使转染

基本解释 (translations)

transfect

与使转染相关的网络例句 [注：此内容来源于网络，仅供参考]

The appearance of MUC2protein,an intestinal goblet cell marker,was determined as formation of intestinalphenotype.

将pcDNA3.1 /Cdx2质粒和Sox2siRNAs分别及共同转染到人胃上皮细胞系GES-1中分别使Cdx2上调和Sox2下调。

Inaddition,we extract total RNA from cultural U251 cell of humanglioma,make coding gene extron amplification of TfR through ReverseTranscription-Polymerase Chain Reaction,construct expressionplasmid of pCDNA3.1-TfR after digestion of enzyme andconjunction,do transfection to U251 cell by liposome afteridentification,cause excess expression,detect the efficiency of transientexpression of TfR protein by pEGFPN1-TfR, sieve positive cell ofpCDNA3.1-TfR through G418, choose positive cell clone, detect theexpression of TfR in anteroposterior period through Western blot,FCM,cell immunochemistry and mRNA through RT-PCR, identify the effect of transfection.

另外，培养人脑胶质瘤U251细胞，进行细胞总RNA抽提，运用RT-PCR方法进行TfR基因的完整编码区外显子的扩增，经过酶切、连接后构建pCDNA3.1-TfR的表达质粒，鉴定正确后按脂质体转染方法转染人胶质瘤U251细胞，使其过量表达，通过pEGFPN1-TfR检测其瞬时转染的效率；用G418对稳定表达pCDNA3.1-TfR的细胞进行筛选，挑选阳性细胞克隆，运用Western blot、流式细胞检测技术和细胞免疫化学以及mRNA半定量的方法检测TfR在转染前后的表达水平，鉴定转染的效果。

We have generated stable, immortalized cell lines of human neural stem cells from primary human fetal telencephalon cultures via a retroviral vector encoding v-myc.

我们用逆转录病毒转染技术使永生性的来源于原代人胚胎端脑组织的神经干细胞株表达v-myc基因。

We hae generated stable, immortalized cell lines of human neural stem cells from primary human fetal telencephalon cultures ia a retroiral ector encoding -myc.

我们用逆转录病毒转染技术使永生性的来源于原代人胚胎端脑组织的神经干细胞株表达-myc基因。

When SA-bFGF-Math1 transferred to the epithelial cells(UEC-4) of utricle,these cells showed the potential to differentiate hair-cell-like cells.

通过脂质体将bFGF-Math1转染大鼠椭圆囊斑的上皮细胞(UEC-4)，可使其分化为新毛细胞。

METHODS: MyoD cDNA fragments were extracted from plasmids pEMSV-MyoD with polymerase chain reaction, and PCR was used to clone the whole-length gene of MyoD. After adding CACC sequence at 5' end, MyoD gene was cloned by orient topology into transfer ventor, pENTR/D-TOPO. Objective gene was transferred into adenoviral expression vector DNA via pENTR/D-TOPO vector. The recombinant adenoviral vectors transfected into HEK293A cells by using lipofectamine were packaged and amplified.

从pEMSV-MyoD质粒上用聚合酶链反应法扩增出MyoD cDNA片段，再通过聚合酶链反应使MyoD基因加上CACC序列接头，经过定向拓扑克隆使目的基因连接到转移载体上，再通过LR酶促反应，将目的基因转移到腺病毒表达载体DNA上，获得MyoD基因重组的腺病毒DNA，用脂质体转染法转染HEK293A细胞，包装扩增出MyoD基因重组的腺病毒。

Ribozyme can inhibit the expression of HBeAg in the cotransfected cells by cleaving the mRNA of HBV.

在核酶与HBV共转染细胞中，核酶通过对HBV mRNA的剪切作用，使HBeAg的表达量明显受到抑制。

Results are as followed:1 Exposure of HELF cells to BP caused c-Jun activation,and increased the activity of MAPK,PI-3K,p53 and cyclin D1 pathway.2 BP-induced c-Jun activation was inhibited by dominant negative mutants of extracellular signal-regulated protein kinase or c-Jun NH_2-terminal kinase,but not by p38,impling that JNK and ERK pathways medicate c-Jun activation induced by BP.3 Overexpression of dominant-negative mutants PI-3K and Akt potently blocked phosphorylations of c-Jun and ERK,but not JNK in response to BP,suggesting that PI-3K/Akt pathway positively regulates BP-induced c-Jun activation through ERK.4 Inhibition of p53 by its chemical or molecular inhibitor markedly increased the phosphorylation levels of c-Jun,Akt and ERK upon BP stimulation,indicating that p53 negatively medicates BP-induced c-Jun activation through PI-3K/Akt/ERK pathway.5 The cell lines expressed TAM67 exhibits no significant affecting normal cell growth properties.6 TAM67 was able to significantly block G_1-S transition and subsequent cell proliferation,suggesting that c-Jun is essential for cell cycle alternations elicited by BP.7 Overexpression of TAM67 impaired BP-induced cyclin D1 activation,decreasing expression of E2F1 and pRb,indicating that c-Jun participates in the modulation of BP-induced activation of cyclin D1/pRb/E2F1 pathway.8 Stably expression of TAM67 led to the increases in the expression levels of p53 and p21,elevating phosphorylation level of p53,clearly indicating that c-Jun regulates p53/p21 pathway activation induced by BRCollectively,PI3K/Akt/ERK pathway mediated BP-induced c-Jun activation through p53-dependent mechanism.

