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   copper-binding domains 在 神经病学 分类中 的翻译结果: 查询用时:0.048秒
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copper-binding domains
相关语句
  铜离子结合区
    [Results] When 1-4 copper-binding domains of ATP7B gene were deleted one by one, the trafficking of ATP7B delayed or diminished.
    【结果】ATP7B基因1-4铜离子结合区逐个缺失后,ATP7B蛋白定向移动减慢至消失;
短句来源
    [Conclusion] The function of six copper-binding domains of ATP7B gene is different. The 1-4 domains induce trafficking of ATP7B within the cell, while the 5-6 copper-binding domains are directly involved in copper transport.
    【结论】ATP7B基因6个铜离子结合区功能不同,其中1-4结合区主要根据铜浓度诱导ATP7B蛋白细胞内定向移动,而5-6结合区则直接参与铜离子细胞外转运。
短句来源
    [Objective] The deletion mutant of copper-binding domains of ATP7B gene was constructed in order to investigate its function in hepatocytes of toxic milk mouse.
    【目的】构建ATP7B基因铜离子结合区缺失突变体,研究其在Tx小鼠肝细胞中的表达及功能。
短句来源
    When 5-6 copper-binding domains were deleted, copper transport stopped.
    5-6铜离子结合区缺失,细胞铜转运功能停滞。
短句来源
  铜离子结合区
    [Results] When 1-4 copper-binding domains of ATP7B gene were deleted one by one, the trafficking of ATP7B delayed or diminished.
    【结果】ATP7B基因1-4铜离子结合区逐个缺失后,ATP7B蛋白定向移动减慢至消失;
短句来源
    [Conclusion] The function of six copper-binding domains of ATP7B gene is different. The 1-4 domains induce trafficking of ATP7B within the cell, while the 5-6 copper-binding domains are directly involved in copper transport.
    【结论】ATP7B基因6个铜离子结合区功能不同,其中1-4结合区主要根据铜浓度诱导ATP7B蛋白细胞内定向移动,而5-6结合区则直接参与铜离子细胞外转运。
短句来源
    [Objective] The deletion mutant of copper-binding domains of ATP7B gene was constructed in order to investigate its function in hepatocytes of toxic milk mouse.
    【目的】构建ATP7B基因铜离子结合区缺失突变体,研究其在Tx小鼠肝细胞中的表达及功能。
短句来源
    When 5-6 copper-binding domains were deleted, copper transport stopped.
    5-6铜离子结合区缺失,细胞铜转运功能停滞。
短句来源
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  copper-binding domains
The inferred yellow-poplar laccase gene products were highly related to one another (79-91% at the amino acid level) and showed significant similarity to other blue copper oxidases, especially with respect to the copper-binding domains.
      
A high degree of sequence conservation was found with the copper-binding domains of the 59 kDa tomato PPO as well as hemocyanins and tyrosinases from a wide diversity of taxa.
      
Alignments of the predicted amino acid sequences highlighted regions of variable sequence flanked by the highly conserved copper-binding domains that characterize members of this enzyme family.
      
The Atx1 copper chaperone binds Cu(I) and interacts directly with the copper-binding domains of a P-type ATPase copper transporter, its physiological partner.
      


Objective: To investigate the pathogenesis of Wilson disease (WD) by detecting its gene products encoded by WD gene (ATP7B). Methods Patients diagnosed as WD were analyzed by SDS-PAGE in conjunction with Western blot. Two antibodies were used, which are specially against the sixth copper binding domain (Anti-CuBD) and ATP binding domain (Anti-ABD) of WD protein. Results The WD proteins were not expressed in two patients when using antiCuBD, and poorly expressed when using anti-ABD. Conclusions WD...

Objective: To investigate the pathogenesis of Wilson disease (WD) by detecting its gene products encoded by WD gene (ATP7B). Methods Patients diagnosed as WD were analyzed by SDS-PAGE in conjunction with Western blot. Two antibodies were used, which are specially against the sixth copper binding domain (Anti-CuBD) and ATP binding domain (Anti-ABD) of WD protein. Results The WD proteins were not expressed in two patients when using antiCuBD, and poorly expressed when using anti-ABD. Conclusions WD is highly heterogeneous in clinical manifestations and inheritance pattern. Two WD patients might simultaneously have exon 5 mutations and exon 8 mutations. The study of WD gene products would probe into the pathogenesis of WD.

