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血管内皮生长因子(begf)936tc基因多态性与vegf转录活性关系的研究,多态性,单核苷酸多态性,基因多态性,对象的多态性,基因的多态性,遗传多态性,面向对象多态性,java多态性,多态性条带
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低氧对食管癌Eca109细胞体内外侵袭转移的影响及机制研究.pdf
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中文摘要低氧对食管癌Ecal09细胞体内外侵袭转移的影响及机制研究摘要食管癌是最常见的恶性肿瘤之一,发病率高且疗效差。目前手术和放疗是食管癌的主要治疗手段。近年来随着诊疗技术的提高和不断改进,食管癌患者的生存率有了提高,但是疗效仍不尽人意,5年生存率仍徘徊在 15%左右。术后和放疗后的局部复发和转移是影响食管癌患者预后的主要因素。因此深入研究食管癌局部浸润和转移的机制并探索有效的治疗措施,对食管癌的防治具有重大意义。近年来许多研究发现,低氧是实体肿瘤中存在的一种普遍现象,是其微环境的基本特征之一。作为一种应激源,低氧能激活肿瘤细胞内的一系列基因作出应答反应,使很多基因转录活性发生改变,其基因产物可引起肿瘤细胞发生一系列生物学行为的改变。目前研究表明,肿瘤细胞为了在低氧环境中保持能量供应,不仅促血管生成能力极大提高,对于放化疗的抗拒性增加,其侵袭性还极大增强,更易于发生远处转移,从而导致治疗失败。在这一过程中,低氧诱导因子.1(hypoxia induciblefactor-1,HIF.1) 起着关键作用,但其复杂的作用机制目前还不十分清楚。HIF—l作为低氧环境中起中枢纽带作用的转录因子,已成为近年来的研究热点。 HIF.1是由HIF.1Q和HIF.113两个亚单位组成的一种异源二聚体。常氧条件下,HIF.1Q很容易被降解,其途径是泛素.蛋白水解酶复合体;而在低氧条件下,降解过程被阻断,导致HIF.1Q积聚,并与HIF.1 B形成活性形式,影响多种靶基因的表达。HIF.1靶基因结构上均含有低氧反应元件(hypoxia response element,HRE),HRE是被调控基因的启动子或增强子中包含的一段特定的核苷酸序列,其核心序列是5’.RCGTG.3’。活化的HIF.1与其靶基因的HRE结合后,形成转录起始复合物,调节靶基因的转录。由于HIF.1Q在低氧诱导肿瘤细胞发生的一系列适应性反应中发挥着重要作用。因此,深入研究HIF.1 Q与肿瘤的侵袭和转移的关系有着重要意义。 RNA干扰(RNA interference,RNAi)是近些年发现的一种反义基因中文摘要技术,自1998年Fire等首次发现以来,迅速应用于基因功能的研究。RNAi 技术是将目的基因所对应的小分子双链RNA导入靶细胞内,导致其相应的mRNA降解,从而阻断特定基因的表达。本研究首先通过观察体外 CoCl2诱导低氧对食管癌细胞中HIF.1 Q、E.钙黏蛋白及基质金属蛋白酶.2(MMP.2)表达的影响,采用哺乳动物雷帕霉素靶向(mTOR)通道阻断剂一雷帕霉素(rapamycin)进行干预,检测Ecal09细胞迁移和侵袭能力的变化,探讨低氧对食管癌迁移及侵袭能力的影响及其作用机制;其次, 通过脂质体介导、质粒连接HIF.1 Q短发卡状RNA(short hairRNA。 shRNA)的RNAi技术,检测HIF.1 Q沉默对食管癌Ecal09细胞迁移能力的变化,以及E.钙黏蛋白、MMP.2及Snail的表达情况,进一步探讨其具体的分子作用机制;最后,通过建立裸鼠移植瘤模型,探讨RNAi 沉默HIF.1a对食管癌Ecal09细胞体内侵袭转移能力的影响。第一部分低氧对食管癌Eeal09细胞体外迁移及侵袭的影响目的:探讨低氧对食管癌迁移及侵袭能力的影响及其作用机制。方法:采用CoCl2化学低氧法模拟肿瘤低氧微环境,半定量RT-PCR 和免疫细胞化学分别检测不同低氧时相时食管癌Ecal09细胞中HIF.1 Q、 E.钙黏蛋白及MMP.2 mRNA及蛋白的表达。Western blot检测rapamycin 联合低氧处理Ecal09细胞后,HIF—l Q、E.钙黏蛋白及MM.2蛋白的表达变化。细胞划痕试验和Transwell实验检测rapamycin联合低氧对Ecal09 细胞迁移及侵袭能力的影响。结果:Ecal09细胞在低氧状态下,HIF.1 amRNA无明显变化,仅蛋白表达增多;E.