结果显示：1BP刺激细胞可促进c-Jun活化，并伴随着MAPK、PI-3K、p53和cyclinD1通路各组成成分的活性增强。2利用MAPK通路的显性失活突变体分别阻断细胞外信号调节激酶和c-Jun氨基末端激酶活性，均可明显抑制BP诱导的c-Jun活化，但阻断p38活性对BP引起的c-Jun活化无明显影响，提示JNK和ERK通路参与调控BP诱导的c-Jun活化。3过表达PI-3K和Akt的显性失活突变体也可显著抑制BP诱导的c-Jun活化，并降低磷酸化ERK的表达水平，但对磷酸化JNK的表达水平无明显影响，说明PI-3K/Akt通路通过ERK正性调控了BP诱导的c-Jun活化。4p53的化学/分子抑制剂能使BP作用的细胞内c-Jun活性明显增加，并同时诱导Akt和ERK的磷酸化水平的升高，表明p53可通过PI-3K/Akt/ERK通路对BP诱导的c-Jun活化进行负性调控。5随后观察转染细胞的生长情况，发现TAM67对细胞正常生长和形态无明显影响。6稳定表达TAM67可有效抑制BP诱导的S期细胞数的增加，提示c-Jun在BP致细胞周期改变的过程中发挥了重要作用。7TAM67过表达能够抑制BP诱导的cyclin D1活化，降低磷酸化Rb以及E2F1蛋白表达水平，表明c-Jun参与调控BP诱导的cyclin D1/Rb/E2F1通路的活化。8过表达TAM67可使BP刺激的细胞中p53、p21总蛋白以及p53磷酸化的表达水平明显升高，可见c-Jun也参与调控BP诱导的p53/p21通路活化。

CaN Aβ gene silencing can reduce myocardial hypertrophy in cultured cells, si1280 (21bp) of CaN Aβ gene is the most effective target site for siRNA. The method of intrapericardial injection of plasmid, microbubbles and erzymes can improve transfection efficiency of non-viral plasmid with satisfying targeted transfection. But the scope of transfected myocytes is still limited. CaN Aβ shRNA expressing plasmid transfection in vivo by pericardial injection results in decreased CaN Aβ protein expression of small part of myocytes, and CaN Aβ mRNA only shows decreased trend. The dosage of non-viral vector and the parameters of ultrasound energy should be optimized in further study.

结论RNAi技术抑制CaN Aβ基因表达可有效减轻Ald诱导的心肌细胞肥大程度；CaN Aβ基因中si1280(21bp)片段为实现RNAi的更有效片段；微泡+酶类心包腔内注射超声导入的方法可有效改善非病毒载体在体心肌的转染效率，同时具有一定的靶向性，但总的转染范围仍然有限；采用这一方法进一步进行&一肾一夹&心肌肥大模型大鼠在体心肌细胞的CaNAβ的RNAi干预，发现心肌肥大大鼠心外膜下局部心肌细胞CaN Aβ蛋白水平降低，CaN AβmRNA水平虽有下降趋势，但无统计学差异，提示质粒的用量及超声导入的参数有待进一步研究使其优化。

Part II The experiment study on anti-tumour effect of dendritic cells derived from peripheral blood monocyte of patients with oral cancer after pulsed by tumour antigen in different ways. Collected 50ml peripheral blood from each patients and volunteers to induced DC in vitro. We parted the test group and control group into three subgroups respectively, untreated group A, freezed and thawn group B, RNA transfected group C. To group A, after induced DCs for five days , we added 200U/mlTNF-α in each hole and cultured on. To group B, we added protein antigen (DC/ tumor cells = 1 : 1 ,each hole) for 4h at 5d, and then added 200U/mlTNF-α in each hole and cultured on. To group C, transfected immature DC with tumor cell RNA(DC:RNA=1×105/ml: 5ug)at 5d, operated completely with the specification of invitrogen DMRIE-C reagents. After transfection we replaced transfection agent with complete medium, and then added 200U/mlTNF-α in each hole and cultured on.

第二部分口腔癌患者外周血来源的树突状细胞体外负载抗原后抑瘤作用的实验研究无菌采集20例口腔癌患者和20例健康志愿者外周血50ml，分离单个核细胞体外诱导培养DC，并将实验组和对照组细胞各分为三组，A组为未处理组，B组为冻融组，C组为RNA转染组。A组DC在培养5d后，每孔加入TNF-α200U/ml；B组DC培养第5d后，每孔中加入癌细胞蛋白抗原，使DC/肿瘤细胞=1：1，继续培养4h后，每孔加入TNF-α200U/ml；C组将培养至第5d的未成熟DC用肿瘤细胞RNA进行转染(DC：RNA=1×105/ml： 5ug，按照invitrogen DMRIE-C试剂说明书进行操作)，转染结束后用完全培基取代转染剂，每孔加入TNF-α200U/ml。

与使转染相关的网络解释 [注：此内容来源于网络，仅供参考]

arteriogenesis：(動脈形成)

近期研究表明Ang1和VEGF共同基因转染能够更好促进缺血心肌的动脉形成(arteriogenesis)和血管形成. 单纯VEGF 165或Ang1基因转染,仅能使缺血心肌毛细血管密度上升36%,如果二者协同转染,可使血管密度上升75倍(21).