY | COLON-CANCER | INVASION | GENE | GROWTH | TRANSCRIPTION FACTOR | HMGA1a Protein - genetics | MicroRNAs - antagonists & inhibitors | Down-Regulation | Humans | Tumor Suppressor Protein p53 - metabolism | MicroRNAs - metabolism | Uterine Cervical Neoplasms - pathology | HMGA1a Protein - metabolism | beta Catenin - metabolism | Tumor Suppressor Protein p53 - genetics | RNA Interference | Transcription Factor RelA - metabolism | Uterine Cervical Neoplasms - metabolism | Cell Line, Tumor | Female | MicroRNAs - genetics | Antagomirs - metabolism | Colorectal Neoplasms - pathology | HMGA1a Protein - antagonists & inhibitors | Colorectal Neoplasms - metabolism | STAT3 Transcription Factor - metabolism | Wnt Signaling Pathway | RNA, Small Interfering - metabolism | Cellular signal transduction | Chromosomal proteins | Tumor proteins | Gene expression | Cancer cells | Colorectal cancer | NF-κB protein | Deregulation | Target recognition | Wnt protein | p53 Protein | Colorectal carcinoma | MiRNA | Stat3 protein | siRNA | Cervix | Tissues | Ribonucleic acid--RNA | Western blotting | Intermediates | Signal transduction | Signaling | Pathways | Inhibition | Aberration | RelA protein | Cancer | Tumors
Journal Article
Oncogene, ISSN 0950-9232, 09/2017, Volume 36, Issue 36, pp. 5110 - 5121
The MAPK pathway is activated in the majority of melanomas and is the target of therapeutic approaches. Under normal conditions, it initiates the so-called... 
CELLS | ACTIVATION | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | DEDIFFERENTIATION | MITF | CELL BIOLOGY | METASTATIC MELANOMA | GENE | ONCOLOGY | CANCER METASTASIS | GENETICS & HEREDITY | FRA-1 | C-JUN | Cell Proliferation | Transcription Factor AP-1 - genetics | Humans | Transcriptional Activation | Gene Expression Regulation, Neoplastic | Melanocytes - metabolism | Gene Expression Profiling | Transcription Factor AP-1 - metabolism | Nevus - genetics | Cell Transformation, Neoplastic - genetics | Melanoma - genetics | Melanocytes - pathology | Melanoma - metabolism | Skin Neoplasms - pathology | HMGA1a Protein - genetics | Microphthalmia-Associated Transcription Factor - metabolism | Signal Transduction | Cells, Cultured | Proto-Oncogene Proteins c-fos - metabolism | Melanoma - pathology | HMGA1a Protein - metabolism | Cell Transformation, Neoplastic - metabolism | Skin Neoplasms - metabolism | Nevus - pathology | Skin Neoplasms - genetics | Proto-Oncogene Proteins c-fos - genetics | High-Throughput Nucleotide Sequencing | Cell Transformation, Neoplastic - pathology | Microphthalmia-Associated Transcription Factor - genetics | Nevus - metabolism | Cell Movement | Care and treatment | Transcription factors | Melanoma | Development and progression | Genetic aspects | Gene expression | Health aspects | Oncogenes | Microphthalmia-associated transcription factor | Cell proliferation | Chromatin | Transformation | Leukocyte migration | Genes | Activator protein 1 | MAP kinase | Melanocytes | Myc protein | Cell adhesion & migration | Axl protein | Anoikis | Cell migration
Journal Article
Oncogene, ISSN 0950-9232, 08/2012, Volume 31, Issue 34, pp. 3857 - 3865
Previous studies have demonstrated that high mobility group A proteins have a critical role on the onset of human pituitary adenomas. Indeed, both high... 
