|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Mitochondrial transcription termination factor 2 binds to entire mitochondrial DNA and negatively regulates mitochondrial gene expression显示文摘(mTERF2 ) Mitochondrial 抄写结束因素 2 是绑在 mitochondrial DNA 的 mitochondrial 矩阵蛋白质。以前的研究证明了 mTERF2 的 overexpression 能禁止房间增长,但是机制到目前为止一直不是明确的。这研究试图在 vivo 介绍 mTERF2 的有约束力的模式给 mitochondrial DNA (mtDNA ) ,并且在 mtDNA, mRNA 抄写,和蛋白质翻译的复制上调查了 mTERF2 的生物功能。到全部 mtDNA 的 mTERF2 绑定经由染色质 immunoprecipitation 分析被识别。当 mTERF2 是在 HeLa 房间的 overexpressed 时,线粒体基因的 mtDNA 复制效率和表示层次显著地被禁止。mtDNA 内容的抑制水平是有 mRNA 和 mitochondrial 蛋白质表示的减少的层次的一样。总的来说, mTERF2 可能基于它 mtDNA 复制上的否定效果是一个细胞生长禁止者,它最后下面调整在是必要的为的线粒体的氧化 phosphorylation 部件,细胞是的所有精力新陈代谢。 | Weiwei Huang Min Yu Yang Jiao Jie Ma Mingxing Ma Zehua Wang Hong Wu Deyong Tan | 2011 | Acta Biochimica et Biophysica Sinica2011，43，6： | 17 |
| 2 | hMTERF4 knockdown in HeLa cells results in sub-G1 cell accumulation and cell death显示文摘Mitochondrial 活动和房间精力地位在房间周期和房间增长的规定起重要作用。mitochondrial 基因表示的规定为 mitochondrial 活动规定是关键的。mitochondrial 抄写结束因素(MTERF ) 家庭是一组重要 mitochondrial 抄写规章的因素。MTERF13 涉及 mitochondrial 基因抄写和氧化 phosphorylation 的规定,这被表明了。然而,最新的成员 MTERF4 的功能没被描绘。在这研究,人的 MTERF4 全身的开的读物框架被克隆,并且蛋白质结构预言表明那 hMTERF4 蛋白质包含了白氨酸拉链主题,它类似于人的 MTERF13。在 HeLa 房间的表示 pMTERF4 绿的荧光熔化蛋白质局部性线粒体。(3 (4,5 ) dimethylthiahiazo (zy1 ) 3,5diphenytetrazoliumromide )(MTT ) 增长试金和流动 cytometry 分析显示出那 hMTERF4 击倒的导致的 sub-G1 阶段房间累积,而它的 overexpression 支持了房间增长。而且,两倍与 Annexin V 和 PI 染色揭示了那 hMTERF4 击倒的增加的坏死然而并非 apoptosis。在结论,我们的数据建议 hMTERF4 是为房间增长的一个必要因素,它被 mitochondrial 抄写可能调制支持房间增长。 | Min Yu Jie Dai Weiwei Huang Yang Jiao Liang Liu Min Wu Deyong Tan | 2011 | Acta Biochimica et Biophysica Sinica2011，43，5： | 9 |
| 3 | Regulation of the cell cycle via mitochondrial gene expression and energy metabolism in HeLa cells显示文摘人的颈的癌症 HeLa 房间有功能的线粒体。最近的研究建议了那 mitochondrial 新陈代谢在肿瘤房间增长起一个必要作用。不过,房间怎么协调 mitochondrial 动力学和房间周期前进,尚待被澄清。为了调查在函数和房间周期规定, mitochondrial 基因表达式侧面和细胞的 ATP 层次是的 mitochondrial 之间的关系,在现在的学习由房间周期进步分析决定了。HeLa 房间被浆液饥饿在 G0/G1 阶段同步,并且由恢复浆液文化重入房间周期,时间功课实验被执行分析 mitochondrial 抄写管理者的表示, mitochondrial 基因, mitochondrial 膜潜力(MMP ) ,细胞的 ATP 层次,和房间骑车前进。结果证明当逮捕 G0/G1 房间在包含浆液的媒介被刺激时, DNA 和表示的数量在开始在 2 h 时间点增加的线粒体 mRNA 和蛋白质铺平,而 MMP 和 ATP 水平在 4 点提高了 h。而且,在浆液触发了房间周期以后, cyclin D1 表示开始在 4 h 增加。ATP 合成 inhibitoroligomycintreatment 压制了 cyclin D1 和 cyclin B1 表示层次并且堵住了房间周期前进。一起拿,我们的结果建议增加的 mitochondrial 基因表示层次,氧化 phosphorylation 激活,和细胞的 ATP 满足增加是为被触发的重要事件房间周期。最后,我们证明 mitochondrial 基因表示层次和细胞的 ATP 内容紧在调整房间增长被调整并且可能玩一个中央角色。 | Wei Xiong Yang Jiao Weiwei Huang Mingxing Ma Min Yu Qinghua Cui Deyong Tan | 2012 | Acta Biochimica et Biophysica Sinica2012，44，4： | 5 |