钙黏蛋白的mRNA表达明显降低(尸&O.05),同时蛋白表达减少;MMP.2mRNA表达明显升高(P&0.05),蛋白表达也增多。 Rapamycin在低氧状态下可显著抑制HIF.1 Q及MMP.2表达,促进E.钙黏蛋白高表达。经相关性分析,E.钙黏蛋白与HIF。1 a呈负相关(r一0.834, P&0.05 oMMP.2表达与HIF.1 Q呈正相关(r=1.000,P&0.01)。经rapamycin 处理后,Ecal09细胞在低氧条件下,迁移速度减慢,侵袭穿膜细胞数减少(P&O.05)。结论:低氧使Ecal09细胞中HIF.1 Q蛋白表达增多,后者可能通过下调E.钙黏蛋白、上调MMP.2表达促进食管癌在低氧状态下的迁移及侵袭。中文摘要第二部分HIF.1 Q基因RNA干扰慢病毒载体的制备和稳定转染食管癌 Ecal09细胞的建立目的:构建HIF.1 QRNA干扰慢病毒载体,筛选mF.1 Q基因稳定沉默的Ecal09细胞株,检测HIF.1Q沉默对食管癌Ecal09细胞迁移能力的变化,以及E.钙黏蛋白、MMP.2及Snail的表达情况,进一步探讨其分子作用机制。方法:设计3对HIF—lQ基因的反义寡核苷酸片段和一对无义序列, 经过退火及酶切后,克隆入RNA干扰表达载体pGCSIL,体外扩增纯化后,得到重组构建的pGCSIL.HIF.1 Q.shRNA干扰表达载体;通过脂质体 2000介导将pGCSIL.HIF一1 Q.shRNA干扰表达载体转染食管癌Ecal09细胞,利用G418筛选稳定表达株;采用RT-PCR、Western blot方法检测转染pGCSIL.HIF.1 Q.shRNA的Ecal09细胞中HIF.1 Q表达水平的变化; 应用transwell体外细胞跨膜迁移实验检测转染pGCSIL.HIF.1 Q.shRNA 的Ecal09细胞迁移能力的变化。采用Western blot方法检测HIF一1Q沉默后,E.钙黏蛋白、MMP.2及Snail的表达情况。结果:RT-PCR鉴定结果表明成功构建了3个shRNA表达载体 pGC SIL—HIF一1Q—shRNA 1,pGCSIL—HIF一1 Q—shRNA2$1]pGCSIL—HIF一1 Q .shRNA3,并筛选出抑制效果最佳的shRNA表达载体pGCSIL.HIF一1 Q .shRNA2;在转染pGCSIL.HIF.1 Q.shRNA2组Ecal09细胞中HIF.1 12显著低于无关siRNA对照组及未转染组(尸&O.05);Transwell体外迁移实验结果显示:pGCSIL—HIF.1 Q.shRNA2转染组Ecal09细胞穿越微孔的细胞数明显减少(尸&o.05),而无关siRNA对照组及未转染组Ecal09细胞无明显差异(尸&O.05)。有效沉默HIF.1 Q表达后, E.钙黏蛋白表达增强、MMP.2 表达减弱(尸&O.05)。低氧条件下,Snail蛋白表达水平升高,但在转染 pGCSIL.HIF.1 Q.shRNA2组Snail表达明显减弱。经相关性分析,
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缺氧反应元件
HIF-1是肿瘤生长过程中的一个重要调节因子，活化的HIF-1可与缺氧反应元件（hypoxia response elements, HREs）结合，促进许多血管生成相关基因的转录，从而促进肿瘤新生血管的形成，促进肿瘤的增殖和转移。
基于4个网页-
上的缺氧反应元件
...cible factor-1，HIF-1)是90年代初发现的由缺氧诱导产生，能与促红细胞生成素基因上的缺氧反应元件(hypoxia response elements，HRE)结合，从而促进EPO转录的新的转录因子。
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可以将缺氧反应元件
为了提高乏氧条件下Egrl的辐射诱导增强,可以将缺氧反应元件(hypoxia response elements, HREs)与其构建嵌合性启动子,增加Egr-1乏氧条件下的辐射诱导增强特性。
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缺乏缺氧反应元件
但OPN缺乏缺氧反应元件(hypoxia response elements，HRE)，并不受HIF-1α的调控。因此，我们推测OPN可能是继HIF-1α之外，缺氧下肿瘤生物学行为的重要...