microRNA | HMGA | pituitary adenoma | TRANSFORMATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | MOUSE | NATURAL-KILLER-CELL | MOBILITY GROUP A2 | PROLIFERATION | PROTEIN-SYNTHESIS | TUMORS | CELL BIOLOGY | OVEREXPRESSION | ONCOLOGY | GENETICS & HEREDITY | GENE-EXPRESSION | ADENOMAS | Cell Line | HMGA1a Protein - genetics | Pituitary Neoplasms - genetics | Humans | 3' Untranslated Regions - genetics | Pituitary Neoplasms - pathology | Binding Sites - genetics | HMGA1a Protein - metabolism | Pituitary Neoplasms - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Cell Transformation, Neoplastic - metabolism | HMGA Proteins - genetics | Sequence Homology, Nucleic Acid | Blotting, Western | HMGA Proteins - metabolism | Animals | HMGA2 Protein - metabolism | Cell Transformation, Neoplastic - genetics | Base Sequence | HMGA2 Protein - genetics | Cell Line, Tumor | MicroRNAs - genetics | Cell Transformation, Neoplastic - pathology | Care and treatment | MicroRNA | Pituitary gland tumors | Patient outcomes | Physiological aspects | Development and progression | Genetic aspects | Health aspects | Methods | Cancer | Proteins | Pituitary gland | Gene expression | Ribonucleic acid--RNA | Pathogenesis | High mobility group proteins | Trisomy | Prolactin | Pituitary | Transgenic mice | Chromosome 12 | miRNA | Tumorigenesis | mRNA | Adenoma | Growth hormone
Journal Article
PLOS ONE, ISSN 1932-6203, 10/2016, Volume 11, Issue 10, p. e0164258
The HMGA1 architectural transcription factor is an oncogene overexpressed in the vast majority of human cancers. HMGA1 is a highly connected node in the... 
BREAST-CANCER | PATHWAY CHOICE | TRANSCRIPTION FACTOR HMGA2 | GENE | MULTIDISCIPLINARY SCIENCES | HISTONE H1 | LIGATION | DEPENDENT PROTEIN-KINASE | EXPRESSION | NUCLEOTIDE EXCISION-REPAIR | CANCER STEM-CELLS | Chromatin - metabolism | HMGA1a Protein - genetics | Phosphorylation | Humans | Recombinant Proteins - chemistry | Substrate Specificity | Ku Autoantigen - metabolism | Chromatography, High Pressure Liquid | Recombinant Proteins - biosynthesis | HMGA1a Protein - metabolism | Comet Assay | Recombinant Proteins - isolation & purification | HMGA2 Protein - metabolism | MCF-7 Cells | DNA Repair | HMGA2 Protein - genetics | Cell Line, Tumor | DNA Ligase ATP - metabolism | Histones - metabolism | Microscopy, Fluorescence | Chromatin - chemistry | Cellular proteins | Chromatin | Chromosomal proteins | Ligases | DNA damage | Genes | DNA | Gene expression | DNA repair | Transcription factors | Homology | Biochemistry | Kinases | Cancer therapies | Proteins | Architectural engineering | Cell cycle | Physiology | Life sciences | Damage | Repair | Deoxyribonucleic acid--DNA | Cell survival | DNA ligase (ATP) | Breast cancer | Pharmacology | Substrates | High mobility group proteins | Chemotherapy | DNA-dependent protein kinase | Stem cells | Non-homologous end joining | Genetic engineering | Histone H1 | Cancer | Deoxyribonucleic acid
Journal Article
Journal Article
BMC cancer, ISSN 1471-2407, 2014, Volume 14, Issue 1, pp. 694 - 694
Journal Article
Nature Medicine, ISSN 1078-8956, 07/2005, Volume 11, Issue 7, pp. 765 - 773
Journal Article
Circulation Research, ISSN 0009-7330, 02/2012, Volume 110, Issue 3, pp. 394 - 405
Journal Article
Histopathology, ISSN 0309-0167, 02/2012, Volume 60, Issue 3, pp. 397 - 404
Piscuoglio S, Zlobec I, Pallante P, Sepe R, Esposito F, Zimmermann A, Diamantis I, Terracciano L, Fusco A & Karamitopoulou E 
(2012) Histopathology 60, 397–404...