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Oncogene, ISSN 0950-9232, 01/2012, Volume 31, Issue 1, pp. 80 - 92
Acute myeloblastic leukemia (AML) is characterized by the accumulation of abnormal myeloblasts (mainly granulocyte or monocyte precursors) in the bone marrow... 
granulocyte/monocyte differentiation | microRNA | acute myeloblastic leukemia | RBSP3-pRB-E2F1 pathway | CANCER-CELLS | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | MICRORNAS | FREQUENT ALTERATIONS | BINDING PROTEIN | RETINOBLASTOMA PROTEIN PATHWAY | CELL BIOLOGY | CYCLE CONTROL | ONCOLOGY | GENETICS & HEREDITY | E2F1 | PROGNOSTIC-SIGNIFICANCE | CARCINOMA | Phosphorylation | Tumor Suppressor Proteins - antagonists & inhibitors | Cell Survival | Leukemia, Myeloid, Acute - pathology | Humans | Retinoblastoma Protein - metabolism | Male | Leukemia, Myeloid, Acute - etiology | E2F1 Transcription Factor - metabolism | Tumor Suppressor Proteins - physiology | MicroRNAs - analysis | Tumor Suppressor Proteins - genetics | Cell Line, Tumor | Female | Cell Differentiation | MicroRNAs - physiology | Leukemia, Myeloid, Acute - genetics | Physiological aspects | Tumor suppressor genes | Genetic aspects | Research | Cell differentiation | Health aspects | Phosphates | Leukemia | Tumors | Cell proliferation | Osteoprogenitor cells | Cell survival | non-coding RNA | Myeloid leukemia | Data processing | Acute myeloblastic leukemia | Blast | Survival | Blood | Hemopoiesis | Monocytes | Etiology | Cell cycle | Stem cells | Bone marrow | Leukemogenesis | miRNA | Differentiation | Leukocytes (granulocytic) | Acute myeloid leukemia | Cancer | Index Medicus | granulocyte | monocyte differentiation | Original | RBSP3–pRB–E2F1 pathway
Journal Article
Journal of Cellular Physiology, ISSN 0021-9541, 02/2018, Volume 233, Issue 2, pp. 1213 - 1221
We propose that E2F1 interactive with BRCA1 pathway induces HCC two different small molecule metabolism or cell cycle regulation via mitochondrion or CD4+T to... 
high | feedback‐interactive | E2F1 | HCC | pathway | BRCA1 | from mitochondrion or membrane to cytosol | CD4+T‐related cell cycle regulation | small molecule metabolism | CD4+T-related cell cycle regulation | high E2F1 feedback-interactive BRCA1 pathway | TRANSFORMATION | SIGNAL | SYSTEMS-THEORETICAL ANALYSIS | PHYSIOLOGY | BIOCOMPUTATION | TUMOR HEPATITIS/CIRRHOTIC TISSUES | LARGE GENE LISTS | CELL BIOLOGY | COMPUTATIONAL NETWORK | HUMAN HEPATOCELLULAR-CARCINOMA | EXPRESSION | Cell Cycle - genetics | Humans | Gene Expression Regulation, Neoplastic | Databases, Genetic | CD4-Positive T-Lymphocytes - immunology | Cell Transformation, Neoplastic - genetics | BRCA1 Protein - metabolism | Carcinoma, Hepatocellular - genetics | Liver Neoplasms - pathology | Carcinoma, Hepatocellular - immunology | Energy Metabolism - genetics | Liver Neoplasms - genetics | Signal Transduction | CD4-Positive T-Lymphocytes - metabolism | Computational Biology | Liver Neoplasms - immunology | Mitochondria - metabolism | E2F1 Transcription Factor - metabolism | Mitochondria - pathology | Cell Transformation, Neoplastic - metabolism | BRCA1 Protein - genetics | Cell Transformation, Neoplastic - immunology | Feedback, Physiological | Carcinoma, Hepatocellular - pathology | Liver Neoplasms - metabolism | Cytosol - metabolism | Cell Transformation, Neoplastic - pathology | E2F1 Transcription Factor - genetics | Carcinoma, Hepatocellular - metabolism | Physiological aspects | Analysis | Cell cycle | Protein binding | Binding | Enrichment | Regulations | BRCA1 protein | Activation | Breast cancer | Metabolism | Cytosol | E2F1 protein | CD4 antigen | E2F protein | Feedback | Deoxyribonucleic acid--DNA | Cancer | Index Medicus
Journal Article
Journal of Cell Science, ISSN 0021-9533, 12/2010, Volume 123, Issue 23, pp. 4095 - 4106
Journal Article
Journal Article
Nature, ISSN 0028-0836, 07/2010, Volume 466, Issue 7306, pp. 637 - 641
Gain-of-function mutations in leucine-rich repeat kinase 2 (LRRK2) cause familial as well as sporadic Parkinson's disease characterized by age-dependent... 