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The result of the sequence analysis suggested that many kinds of nonbiological stress response elements are contained in the promoter,such as ABRE,DRE/C-repeat,MBS(MYB binding site involved in drought-inducibility),and so on.
序列分析显示,该启动子中存在多种非生物胁迫反应元件,如ABA反应元件ABRE、干旱反应元件DRE/C-repeat以及MYB结合位点MBS(MYB binding site involved in drought-inducibility)等。
Hypoxia-inducible factor 1 (HIF-1) is an important transcription factor found in the begining of 1990's, which could combine with the hypoxia response elements (HRE) in the gene of EPO to induce the transcription of HIF-1. HIF-1 is made up of two subunits: a and β, HIF-la is a regulating subunit: hypoxia can regulates its stability, subcellular orientation ,and the function of transcription.
缺氧诱导因子HIF-1(hypoxia-inducible factor-1，HIF-1)是90年代初发现的由缺氧诱导产生，能与促红细胞生成素基因上的缺氧反应元件(hypoxia response elements，HRE)结合，从而促进EPO转录的新的转录因子。
Conclusion The TPA response elements of NGAL gene located on -416~+84 position of its 5′ flanking region in the esophageal cancer cells.
结论食管癌细胞NGAL基因5′侧翼416～+84区段存在着TPA反应元件。
Conclusion: Expression of TTF1 in vitro can be used in the further research of interaction of TTF1 and its DNA response elements and others transcription factors.
结论:能方便地获得TTF1体外翻译蛋白,为进一步研究TTF1蛋白与相应的DNA反应元件及其他转录因子的相互作用奠定了基础。
LXRs binding with retinoid X receptors (RXRs) to form LXR-RXR heterodimer, which can be activated by ligands of LXRs and/or RXRs. LXR-RXR heterodimer regulate the expression of target genes by interacting with LXR response elements (LXRE).
LXRs与维甲酸X受体(retinoid X receptors, RXRs)形成的异源二聚体可被LXRs配体和/或RXRs配体激活,通过与靶基因上的肝X受体反应元件(LXR response elements, LXRE)结合,调节靶基因转录。
Identification of TPA Response Elements in NGAL 5′ Flanking Region of the Esophageal Cancer Cells
食管癌细胞NGAL5′侧翼区存在TPA应答元件
investigate
dihydroxyvitamin
expression
adenocarcinoma
possibility
inhibitory
目的：　研究1，25－二羟维生素D3 对结肠癌细胞系Caco－2 细胞中报告基因表达的作用，并探讨在报告载体pGL2 序列中存在潜在的抑制性维生素D应答元件（VDRE）的可能性。
A Prostate
specific Protein Factor Inhibits the Interaction
of Androgen
Receptors with Hormone Response Elements
前列腺专一蛋白因子抑制雄激素受体与其应答元件作用
Conclusion:Missense mutation of Tyr486Asp in Exon 5 of UGT1A1 gene is the pathogenic factor of the CNⅡcase in the family and recessively inherited. The mutation has no influence on the response elements of pheniharbital in the promoter re- gion.
结论:Tyr486Asp突变是本例CN—Ⅱ家系的致病性基因,该突变不影响UGT1A1基因启动子区苯巴比妥酸的应答元件,其遗传规律符合常染色体隐性遗传。
The analysis by bioinformatics showed that there is the structural character responding to TPA induction in the gene and at least 3 putative TPA response elements in-657～(-417) position.
生物信息学分析显示,NGAL5′侧翼-657~-417区段至少存在3个潜在的TPA应答元件,表明有应答TPA刺激的结构基础.
The 5′ flanking sequences had four predicted TATA motifs (-25--30 bp, -260--265 bp, -337--342 bp and -715--720 bp), two predicted CCAAT motifs (-389--393 bp and -720--724 bp) and two predicted ABA response elements (-112--116 bp and -397--401 bp).
在-25～-30bp、-260～-265bp、-337～-342bp以及-715～-720bp含有推测的TATA box(TATAAA),在-389～-393bp和-720～-724bp含有推测的CAAT box(CCAAT),以及在-112～-116bp和-397～-401bp含有推测的ABA作用元件CACGT。
These results suggest that the spatiotemporal expression response elements of OsGSTL1 existed in the 5′-upstream region between –2 155 and –1 224 bp.
