机译:仅BH3分子Bim和Puma在Pdx1缺乏症的β细胞死亡中的作用
Department of Medicine, University of Chicago, Chicago, IL;
Department of Medicine, University of Chicago, Chicago, IL;
Department of Medicine, University of Chicago, Chicago, IL;
Department of Medicine, University of Chicago, Chicago, IL;
Department of Medicine, University of Chicago, Chicago, IL;
Human Oncology and Pathogenesis Program and Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY;
Department of Medicine, University of Chicago, Chicago, IL;
Department of Medicine, University of Chicago, Chicago, IL;
机译:仅BH3分子Bim介导IRS2缺乏症中的β细胞死亡
机译:NF-κB调节剂Bcl-3和仅BH3蛋白Bim和Puma控制活化T细胞的死亡
机译:Puma与Bim协同作用,Bim是限速BH3蛋白,在淋巴细胞发育过程中的细胞死亡中诱导凋亡
机译:外源表达人胰腺β细胞转录因子PDX1,MAFA,NGN3的人唾液腺细胞的转录组(RNA-seq)分析
机译:通过使用转录因子基因Pdx1,Ngn3和MafA,将不同类型的细胞重编程为胰腺β细胞。
机译:仅BH3分子Bim和Puma在Pdx1缺乏症的β细胞死亡中的作用
机译:NF-κB调节剂Bcl-3和仅BH3蛋白Bim和Puma控制活化T细胞的死亡