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The TIP30 Protein Complex, Arachidonic Acid and Coenzyme A Are Required for Vesicle Membrane Fusion  [PDF]
Chengliang Zhang, Aimin Li, Shenglan Gao, Xinchun Zhang, Hua Xiao
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0021233
Abstract: Efficient membrane fusion has been successfully mimicked in vitro using artificial membranes and a number of cellular proteins that are currently known to participate in membrane fusion. However, these proteins are not sufficient to promote efficient fusion between biological membranes, indicating that critical fusogenic factors remain unidentified. We have recently identified a TIP30 protein complex containing TIP30, acyl-CoA synthetase long-chain family member 4 (ACSL4) and Endophilin B1 (Endo B1) that promotes the fusion of endocytic vesicles with Rab5a vesicles, which transport endosomal acidification enzymes vacuolar (H+)-ATPases (V-ATPases) to the early endosomes in vivo. Here, we demonstrate that the TIP30 protein complex facilitates the fusion of endocytic vesicles with Rab5a vesicles in vitro. Fusion of the two vesicles also depends on arachidonic acid, coenzyme A and the synthesis of arachidonyl-CoA by ACSL4. Moreover, the TIP30 complex is able to transfer arachidonyl groups onto phosphatidic acid (PA), producing a new lipid species that is capable of inducing close contact between membranes. Together, our data suggest that the TIP30 complex facilitates biological membrane fusion through modification of PA on membranes.
CC3/TIP30 affects DNA damage repair
Sylvia Fong, Frank King, Emma Shtivelman
BMC Cell Biology , 2010, DOI: 10.1186/1471-2121-11-23
Abstract: We found that forced expression of CC3 in CC3-negative cells strongly delays the repair of UV-induced DNA damage. Exogenously introduced CC3 negatively affects expression levels of DDB2/XPE and p21CIP1, and inhibits induction of c-FOS after UV exposure. In addition, exogenous CC3 prevents the nuclear accumulation of P21CIP in response to UV. These changes in the levels/localization of relevant proteins resulting from the enforced expression of CC3 are likely to contribute to the observed delay in DNA damage repair. Silencing of CC3 in CC3-positive cells has a modest delaying effect on repair of the UV induced damage, but has a much more significant negative affect on the translesion DNA synthesis after UV exposure. This could be related to the higher expression levels and increased nuclear localization of p21CIP1 in cells where expression of CC3 is silenced. Expression of CC3 also inhibits repair of oxidative DNA damage and leads to a decrease in levels of nucleoredoxin, that could contribute to the reduced viability of CC3 expressing cells after oxidative insult.Manipulation of the cellular levels of CC3 alters expression levels and/or subcellular localization of proteins that exhibit nucleocytoplasmic shuttling. This results in altered responses to genotoxic stress and adversely affects DNA damage repair by affecting the recruitment of adequate amounts of required proteins to proper cellular compartments. Excess of cellular CC3 has a significant negative effect on DNA repair after UV and oxidant exposure, while silencing of endogenous CC3 slightly delays repair of UV-induced damage.The human gene CC3/TIP30 was originally identified as a metastasis-suppressor of variant small cell lung carcinoma (vSCLC) [1]. CC3 is a phylogenetically conserved protein whose expression is absent or much reduced in a variety of aggressive or metastatic tumors such as vSCLC [1], neuroblastoma and glioblastoma [2,3], metastatic breast cancer [4], gastric cancer [5], hepatocellular carc
力达霉素诱导人胃癌bgc823细胞凋亡和抑制裸鼠移植瘤生长  [PDF]
张胜华,陈静,江敏,甄永苏
药学学报 , 2008,
Abstract: 观察力达霉素(ldm)对人胃癌bgc823细胞的诱导凋亡作用及体内抗肿瘤活性。采用mtt法观察ldm对人胃癌bgc823细胞增殖的抑制作用。利用annexinv-fitc/pi双染结合流式细胞仪和脱氧核糖核酸末端转移酶介导的缺口末端标记技术检测细胞凋亡的改变。采用westernblotting法检测细胞中vegf蛋白的表达情况。建立裸鼠胃癌皮下移植瘤模型,观察ldm的体内抗肿瘤活性。ldm能够明显抑制bgc823细胞增殖,诱导细胞凋亡,降低细胞vegf蛋白的表达,抑制胃癌裸鼠移植瘤的生长。ldm剂量0.02和0.04mg·kg-1的抑瘤率分别为57%和72%(p<0.01)。ldm可诱导胃癌细胞凋亡并抑制裸鼠移植肿瘤的生长。
'92德布罗意年  [PDF]
沈惠川
物理 , 1994,
Abstract: ?1992年8月15日,是伟大的思想家和物理学家路易·德布罗意(lonisdebroglie,1892-1987)100周年诞辰。在世界各地所举行的各种形式的纪念活动中,最重要的和最引人注目的无疑应当首推以法国科学院和德布罗意基金委员会为中心的学术举措。他们的学术举措主要有以下几个方面一、会议1.1992年5月15日至2?...
