The Cell Cycle-regulated Protein Human GTSE-1 Controls DNA Damage-induced Apoptosis by Affecting p53 Function
Copyright policy )The Cell Cycle-regulated Protein Human GTSE-1 Controls DNA Damage-induced Apoptosis by Affecting p53 Function
GTSE-1 (G2 and S phase-expressed-1) protein is specifically expressed during S and G2 phases of the cell cycle. It is mainly localized to the microtubules and when overexpressed delays the G2 to M transition. Here we report that human GTSE-1 (hGTSE-1) protein can negatively regulate p53 transactivation function, protein levels, and p53-dependent apoptosis. We identified a physical interaction between the C-terminal regulatory domain of p53 and the C-terminal region of hGTSE-1 that is necessary and sufficient to down-regulate p53 activity. Furthermore, we provide evidence that hGTSE-1 is able to control p53 function in a cell cycle-dependent fashion. hGTSE-1 knock-down by small interfering RNA resulted in a S/G2-specific increase of p53 levels as well as cell sensitization to DNA damage-induced apoptosis during these phases of the cell cycle. Altogether, this work suggests a physiological role of hGTSE-1 in apoptosis control after DNA damage during S and G2 phases through regulation of p53 function.
- University of Udine Italy
- AREA Science Park Italy
- University of Milan Italy
- University of Trieste Italy
- Consorzio Interuniversitario per le Biotecnologie Italy
G2 Phase, Blotting, Western, Genetic Vectors, Down-Regulation, Mitosis, Apoptosis, Biochemistry, Genes, Reporter, Antibodies, Monoclonal; Blotting, Western; Cell Cycle; Down-Regulation; Flow Cytometry; G2 Phase; Gene Silencing; Genes, Reporter; Genetic Vectors; Humans; Microscopy, Fluorescence; Microtubule-Associated Proteins; Mitosis; Plasmids; Precipitin Tests; Protein Binding; Protein Structure, Tertiary; RNA, Small Interfering; S Phase; Transfection; Tumor Cells, Cultured; Tumor Suppressor Protein p53; Apoptosis; DNA Damage; Biochemistry, Apoptosis ; DNA Damage ; Antibodies, Monoclonal ; Blotting, Western ; Cell Cycle ; Down-Regulation ; Flow Cytometry ; G2 Phase ; Gene Silencing ; Genes, Reporter ; Genetic Vectors ; Humans ; Microscopy, Fluorescence ; Microtubule-Associated Proteins ; Mitosis ; Plasmids ; Precipitin Tests ; Protein Binding ; Protein Structure, Tertiary ; RNA, Small Interfering ; S Phase ; Transfection ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53, Humans, Gene Silencing, RNA, Small Interfering, Molecular Biology, Cell Cycle, Antibodies, Monoclonal, Cell Biology, Flow Cytometry, Precipitin Tests, Protein Structure, Tertiary, Microscopy, Fluorescence, Microtubule-Associated Proteins, DNA Damage, Plasmids, Protein Binding
G2 Phase, Blotting, Western, Genetic Vectors, Down-Regulation, Mitosis, Apoptosis, Biochemistry, Genes, Reporter, Antibodies, Monoclonal; Blotting, Western; Cell Cycle; Down-Regulation; Flow Cytometry; G2 Phase; Gene Silencing; Genes, Reporter; Genetic Vectors; Humans; Microscopy, Fluorescence; Microtubule-Associated Proteins; Mitosis; Plasmids; Precipitin Tests; Protein Binding; Protein Structure, Tertiary; RNA, Small Interfering; S Phase; Transfection; Tumor Cells, Cultured; Tumor Suppressor Protein p53; Apoptosis; DNA Damage; Biochemistry, Apoptosis ; DNA Damage ; Antibodies, Monoclonal ; Blotting, Western ; Cell Cycle ; Down-Regulation ; Flow Cytometry ; G2 Phase ; Gene Silencing ; Genes, Reporter ; Genetic Vectors ; Humans ; Microscopy, Fluorescence ; Microtubule-Associated Proteins ; Mitosis ; Plasmids ; Precipitin Tests ; Protein Binding ; Protein Structure, Tertiary ; RNA, Small Interfering ; S Phase ; Transfection ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53, Humans, Gene Silencing, RNA, Small Interfering, Molecular Biology, Cell Cycle, Antibodies, Monoclonal, Cell Biology, Flow Cytometry, Precipitin Tests, Protein Structure, Tertiary, Microscopy, Fluorescence, Microtubule-Associated Proteins, DNA Damage, Plasmids, Protein Binding
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