机译:mRNA出口因子Dbp5的C端结构揭示了ATPase激活因子Gle1的相互作用表面
Divisions of Cell and Developmental Biology, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3200;
Divisions of Cell and Developmental Biology, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3200 Institute of Biochemistry, Eidgenossiche Technische Hochschule, 8093 Zurich, Switzerland;
Divisions ofBiochemistry and Molecular Biology, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3200 Institute of Molecular Biology and Biophysics, Eidgenossiche Technische Hochschule, 8093 Zurich, Switzerland;
Divisions ofBiochemistry and Molecular Biology, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3200;
Divisions of Cell and Developmental Biology, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3200;
crystal structure; DExD/H-box; nuclear pore complex;
机译:mRNA输出需要激活DExD / H-box蛋白Dbp5的核孔蛋白Gle1及其共激活因子InsP(6)。
机译:肌醇六磷酸和Gle1激活DEAD-box蛋白Dbp5进行核mRNA输出。
机译:穿梭的mRNA出口因子Gle1和核孔蛋白hCG1之间的相互作用:Hsp70 mRNA出口的保守机制。
机译:比较因子Hydro亲水和疏水表面的接触活化以及与前激肽释放酶和因子Inter的相互作用
机译:MKRN2与GLE1相互作用,负面调节mRNA核导出和视网膜发育
机译:mRNA出口因子Dbp5的C端结构揭示了ATPase激活因子Gle1的相互作用表面
机译:mRNA出口因子Dbp5的C端结构揭示了ATPase激活因子Gle1的相互作用表面