而OsGSTL1启动子的时空表达相关元件可能位于OsGSTL1翻译起始位点5′端上游–2155bp至–1224bp范围内。
The Construction of ERα Expression Vector Containing Vitamin D_3 Response Elements, and Its Effects on ER-negative Breast Cancer Cells in Combination with Tamoxifen
1α，25二羟维生素D_3靶控ERα基因表达载体构建及其联合他莫西芬对ER阴性乳腺癌细胞抑制效应的研究
Methods A recombinant pTKS3-CAT was constructed by inserting CRP-APRE,a sequence composed of seven copy Stat3 response elements upstream of promoter and a chloramphenicol acetyltransferase (CAT) gene downstream of promoter.
方法将Stat3特异结合序列CRP-APRE克隆到诱导表达型载体pGL2转录启始位点上游,选择氯霉素乙酰转移酶基因(CAT)作为报告基因克隆在转录启始位点下游,构建重组质粒pTKS3-CAT。
Specific activity of the promoter containing Myc-Max response elements in c-myc
overexpressing cells
Myc-Max作用序列启动子在c-myc过表达细胞中的特异启动活性
查询“response elements”译词为用户自定义的双语例句&&&&我想查看译文中含有：的双语例句
为了更好的帮助您理解掌握查询词或其译词在地道英语中的实际用法，我们为您准备了出自英文原文的大量英语例句，供您参考。&&&&&&&&&&&& Previous work from this laboratory has demonstrated that the induction of c-fos by angiotensin (Ang) Ⅱ in vascular smooth muscle cells (VSMC) is mediated by at least two enhancer elements, the serum response element (SRE) and the cyclic AMP response element (CRE). These two elements appear to act independently and equally. The current study is aimed at identifying the trans-acting proteins that interact with these enhancer ele-.ments to mediate this response. Rat aortic smooth muscle... Previous work from this laboratory has demonstrated that the induction of c-fos by angiotensin (Ang) Ⅱ in vascular smooth muscle cells (VSMC) is mediated by at least two enhancer elements, the serum response element (SRE) and the cyclic AMP response element (CRE). These two elements appear to act independently and equally. The current study is aimed at identifying the trans-acting proteins that interact with these enhancer ele-.ments to mediate this response. Rat aortic smooth muscle (RASM) cells were grown in culture and made quiescent by placing them in a defined serum-free media for 48 hours.Aug Ⅱor vehicle was then added, the cells harvested 30 minutes later and nuclear extracts isolated. Gel mobility shift assay were then performed.gel shifts done with wild type SRE oligonucleotide demonstrated that two specific proteins bound to this element.Mutations in central CArG box of the SRE inhibited binding but mutations in the ets binding site in the SRE had no effect. Extracts from Aug Ⅱor vehicle treated cells demonstrated an identical pattern of binding. Similar experiments performed with CRE noligonucleotide identified three proteins which bound to CRE. Again,no differences were observed between vehicle and AugⅡtreated extracts. An antibody to serum response factor(SRF),which binds to the SRE, supershifted the proteins that bound to the SRE. When gel shifts with RASM cells extracts were compared to gel shifts from either NIH 3T3 fibroblast cell extraes of HeLa cell extracts,a different pattern of protein binding was observed using the SRE oligonucleotide.In contrast to the studies with the SRF antibody,an antibody to CRE binding protein (CREB)-43, the most common CREB protein, failed to recognize protein from RASM extract in a supershift assay. When the gel shift pattern with the CRE oligonucleotide between RASM, 3T3 and HeLa cell extracts was compared,no similarity was seen. Taken together,'these data suggest that stimulation of c-for in VSMC's occurs via activation of a unique set of proteins. Activation of these proteins is not due to new protein synthesis. Further work will be aimed at identifying these proteins and studying their mechanism of activation in VSMC's.ＭＵＬＴＩＰＬＥＴＲＡＮＳ－ＡＣＴＩＮＧＦＡＣＴＯＲＳＭＥＤＩＡＴＥＴＨＥＩＮＤＵＣＴＩＯＮＯＦＣ－ＦＯＳＩＮＶＡＳＣＵＬＡＲＳＭＯＯＴＨＭＵＳＣＬＥＣＥＬＬＳＣｈｅｎＹａｎｑｕｎ；ＢａｒｔｅｋＲｙｄｚｅｗｓｋｉ，ＡｌｌｅｎＪ．