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肌动蛋白

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Furthermore,we observed that TH1 localized to focal adhesions and filopodia in the leading edge of cells,where TH1 reduced cell migration through affecting actin and adhesion dynamics.

此外,我们还观察到TH1定位于迁移细胞前沿的粘附斑和纤维伪足上,并且通过影响肌动蛋白和粘附动力学变化干扰了细胞的迁移。

These structures include filopodia, lamellipodia, stress fiber and focal adhesion.

已知与肌动蛋白相关的细胞结构主要有:丝状伪足、板状伪足、粘着斑和张力纤维。

Cdc42 and Rac1 have similar effects on cytoskeleton. They both promote the actin polymerization in the cell and profit the formation of filopodia and lamelipodia respectively.

Cdc42和Rac促进细胞内肌动蛋白聚合,分别有利于丝状伪足和片状伪足的形成;而RhoA可能具有与Cdc42 和Rac相反的效果,通常造成细胞边缘和突起的收缩及胞体变圆。

Thus the actin-based structures which have tight relation with the migration of VSMC take part in the development of restenosis. These structures include filopodia, lamellipodia, stress fiber and focal adhesion.

已知与肌动蛋白相关的细胞结构主要有:丝状伪足、板状伪足、粘着斑和张力纤维。

Results From the fourth week, in diabetic rats, the contents of AGEs in plasma and the abdominal aorta increased, the relative area of α-SM-actin in the abdominal aorta decreased, the density of nucleus of VSMC increased, and mitochondria and rough endoplasmic reticules in VSMC increased.

结果 从4周起,DM大鼠血浆和腹主动脉的AGEs显著增多;腹主动脉α-SM-肌动蛋白的相对面积减小,VSMC的细胞核密度增大,线粒体和粗面内质网增多。

Thus, we can conclude that the persistent expression of actin during late stage of baculoviral infection inhibited the polyhedrin expression, and then the formation of polyhedra.

本研究的结果表明,晚期持续表达的外源肌动蛋白抑制了多角体基因的转录和表达,从而导致多角体不能正常产生。

It can be concluded that the persistently expression of actin during late stage of baculovirus infection inhibit the polyhedrin expression, and then the formation of polyhedra.

结果表明,晚期表达的外源肌动蛋白抑制了多角体基因的转录和表达,从而导致多角体不能正常产生。

So the large-scale structures of actin filaments forming in low concentration protein solution via self-organization without any F-actin dynamic interfering factors such as phalloidin etc.

同时,对肌动蛋白自组织分支纤维结构的拓扑形态进行了分形构造的数学描述,以有助于自组织纤维结构2D构型的确定和分析。

Cytoplasmic actin microfilament systems were localized in the freshly isolated onion protoplasts of bulb parenchyma cells using TRITC labelled phalloidin probe in the present study.

使用四甲基罗丹明标记的鬼笔环碱探针,以新分离的洋葱鳞茎薄壁细胞原生质体为材料,观察了细胞胞质肌动蛋白微丝骨架的结构与形态。

Lamblia were cultivated axenically with modified TYI-S-33 medium contained dihydroartemisinin (0.002 mg/L) for 12 h and then stained by rhodanmine phalloidin and paclitaxel (P22310). The cytoskeletons of the organisms were detected and analyzed by flow cytometry, and then observed by confocal microscopy.RESULTS: The cytoskeleton of trophozoites was markedly damaged after treatment with 0.002 mg/L dihydroartemisinin for 12 h.

将用含双氢青蒿素的改良TYI-S-33培养基培养后的蓝氏贾第鞭毛虫滋养体,用专一性结合f-肌动蛋白的荧光染料罗丹明-鬼笔环肽(rhodanmine phalloidin, RDP)标记微丝,结合微管的紫杉醇(Paclitaxel, Oregen Green 488, P22310)标记微管,用流式细胞术检测、分析,用激光共聚焦显微镜(confocal microscopy, CFM)观察滋养体微丝和微管的变化。

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