目的 对肝豆状核变性(WD)基因编码产物WD蛋白进行检测,探讨WD的发病机制。方法 应用Western-blot蛋白印迹技术对诊断为WD的患者进行WD蛋白的研究。结果 发现患者WD蛋白在肝内表达缺失或者含量改变。结论 WD患者可能同时存在有WD基因exons和exon5的突变,直接检测WD基因产物为进一步研究WD的病理机制奠定了基础。

[Objective] The deletion mutant of copper-binding domains of ATP7B gene was constructed in order to investigate its function in hepatocytes of toxic milk mouse. [ Methods] The deletion mutant expression vectors of ATP7B gene were constructed by means of long distance PCR and plas-mid-recombination. The hepatocytes of toxic milk mouse were transfected by recombinant plasmid mediated by liposome, cultured in high and low copper concentration. The trafficking of mutant ATP7B and its ability to transport copper...

[Objective] The deletion mutant of copper-binding domains of ATP7B gene was constructed in order to investigate its function in hepatocytes of toxic milk mouse. [ Methods] The deletion mutant expression vectors of ATP7B gene were constructed by means of long distance PCR and plas-mid-recombination. The hepatocytes of toxic milk mouse were transfected by recombinant plasmid mediated by liposome, cultured in high and low copper concentration. The trafficking of mutant ATP7B and its ability to transport copper were observed. [Results] When 1-4 copper-binding domains of ATP7B gene were deleted one by one, the trafficking of ATP7B delayed or diminished. When 5-6 copper-binding domains were deleted, copper transport stopped. [Conclusion] The function of six copper-binding domains of ATP7B gene is different. The 1-4 domains induce trafficking of ATP7B within the cell, while the 5-6 copper-binding domains are directly involved in copper transport.

【目的】构建ATP7B基因铜离子结合区缺失突变体,研究其在Tx小鼠肝细胞中的表达及功能。【方法】利用长片断PCR和质粒重组技术构建不同铜离子结合区的缺失体,脂质体介导转染Tx小鼠肝脏细胞,然后进行高铜、低铜孵育,观察ATP7B突变蛋白在细胞内的定向移动及对铜离子转运功能的影响。【结果】ATP7B基因1-4铜离子结合区逐个缺失后,ATP7B蛋白定向移动减慢至消失;5-6铜离子结合区缺失,细胞铜转运功能停滞。【结论】ATP7B基因6个铜离子结合区功能不同,其中1-4结合区主要根据铜浓度诱导ATP7B蛋白细胞内定向移动,而5-6结合区则直接参与铜离子细胞外转运。

Objective To investigate the copper transporting ability of Wilson protein, and the mechanism of zinc therapy. Methods Using RT-PCR to amplify a 1.95 kb copper binding domain fragment of Wilson protein (WCBD) and cloning it to pGEX-4T-1, the GST-WCBD was expressed in BL-21 under the IPTG induction. Purified the GST-WCBD with GST-columns, cleaved the GST part with Thrombin and acquired the WCBD. The metal binding properties to Cu(Ⅱ), Zn(Ⅱ), Fe(Ⅲ), Ni(Ⅱ), Ag(Ⅰ) with IMAC and 65 Zn blotting analysis were...

Objective To investigate the copper transporting ability of Wilson protein, and the mechanism of zinc therapy. Methods Using RT-PCR to amplify a 1.95 kb copper binding domain fragment of Wilson protein (WCBD) and cloning it to pGEX-4T-1, the GST-WCBD was expressed in BL-21 under the IPTG induction. Purified the GST-WCBD with GST-columns, cleaved the GST part with Thrombin and acquired the WCBD. The metal binding properties to Cu(Ⅱ), Zn(Ⅱ), Fe(Ⅲ), Ni(Ⅱ), Ag(Ⅰ) with IMAC and 65 Zn blotting analysis were carried out. Results The WCBD was found having varying affinities with different metals as follow: Cu(Ⅰ)> Zn(Ⅱ) >Ni(Ⅱ) >Cu(Ⅱ). Zn(Ⅱ) was discovered able to compete with Cu(Ⅰ) in the binding domain. Conclusion Wilson protein delivering copper as Cu(Ⅰ) was suggested to be demonstrated. The capacity of zinc to compete with copper may be a mechanism in zinc treatment to this disease.

目的 研究Wilson蛋白 (ATP7B酶 )的离子结合功能 ,探讨锌剂治疗Wilson病的机制。方法 应用逆转录 聚合酶链反应 (RT PCR)扩增目的基因 ,GST基因融合载体表达并纯化融合蛋白 ,凝血酶酶切并收集目的蛋白 ,应用离子螯合层析和放射性锌印迹技术研究蛋白不同离子的结合能力。结果 ATP7B的离子结合能力为Cu(Ⅰ ) >Zn(Ⅱ ) >Ni(Ⅱ ) >Cu(Ⅱ ) ,并发现锌离子和铜离子对蛋白的结合具有竞争作用。结论 本实验证明了ATP7B以一价铜离子的形式行使其运铜功能 ,ATP7B不仅有结合铜离子的功能 ,而且有结合其他离子的功能 ;铜锌两种金属离子在蛋白结合位点的竞争作用可能是锌剂治疗WD的机制之一。

 
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