Ｎａｆｔｉｌａｎ（Ｄｅ... Previous work from this laboratory has demonstrated that the addition of angiotensin(Aug)Ⅱresults in the rapid transcriptional activation of early growth response gene c-fos.Blockage of this increase completely inhibits the Aug Ⅱinduced increase in vascular smooth muscle cell(VSMC)growth.To explore the molecular mechanism responsible for the induction of c-fos in VSMC,a series of constructs containing portions of c-fos promoter linked to the reporter gene chloramphenicol acetyltransferase(CAT)were used... Previous work from this laboratory has demonstrated that the addition of angiotensin(Aug)Ⅱresults in the rapid transcriptional activation of early growth response gene c-fos.Blockage of this increase completely inhibits the Aug Ⅱinduced increase in vascular smooth muscle cell(VSMC)growth.To explore the molecular mechanism responsible for the induction of c-fos in VSMC,a series of constructs containing portions of c-fos promoter linked to the reporter gene chloramphenicol acetyltransferase(CAT)were used in transient transfection assays.When a construct containing both the well described serum response element(SRE)and the cyclic AMP response element(CRE)was used,no endogenous CAT activity was observed in serum starved cells.The addition of either Ang Ⅱor serum resulted in a marked increase in CAT activity.Mutations in either the SRE or CRE alone which have been demonstrated to inactivate these elements in number of cell types had no effect on c-fos inducibility by either Angll or serum. In contrast,if both elements were mutated in the same construct,inducibility was reduced by 75 %￣80%.Using a construct in which the SRE has been deleted,a mutation in the CRE completely abolished induction of c-fos by either Aug Ⅱor serum. Mobility shift assays demonstrated that tow proteins bind specifically to the SRE and three proteins to CRE. These data demonstrate that the induction of c-fos in VSMC's can be mediated by two distinct enhancer elements each of which can act independently. Future research will be aimed at identifying the proteins that interact with these elemetns delineating the mechanisms by which Ang Ⅱstimulates their activity.ＭＵＬＴＩＰＬＥＥＮＨＡＮＣＥＲＥＬＥＭＥＮＴＳＭＥＤＩＡＴＥＴＨＥＩＮＤＵＣＴＩＯＮＯＦＣ－ＦＯＳＢＹＡＮＧＩＯＴＥＮＳＩＮⅡＩＮＶＡＳＣＵＬＡＲＳＭＯＯＴＨＭＵＳＣＬＥＣＥＬＬＳＣｈｅｎＹａｎｑｕｎ；ＢａｒｔｅｋＲｙｄｚｅｗｓｋｉ，ＡｌｌｅｎＪ．... The site-directed mutagenesis mediated by oliogonucleotide was made to change the structure of the glucocor-ticoid response element(GRE) of HBV. The DNA fragments containing natural GRE or mutant GRE were fused to chloramphenical acetyltransferease (CAT) gene. The human liver-derived cell line hepG2 was co-transfected by hormone receptor expression plasmids and CAT reporter plasmids. The results of CAT assay showed that the GUE-associated DNA fragment of HBV was able to mediate heterologous gene to response... The site-directed mutagenesis mediated by oliogonucleotide was made to change the structure of the glucocor-ticoid response element(GRE) of HBV. The DNA fragments containing natural GRE or mutant GRE were fused to chloramphenical acetyltransferease (CAT) gene. The human liver-derived cell line hepG2 was co-transfected by hormone receptor expression plasmids and CAT reporter plasmids. The results of CAT assay showed that the GUE-associated DNA fragment of HBV was able to mediate heterologous gene to response for dexamethasone,progesterone and estradiol. The fusion of the CAT gene and the GRE-associated DNA fragment without En I decreased the activity of the CAT gene in the absence of hormones.本文用寡聚核苷酸介导的定点突变改造乙型肝炎病毒(HBV)基因中的糖皮质激素应答元件(glucocorticoid response element,GRE),并将改变前后的GRE相关DNA片段与氯霉素乙酰基转移酶(CAT)基因融合,与多种激素受体的表达质粒共转染肝细胞,分别用不同的激素处理,测定CAT基因的表达活性以确定HBV上GRE相关DNA片段对各种激素的应答。结果表明HBV上GRE相关DNA片段能介导异源基因对糖皮质激素、孕激素和雌激素的应答。不含Enl的GRE相关片段与CAT基因融合后,在不加激素诱导的情况下,CAT基因活性明显降低。&nbsp&&&&&相关查询
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