机译:细胞信号传导中的变构相互作用原理
Cancer and Inflammation Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, National Cancer Institute, Frederick, Maryland 21702, United States,Sackler Institute of Molecular Medicine, Department of Human Genetics and Molecular Medicine, Sadder School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel;
Sackler Institute of Molecular Medicine, Department of Human Genetics and Molecular Medicine, Sadder School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel;
Department of Biophysics, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390, United States,Department of Chemistry, Center for Drug Discovery, Design, and Delivery (CD4), and Center for Scientific Computation, Southern Methodist University, 3215 Daniel Avenue, Dallas, Texas 75275, United States;
机译:变构通讯的计算模型揭示了ABL和EGFR激酶突变诱导信号的组织原理。
机译:原理:二聚体GPCR内配体结合位点之间的变构相互作用的模型。
机译:肽抑制剂破坏5-羟色胺5-HT2C受体与磷酸酶和张力蛋白同源物的相互作用,以变构调节细胞信号和行为
机译:新型血糖素旋红素导致选择性细胞信号传导
机译:研究细胞相互作用的微尺度原理和工具
机译:原则信号中的变构相互作用
机译:使用分层模拟方法和颠覆性相互作用的网络建模对HSP90伴侣调节的分子原理进行了分解调节剂:构象选择规定了蛋白质反应和配体特异性功能机制的多样性