| 4 | Prokaryotic Expression, Purification, and Production of Polyclonal Antibody Against Novel Human Serum Inhibited Related Protein I (SI1)显示文摘 | Mingxing Ma Jie Ma Yinghui Shi Hong Wu Wenxiu Zhao Weiwei Huang Yang Jiao Deyong Tan | 2010 | The Protein Journal2010，，2： | 1 |
| 5 | Changes of Plasma tPA and PAI Activities in Patients with Diabetic Retinopathy显示文摘Purpose:To investigate the relationship between the diabetic retinopathy (DR) and the activity of plasma tissue plasminogen activator (tPA) and plasminogen activator inhibitor (PAI).Methods :tPA and PAI activities were measured by chromatogenous substrate assay in plasma samples obtained from patients with and without diabetic retinopathy (n = 42). Retinopathy was determined by stereoscopic color fundus photographs graded according to a modification of Chinese National Fundus Disease Academic Meeting. And 21 sex-age matched normal people were as controls. This study was in a masked fashion.Results:①tPA activity was lower and PAI activity was higher in all of diabetic patients than those in controls (P<0. 001); ②tPA activity was lower and PAI activity was higher in proliferative DR (PDR) subgroup than those in non-DR (NDR) and background-DR (BDR) subgroups (P<0.01,respectively); ③there was no significant difference between BDR and NDR subgroups (P>0. 05); and ④the results also suggested that the | Du Zhenya, Jiang Deyong, Tan Jiaquan, Nie Aiguang, Tang ChaozhenDepartment of Ophthalmology, First Affiliated Hospital, Hunan Medical University Changsha 410008, ChinaDepartment of Ophthalmology, 2nd Affiliated Hospital, Hunan Medical University Changsha 410000,China | 1997 | 眼科学报1997，13，1： | 1 |
| 6 | IL-1β regulates the mouse Fas ligand expression in corneal endothelial cells显示文摘Constitutively expressed Fas ligand (FasL) in several distinct epithelial cell types appears to protect tissues by inducing apoptosis of Fas+ immune cells during inflammatory reactions. To study the rela-tionship of FasL and inflammation process in cornea,we examined the effects of inflammatory cytokine IL-1β on the FasL production,expression and cytotoxic function in corneal endothelial cells. In this paper,we demonstrate that IL-1β inhibits the FasL production and expression in corneal endothelial cells. The promoter activities of FasL in these cells are reduced by IL-1β in a dose-dependent manner. Finally,we also find that IL-1β block the cytotoxic effects of FasL derived from corneal endothelial cells to the Fas+ target cells. These data support the view that FasL derived from corneal endothelial cells modulate inflammation within cornea. | ZHANG Jie Yang Ke TAN DeYong ZENG JunYing Alan FINE | 2007 | Chinese Science Bulletin2007，52，16： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员