在....末端

These above results demonstrated the interaction between these two proteins. To make sure the specific spot where ASH2L and DPY-30-like really interact, we fragmentally expressed ASH2L according to its two important domains, PHD and SPRY. The results of following fragmental pull down tests indicated that the two protein interact at the zone between SPRY domain and the C-terminal of ASH2L.

为了明确ASH2L与GST-DPY30-like相互作用的关键氨基酸序列，我们按ASH2L上的PHD和SPRY两个重要结构域对ASH2L进行了分段表达及分段Pull down，结果表明ASH2L与GST-DPY30-like的作用部位在ASH2L的SPRY结构域到C-末端之间的区域。

By means of GPC,IR,GC-MS,~(13)CNMR,~1HNMR,Methylation analysisetc,structural properties of PST-1 were identified as follows:The Mwof PST-1 was 3.44×10~6 Da and its optical rotation was _D~(20)=+0.110°(c0.1, H_2O); PST-1 constituted 8 simple sugars and the molar ratio was 2,4-Dimethoxy-Mannose:Rhamnose:Ara-binose:Xylose:Galactose:D-Galacturonic acid:Mannose:D-glucuronic acid=2%:5%:24%:9%:3%:1%:46%:10%;The chief bone of PST-1 was 1,3,6-linked-β-D-Man residue and the side chains contained Furanoid and Pyranoid residues.

结合GPC、旋光度测定、IR、GC-MS、~(13)CNMR、~1HNMR、高碘酸氧化法、Smith降解以及甲基化方法等分析测试方法，得到PST-1的单糖组成及结构表征，实验结果如下：红豆杉多糖PST-1是重均分子量为3.44×10~6 Da的支链多糖，旋光度为20D=+0.110~0(c0.1，H_2O)；PST-1单糖组成为：2，4-Dimethoxy-Mannose：Rhamnose：Arabinose：Xylose：Galactose：D-Galacturonic acid：Mannose：D-glucuronic acid=2％：5％：24％：9％：3％：1％：46％：10％；PST-1的骨架结构为：具有1，3，6-连接的β-D-甘露糖残基骨架，侧链分枝包括非还原末端的呋喃型α-L-阿拉伯糖残基、吡喃型α-L-阿拉伯糖残基、β-D-木糖残基、β-D-甘露糖残基、2，4-二氧甲基-β-D-甘露糖残基和α-D-葡萄糖醛酸残基；侧链的糖残基也可能存在2，5-二氧-取代呋喃型α-L-阿拉伯糖基、3-氧-取代的β-D-木糖残基、6-氧-取代的α-D-半乳糖醛酸残基、6-氧-取代的α-D-半乳糖残基、4-氧-取代的α-D-葡萄糖醛酸残基和2-氧-取代的α-L-鼠李糖残基，同时后者也可能穿插在主链上。

The sugar cane spring sugar cane mostly for the autumn goods in stock,after has stored up for a winter, is extremely easy to deteriorate,appears the cotton wool shape or furriness white matter in the sugarcane terminal.

甘蔗春季的甘蔗大多为秋季的存货，储存了一个冬天后，极易变质，在甘蔗末端出现絮状或茸毛状的白色物质。

Seeds very numerous, fusiform, with long, narrow wings at both ends.

非常多，纺锤形的种子，具长，狭窄翅在两末端。

Although the structure contained one molecule per asymmetric unit, the functional unit of CnbG proved to be hexameric with 32 symmetry.

结构表明，不对称单位包含一个分子，，每个分子由63个氨基酸残基组成，形成β-α-β模体，此外在序列中央有一个310-螺旋，C-末端也有1个小的α-螺旋。

A hipped roof has sloping sides and ends meeting at incline d projecting angles called hips.

带斜脊的屋顶有倾斜的侧面和在斜向突出的拐角处汇合的末端。

A hipped roof has sloping sides and ends meeting at inclined projecting angles called hips.

带斜脊的屋顶有倾斜的侧面和在斜向突出的拐角处汇合的末端。

The renal function and histopathological changes were evaluated at 1,2,4,8,12,16,26 and 40 weeks after operation finished.

在1、2、4、8、12、16、26和40周，用原位末端标记法、免疫组化、RT-PCR、Western—blot分别检测细胞凋亡、caspase-3，-8，-9的mRNA和蛋白质的水平。

A small hooklike projection or process,as at the end of a bone .

翅钩；钩形突一种小的钩状突起或隆起，比如在头的末端

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。

In the United States, chronic alcoholism and hepatitis C are the most common ones.

在美国，慢性酒精中毒，肝炎是最常见的。

If you have any questions, you can contact me anytime.

如果有任何问题，你可以随时联系我。