PATHWAYS | KINASE-ACTIVITY | GENE | LET-7 MICRORNA | 4E-BP | MULTIDISCIPLINARY SCIENCES | DISTINCT ROLES | MUTATIONS | DROSOPHILA | PARKINSONS-DISEASE | CELL-DEATH | Up-Regulation | Protein Biosynthesis | MicroRNAs - antagonists & inhibitors | Humans | Male | MicroRNAs - metabolism | Neurons - cytology | Drosophila Proteins - metabolism | RNA, Messenger - metabolism | Drosophila Proteins - biosynthesis | Trans-Activators - genetics | Eukaryotic Initiation Factor-2 - metabolism | Female | Neurons - metabolism | Parkinson Disease - metabolism | Trans-Activators - biosynthesis | Dopamine - metabolism | Protein-Serine-Threonine Kinases - metabolism | Eukaryotic Initiation Factors - metabolism | Cell Line | RNA-Induced Silencing Complex - antagonists & inhibitors | Down-Regulation | RNA, Messenger - genetics | Protein-Serine-Threonine Kinases - genetics | E2F1 Transcription Factor - metabolism | Eukaryotic Initiation Factors - biosynthesis | Parkinson Disease - genetics | Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 | Animals | RNA-Induced Silencing Complex - metabolism | Argonaute Proteins | Protein Binding | Trans-Activators - metabolism | E2F1 Transcription Factor - biosynthesis | MicroRNAs - genetics | Drosophila Proteins - genetics | RNA-Induced Silencing Complex - chemistry | E2F1 Transcription Factor - genetics | Drosophila melanogaster | Parkinson Disease - etiology | Models | Genetic aspects | Genetic translation | Phosphotransferases | Proteins | Statistical analysis | Insects | Neurons | Cell cycle | Cell division | Mutation | Kinases | Binding sites | Apoptosis | Index Medicus
Journal Article
Cellular Signalling, ISSN 0898-6568, 05/2013, Volume 25, Issue 5, pp. 1086 - 1095
Journal Article
Journal of Cellular Physiology, ISSN 0021-9541, 02/2018, Volume 233, Issue 2, pp. 1312 - 1320
The results were suggested that heavy ion IR could induce p53 −/− cancer cells apoptosis via E2F1 signal pathway. Our study provides a scientific rationale for... 
E2F1 | apoptosis | cancer cells | radioresistance | carbon ion irradiation | HEAD | TRANSLOCATION | PHYSIOLOGY | DNA-DAMAGE | RETINOBLASTOMA GENE | CANCER | P53 | CELL BIOLOGY | RESISTANCE | TUMOR-SUPPRESSOR | HUMAN HEPATOCELLULAR-CARCINOMA | IONIZING-RADIATION | Up-Regulation | Apoptosis - radiation effects | Humans | Radiation Tolerance | Caspase 3 - metabolism | Gene Expression Regulation, Neoplastic | Tumor Suppressor Protein p53 - genetics | G2 Phase Cell Cycle Checkpoints - radiation effects | Carcinoma, Hepatocellular - drug therapy | Heavy Ion Radiotherapy | Carcinoma, Hepatocellular - genetics | Liver Neoplasms - pathology | Signal Transduction - radiation effects | Liver Neoplasms - enzymology | A549 Cells | Liver Neoplasms - genetics | Tumor Suppressor Protein p53 - metabolism | bcl-2-Associated X Protein - metabolism | Carcinoma, Hepatocellular - enzymology | E2F1 Transcription Factor - metabolism | Hep G2 Cells | Liver Neoplasms - radiotherapy | Carcinoma, Hepatocellular - pathology | E2F1 Transcription Factor - genetics | Dose-Response Relationship, Radiation | Tumor proteins | Apoptosis | Cell survival | Bax protein | p53 Protein | Caspase | Radioresistance | Hepatoma | Radiation therapy | Rubidium | Caspase-3 | Low level | E2F1 protein | Proteins | E2F protein | Signaling | Ion irradiation | Clonal deletion | Cell fate | Deletion | Irradiation | Cancer | Tumors | Index Medicus
Journal Article
Nature Medicine, ISSN 1078-8956, 04/2016, Volume 22, Issue 4, pp. 369 - 378
Journal Article