机译:DNA损伤和p53途径的激活介导脂肪细胞代谢和分泌功能的改变。
INSERM, UMR 1065, C3M, Team 7 Molecular and Cellular Physiopathology of Obesity and Diabetes, Nice, France,Universite Cote d'Azur, C3M, Nice, France;
INSERM, UMR 1065, C3M, Team 7 Molecular and Cellular Physiopathology of Obesity and Diabetes, Nice, France,Universite Cote d'Azur, C3M, Nice, France;
INSERM, UMR 1065, C3M, Team 7 Molecular and Cellular Physiopathology of Obesity and Diabetes, Nice, France,Universite Cote d'Azur, C3M, Nice, France;
INSERM, UMR 1065, C3M, Team 7 Molecular and Cellular Physiopathology of Obesity and Diabetes, Nice, France,Universite Cote d'Azur, C3M, Nice, France;
INSERM, UMR 1065, C3M, Team 7 Molecular and Cellular Physiopathology of Obesity and Diabetes, Nice, France,Universite Cote d'Azur, C3M, Nice, France;
Universite Cote d'Azur, C3M, Nice, France,INSERM, UMR 1065, C3M, Team 2 Cell Death, Differentiation and Cancer, Nice, France;
INSERM, UMR 1065, C3M, Team 7 Molecular and Cellular Physiopathology of Obesity and Diabetes, Nice, France,Universite Cote d'Azur, C3M, Nice, France;
INSERM, UMR 1065, C3M, Team 7 Molecular and Cellular Physiopathology of Obesity and Diabetes, Nice, France,Universite Cote d'Azur, C3M, Nice, France;
INSERM, UMR 1065, C3M, Team 7 Molecular and Cellular Physiopathology of Obesity and Diabetes, Nice, France,Universite Cote d'Azur, C3M, Nice, France,INSERM, UMR 1062, Nutrition, Obesity and Risk of Thrombosis, Marseille, France;
CNRS, UMR 8199, Lille Pasteur Institute, Lille, France,Lille University, Lille, France,European Genomic Institute for Diabetes, Lille, France;
CNRS, UMR 8199, Lille Pasteur Institute, Lille, France,Lille University, Lille, France,European Genomic Institute for Diabetes, Lille, France;
CNRS, UMR 8199, Lille Pasteur Institute, Lille, France,Lille University, Lille, France,European Genomic Institute for Diabetes, Lille, France;
Universite Cote d'Azur, C3M, Nice, France,INSERM, UMR 1065, C3M, Team 2 Cell Death, Differentiation and Cancer, Nice, France;
CNRS, UMR 8199, Lille Pasteur Institute, Lille, France,Lille University, Lille, France,European Genomic Institute for Diabetes, Lille, France,Department of Genomics of Common Disease, School of Public Health, Imperial College London, Hammersmith Hospital, London, U.K.;
INSERM, UMR 1065, C3M, Team 7 Molecular and Cellular Physiopathology of Obesity and Diabetes, Nice, France,Universite Cote d'Azur, C3M, Nice, France;
INSERM, UMR 1065, C3M, Team 7 Molecular and Cellular Physiopathology of Obesity and Diabetes, Nice, France,Universite Cote d'Azur, C3M, Nice, France;
机译:细胞周期蛋白依赖性激酶和P53途径被独立激活,并在DNA损伤后介导神经元中的Bax激活。
机译:P53对环境致癌物质苯并[A]芘的DNA损伤和代谢活化的影响:TRP53(+ /加),TRP53(+/-)和TRP53( - / - )小鼠中的作用
机译:P53对TRP53(+ / +),TRP53(+/-)和TRP53(-)中2-氨基-1-甲基-6-苯基咪唑并[4,5-b]吡啶(PHIP)的DNA损伤和代谢活化的影响/-) 老鼠
机译:对p53途径动力学差异调节所控制的DNA损伤的反应决定生存或死亡
机译:E2F3a作为癌基因起作用,并诱导DNA损伤反应途径介导的细胞凋亡。
机译:细胞周期蛋白依赖性激酶和P53途径被独立激活并介导DNA损伤后神经元中的Bax激活。
机译:DNA损伤和p53途径的激活介导脂肪细胞代谢和分泌功能的改变标题:肥胖脂肪细胞中的DNA损伤和p53