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Cell death and differentiation, ISSN 1476-5403, 2006, Volume 13, Issue 6, pp. 962 - 972
.... They encode for multiple p63, p73 or p53 proteins containing different protein domains (isoforms) due to multiple splicing, alternative promoter and alternative initiation of translation... 
Promoter | Development | Zebrafish | Splice | Drosophila | Cancer | development | P53-DEPENDENT APOPTOSIS | splice | BIOCHEMISTRY & MOLECULAR BIOLOGY | HOMOLOG P63 | TUMOR-SUPPRESSOR GENE | P73 | CELL BIOLOGY | DAMAGE RESPONSE | drosophila | TRANSACTIVATION | P53 FAMILY-MEMBER | promoter | cancer | zebrafish | EXPRESSION | ALTERNATIVELY SPLICED FORM | TRANSFORMED-CELLS | Neoplasms - metabolism | Alternative Splicing | Humans | Promoter Regions, Genetic - genetics | Tumor Suppressor Protein p53 - genetics | DNA-Binding Proteins - metabolism | Cell Differentiation - genetics | Protein Isoforms - metabolism | Neoplasms - genetics | Cell Transformation, Neoplastic - genetics | Tumor Suppressor Proteins - genetics | Trans-Activators - genetics | Apoptosis Regulatory Proteins - genetics | Cell Cycle Proteins - genetics | Transcription, Genetic | Nuclear Proteins - genetics | Tumor Suppressor Proteins - metabolism | Cell Cycle Proteins - metabolism | Tumor Suppressor Protein p53 - metabolism | Nuclear Proteins - metabolism | DNA - metabolism | DNA-Binding Proteins - genetics | Cell Transformation, Neoplastic - metabolism | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | DNA - genetics | Tumor Protein p73 | Animals | Trans-Activators - metabolism | Mice | Transcription Factors | Mutation | Evolution, Molecular | Protein Isoforms - genetics
Journal Article
Journal Article
Journal Article
Cell Cycle, ISSN 1551-4005, 2014, Volume 8, Issue 16, pp. 2502 - 2508
The Akt (PKB) protein kinases are critical regulators of human physiology that control an impressive array of diverse cellular functions, including the modulation of growth, survival, proliferation and metabolism... 
Binding | Proteins | Landes | Calcium | Bioscience | Biology | Cell | Cycle | Cancer | Organogenesis | Glucose homeostasis | Akt2 | Isoforms | Akt1 | Akt | GLUT4 | Metabolism | Cellular growth | Signaling specificity | signaling specificity | GLUT4-CONTAINING VESICLES | STIMULATED GLUT4 TRANSLOCATION | GTPASE-ACTIVATING-PROTEIN | isoforms | PLASMA-MEMBRANE | MICE LACKING | CELL BIOLOGY | cellular growth | glucose homeostasis | SKELETAL-MUSCLE | GLUCOSE-HOMEOSTASIS | SIGNALING PATHWAY | CELL-MIGRATION | INSULIN-RESISTANCE | metabolism | cancer
Journal Article
The EMBO Journal, ISSN 0261-4189, 02/2011, Volume 30, Issue 4, pp. 783 - 795
.... During the EMT process, TGF‐β induced isoform switching of fibroblast growth factor (FGF) receptors, causing the cells to become sensitive to FGF‐2. Addition of FGF‐2 to TGF‐β... 
FGF‐2 | TGF‐β | δEF1 | FGF receptor | EMT | FGF-2 | TGF-β | CELLS | dEF1 | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | INDUCTION | IDENTIFICATION | SUPPRESSION | FIBROBLASTS | CELL BIOLOGY | PROSTATE ADENOCARCINOMA | COREPRESSORS | TGF-beta | TUMOR-GROWTH | PROGRESSION | Neoplasms - metabolism | Protein Binding - genetics | Myofibroblasts - physiology | Epithelial-Mesenchymal Transition - physiology | Homeodomain Proteins - metabolism | Humans | Actins - metabolism | Fibroblast Growth Factor 2 - pharmacology | Epithelial-Mesenchymal Transition - drug effects | Epithelial-Mesenchymal Transition - genetics | Actins - genetics | DNA-Binding Proteins - metabolism | Myofibroblasts - metabolism | Cell Differentiation - genetics | Protein Isoforms - metabolism | Neoplasms - genetics | Protein Binding - drug effects | Receptors, Fibroblast Growth Factor - genetics | Fibroblast Growth Factor 2 - metabolism | Gene Expression Regulation, Neoplastic - drug effects | Cell Differentiation - physiology | Neoplasm Invasiveness | Alternative Splicing - genetics | Cells, Cultured | Transforming Growth Factor beta - physiology | Alcohol Oxidoreductases - metabolism | Signal Transduction - genetics | Myofibroblasts - drug effects | Protein Isoforms - physiology | Transcription Factors - metabolism | Transforming Growth Factor beta - pharmacology | Alternative Splicing - drug effects | Cell Differentiation - drug effects | Models, Biological | Receptors, Fibroblast Growth Factor - metabolism | Neoplasms - pathology | Protein Isoforms - genetics | Zinc Finger E-box-Binding Homeobox 1
Journal Article
Cell Death and Differentiation, ISSN 1350-9047, 09/2016, Volume 23, Issue 9, pp. 1515 - 1528
...), while their neuroprotective effect is attributed to neurotrophic growth factors (e.g., NGF). We here demonstrate that the p53 isoforms Delta 133p53 and p53 beta are expressed in astrocytes... 
MOTOR-NEURONS | STEM-CELLS | DELTA-133P53-ALPHA | ALZHEIMERS-DISEASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | DNA-DAMAGE | P53-BETA | GROWTH | AUTOPHAGY | CELLULAR SENESCENCE | EXPRESSION | CELL BIOLOGY | Alternative Splicing | Tumor Suppressor Protein p53 - antagonists & inhibitors | Coculture Techniques | Humans | Neurons - cytology | Serine-Arginine Splicing Factors - metabolism | Serine-Arginine Splicing Factors - genetics | Autophagy - drug effects | Tumor Suppressor Protein p53 - genetics | Alzheimer Disease - pathology | Brain - metabolism | Protein Isoforms - metabolism | RNA Interference | Cellular Senescence | Neurons - metabolism | Interleukin-6 - metabolism | Sequestosome-1 Protein - metabolism | Astrocytes - cytology | Astrocytes - drug effects | Interleukin-6 - genetics | Sequestosome-1 Protein - antagonists & inhibitors | Cells, Cultured | Neuroprotection - physiology | Tumor Suppressor Protein p53 - metabolism | Genetic Vectors - metabolism | Genetic Vectors - genetics | Serine-Arginine Splicing Factors - antagonists & inhibitors | Leupeptins - pharmacology | Sequestosome-1 Protein - genetics | Amyotrophic Lateral Sclerosis - pathology | Alzheimer Disease - metabolism | Amyotrophic Lateral Sclerosis - metabolism | Brain - pathology | Protein Isoforms - antagonists & inhibitors | Astrocytes - metabolism | Protein Isoforms - genetics | RNA, Small Interfering - metabolism | Index Medicus | Original Paper
Journal Article