银杏叶提取物对泪腺腺样囊性癌ACC-2细胞增殖及Survivin,TIP30基因表达的影响  [PDF]
牛坡,赵新霞,燕飞,周雍明,简鹏
中国中药杂志 , 2014,
Abstract: 探讨银杏叶提取物(EGB)对泪腺腺样囊性癌ACC-2细胞增殖、凋亡的影响,并从基因和蛋白水平上分析EGB对Survivin和TIP30基因表达的影响。不同浓度EGB处理体外培养的人泪腺腺样囊性癌ACC-2细胞,应用MTT法检测细胞增殖;AnnexinV/PI双染色流式细胞仪检测细胞凋亡和细胞周期;RT-PCR和Westernblotting分析Survivin,TIP30基因和蛋白的表达。结果发现EGB对ACC-2细胞的体外增殖具有抑制作用,量效关系显著,与对照组比较有统计学差异(P<0.01),半数抑制浓度(IC50)为88mg·L。经流式细胞仪检测表明,EGB能使ACC-2细胞G0/G1期逐渐增加,G2/M期和S期逐渐减少,并且随着剂量的增加,ACC-2细胞凋亡率明显增加(P<0.05或P<0.01)。RT-PCR与Western杂交结果一致表明随着EGB浓度的升高,Survivin基因表达明显减少(P<0.01),而TIP30基因表达则显著提高(P<0.01)。因此,EGB能有效抑制人泪腺腺样囊性癌ACC-2细胞Survivin基因表达,并促进TIP30的表达,诱导ACC-2细胞凋亡,从而抑制肿瘤细胞增殖。该研究为中药成分在肿瘤治疗中的应用提供了一定的理论和实验依据。
古音研究中的“以义正音”  [PDF]
黄易青
北京师范大学学报(社会科学版) , 2012,
Abstract: ?“以义正音”是乾嘉时代学术领袖戴震提出的重要主张。其主要内涵是,根据字词的意义和规律性的意义关系,可以确定它们的古音地位,以及古音之间的关系,进而发现古音演变的轨迹。清代小学的最重要理论和方法,在于音义互求。以义正音与因声求义二者,是音义互求中不可分割的两个方面。清代以后,因声求义的理论和方法得到很好的总结和继承,而以义正音,因为要以对词义和意义关系的认识为起点去推证古音,有更大的难度,所以还没有得到总结。清代小学形音义互求的学术大背景以及戴震本人的古音学旨趣和治学特点等,是以义正音提出的学术条件。以义正音的语言学基本原理是音义结合具有内在关系,这种方法具有严密的论证逻辑。戴震和他的大弟子、著名学者段玉裁的音义互求的实践,包含着以义正音的理论和方法,他们的古音学结论,从以义正音的角度可以得到更好的理解。以义正音的理论的方法,对现代古音研究也有重要的作用。
德布罗意和狄拉克
沈惠川
现代物理知识 , 1995,
Abstract: 德布罗意同狄拉克之间的关系,甚至比他同薛定谔之间的关系还来得密切:德布罗意和他的二哥莫里斯·德布罗意由于研究X射线的吸收、散射及其光谱的缘由,很早就同英国曼彻斯特大学的卢瑟福及其在剑桥大学三一学院的乘龙快婿福勒有学术联系。德布罗意1923年10月13日发表于英国《自然》杂志第112卷2815期540页题名为“波和量子”的论文,就是由福勒推荐的。德布罗意和福勒后来还经常进
《滕学义建祠碑》考释  [PDF]
梁勇,姜新
东南文化 , 2000,
Abstract: ????光绪年间所立的《滕学义建祠碑》,所记史实是研究淮军及捻军起义的宝贵资料。
书籍封面设计中的“象”与“意”  [PDF]
潜铁宇,王文
包装工程 , 2014,
Abstract: 目的 研究书籍封面设计的“象”与“意”之间的表现形式和相互关系。方法 书籍封面所具有的文化特性出发,阐述封面设计“意”的来源与作用,分析封面设计“象”的构思、编排及“意”的表达。结论 书籍封面设计是“象”和“意”的艺术,“象”是躯体并依附于“意”,“意”是灵魂,表现为“象”,又决定“象”。
明儒“意”论分歧及其发展  [PDF]
张锦枝
安徽师范大学学报(人文社会科学版) , 2014,
Abstract: 明儒关于《大学》诚意之“意”的定位大体可分两种以意为心之所发,有善有恶,不具有主宰的意义;以意为心之所存,纯善无恶,是心之主宰。宋代学者思想中已体现出“意”定位之二重性,至明中叶王阳明这种分歧和矛盾更为突出,而其后学或在其“有善有恶意之动”的基础上提出“无意之意”,以超越形下的善恶观念;或发展了“意”的第二种涵义,提出意为心之所存,来解决阳明思想中的矛盾,刘蕺山即是这一支诚意说的集大成者。在此过程中,诚意工夫的重点亦由“诚”逐渐落实到“意”。
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