机译:顺式致死性遗传相互作用减弱并改变p53肿瘤发生
Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461 Department of Pharmaceutical and Biomedical Sciences, University of South Carolina, Columbia, SC 29208;
rnDepartment of Medicine, Mount Sinai School of Medicine, New York, NY 10029;
rnDepartment of Genetics and Genomic Sciences, Mount Sinai School of Medicine, New York, NY 10029;
rnLudwig Institute for Cancer Research, Departments of Medicine and Cellular and Molecular Medicine, and Cancer Center, University of California San Diego, La Jolla, CA 92093;
rnHarvard Medical School-Partners Healthcare Center for Genetics and Genomics, Harvard Medical School, Boston, MA 02115;
rnDepartment of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461;
DNA repair; genome instability; loss of heterozygosity; murine model; tumor suppressor gene;
机译:肿瘤抑制因子Brca1和p53在细胞凋亡,细胞周期和肿瘤发生中的遗传相互作用。
机译:E2F1 / YY1反应位点和推定的p53位点的顺式遗传变异与正常人支气管上皮中ERCC5(XPG)转录本的等位基因特异性表达改变有关。
机译:E2F1 / YY1反应位点和推定的p53位点的顺式遗传变异与正常人支气管上皮中ERCC5(XPG)转录本的等位基因特异性表达改变有关
机译:P53缺陷小鼠中的自发性和辐射诱导的肿瘤发生
机译:小鼠中p53和Fas系统缺陷导致繁殖,发育和肿瘤发生改变。
机译:顺式致死性遗传相互作用减弱并改变p53肿瘤发生
机译:顺式致死性遗传相互作用减弱并改变p53肿瘤发生