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您的检索式：作者名="Wenyan SHE"
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| 1 | Overexpression of a dominant-negative mutant of SIRT1 in mouse heart causes cardiomyocyte apoptosis and early-onset heart failure显示文摘SIRT1,a mammalian ortholog of yeast silent information regulator 2(Sir2),is an NAD+-dependent protein deacetylase that plays a critical role in the regulation of vascular function.The current study aims to investigate the functional significance of deacetylase activity of SIRT1 in heart.Here we show that the early postnatal hearts expressed the highest level of SIRT1deacetylase activity compared to adult and aged hearts.We generated transgenic mice with cardiac-specific expression of a dominant-negative form of the human SIRT1(SIRT1H363Y),which represses endogenous SIRT1 activity.The transgenic mice displayed dilated atrial and ventricular chambers,and died early in the postnatal period.Pathological,echocardiographic and molecular phenotype confirmed the presence of dilated cardiomyopathy.Terminal deoxynucleotidyl transferase-mediated dUTP nick-end-labeling analysis revealed a greater abundance of apoptotic nuclei in the hearts of transgenic mice.Furthermore,we show that cardiomyocyte apoptosis caused by suppression of SIRT1 activity is,at least in part,due to increased p53acetylation and upregulated Bax expression.These results indicate that dominant negative form of SIRT1(SIRT1H363Y)overexpression in mouse hearts causes cardiomyocyte apoptosis and early-onset heart failure,suggesting a critical role of SIRT1 in preserving normal cardiac development during the early postnatal period. | MU WenLi ZHANG QingJun TANG XiaoQiang FU WenYan ZHENG Wei LU YunBiao LI HongLiang WEI YuSheng LI Li SHE ZhiGang CHEN HouZao LIU DePei | 2014 | Science China(Life Sciences)2014，57，9： | 12 |
| 2 | AAZ2 induces mitochondrial-dependent apoptosis by targeting PDK1 in gastric cancer显示文摘Drastic surges in intracellular reactive oxygen species(ROS)induce cell apoptosis,while most chemotherapy drugs lead to the accumulation of ROS.Here,we constructed an organic compound,arsenical N-(4-(1,3,2-dithiarsinan-2-yl)phenyl)acrylamide(AAZ2),which could prompt the ROS to trigger mitochondrial-dependent apoptosis in gastric cancer(GC).Mechanistically,by targeting pyruvate dehydrogenase kinase 1(PDK1),AAZ2 caused metabolism alteration and the imbalance of redox homeostasis,followed by the inhibition of phosphoinositide-3-kinase(PI3K)/protein kinase B(AKT)/mammalian target of rapamycin(mTOR)pathway and leading to the activation of B-cell lymphoma 2(Bcl2)/Bcl2-associated X(Bax)/caspase-9(Cas9)/Cas3 cascades.Importantly,our in vivo data demonstrated that AAZ2 could inhibit the growth of GC xenograft.Overall,our data suggested that AAZ2 could contribute to metabolic abnormalities,leading to mitochondrial-dependent apoptosis by targeting PDK1 in GC. | Yi LI Wenyan SHE Xiaoran XU Yixin LIU Xinyu WANG Sheng TIAN Shiyi LI Miao WANG Chaochao YU Pan LIU Tianhe HUANG Yongchang WEI | 2023 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2023，24，3： | 0 |
| 3 | 内质网跨膜蛋白EPG-3/VMP1激活钙通道SERCA来调节ER与隔离膜的互作显示文摘文章简介细胞自噬是生物体内高度保守的降解途径。细胞通过形成双层膜结构的自噬小体,包裹部分细胞质或受损细胞器,并将之运送到溶酶体进行降解,这一过程被称为自噬。 | Yan G.Zhao Yong Chen Guangyan Miao Hongyu Zhao Wenyan Qu Dongfang Li Zheng Wang Nan Liu Lin Li She Chen Pingsheng Liu Du Feng 张宏 | 2018 | 科学新闻2018，0，4： | 0 |
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