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作 者:KaiCHEN DanLI YuHuiJIANG WeiJuanYAO XinJuanWANG XiaoChaoWEI JingGAO LiDeXIE ZongYiYAN ZongYaoWEN ShuCHIEN
机构地区:[1]HemorheologyCenter,DepartmentofBiophysics,SchoolofBasicMedicalSciences,PekingUniversity,Beijing,100083,China. [2]DepartmentofBiochemicalandMolecularBiology,SchoolofBasicMedicalSciences,PekingUniversity,Beijing,100083,China. [3]DepartmentofUrology,MedicalCenter,NewYorkUniversity,USA. [4]DepartmentofMechanicsandEngineeringScience,PekingUniversity,Beijing100871,China. [5]DepartmentofBioengineeringandWhitakerInstituteofBiomedicalEngineering,UniversityofCalifornia,SanDiego,LaJolla,CA92093-0412,USA
出 处:《Cell Research》2004年第2期161-168,共8页细胞研究(英文版)
基 金:This work was supported by The National Natural Science Foundation of China(No.30270355,No.39930110);a Doctoral Funding(No.20010001082).
摘 要:The cDNA fragment of human TRAIL (TNF-related apoptosis inducing ligand) was cloned into RevTet-On, a Tetregulated and high-level gene expression system. The gene expression system was constructed in a human leukemic cell line: Jurkat. By using RevTet-On TRAIL gene expression system in Jurkat as a cell model, we studied the influence of TRAIL gene on the changes of cellular apoptosis before and after the TRAIL gene expression, which was induced by adding tetracycline derivative doxycycline (Dox). The results indicated that the cellular apoptosis ratio was largely dependent on the TRAIL gene expression level. Moreover, it was found that the apoptosis-inducing TRAIL could cause significant changes in the biophysical properties of Jurkat cells. The cell surface charge density decreased, the membrane fluidity declined, the elastic coefficients K_I increased, and the proportion of α-helix in membrane protein secondary structure decreased. Thus, the apoptosis-inducing TRAIL gene caused significant changes on the biomechanic properties of Jurkat cells.
关 键 词:TRAIL Tet gene expression system JURKAT apoptosis.
分 类 号:R329.2[医药卫生—人体解剖和组织胚胎学]
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