Analysis of substrate-recognition mode by novel ubiquitin ligase related to endoplasmic reticulum-associated degradation pathway.

与内质网相关降解途径相关的新型泛素连接酶的底物识别模式分析。

基本信息

项目摘要

We have reported previously that Fbs1 and Fbs2 are glycoprotein-specific F-box proteins, which are identified as the endoplasmic reticulum-associated degradation(ERAD)-linked ubiquitin ligase component. Here we report that Fbxo44b, which does not have sugar-binding activity, is involved in ubiquitylation of glycoproteins under the ERAD pathway. In addition, we analyzed the third F-box protein recognizing N-glycoproteins, Fbs3.Fbs3 can interact with glycoproteins modified with not only high-mannose but also complex-type glycans, suggesting that participates in unknown function of glycoproteins endocytosed from the cell surface but not through the ERAD pathway.
我们之前报道过Fbs1和Fbs2是糖蛋白特异性F-box蛋白,被鉴定为内质网相关降解(ERAD)连接的泛素连接酶成分。在这里,我们报告不具有糖结合活性的Fbxo44b参与ERAD途径下糖蛋白的泛素化。此外,我们分析了第三个识别N-糖蛋白的F-box蛋白Fbs3。Fbs3不仅可以与高甘露糖修饰的糖蛋白相互作用,还可以与复合型聚糖修饰的糖蛋白相互作用,表明Fbs3参与从细胞表面内吞的糖蛋白的未知功能但不是通过 ERAD 途径。

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
In vivo function of glycoprotein-specific F-box proteins
糖蛋白特异性 F-box 蛋白的体内功能
  • DOI:
  • 发表时间:
    2010
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Fukunaga K;Fujikawa Y;Esaka M;吉田雪子
  • 通讯作者:
    吉田雪子
SCFFbx2-E3-ligase-mediated degradation of BACE1 attenuates Alzheimer's disease amyloidosis and improves synaptic function.
  • DOI:
    10.1111/j.1474-9726.2010.00632.x
  • 发表时间:
    2010-12
  • 期刊:
  • 影响因子:
    7.8
  • 作者:
    Gong B;Chen F;Pan Y;Arrieta-Cruz I;Yoshida Y;Haroutunian V;Pasinetti GM
  • 通讯作者:
    Pasinetti GM
Characterization of Fbs3 that is the third N-glycoprotein specific F-box protein
第三个 N-糖蛋白特异性 F-box 蛋白 Fbs3 的表征
  • DOI:
  • 发表时间:
    2011
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Eltelib HA;Badejo AA;Fujikawa Y;Esaka M.;吉田雪子
  • 通讯作者:
    吉田雪子
Lectin-like ERAD players in ER and cytosol
Crystallization and preliminary X-ray characterization of the Skp1-Fbg3 complex
Skp1-Fbg3 复合物的结晶和初步 X 射线表征
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YOSHIDA Yukiko其他文献

YOSHIDA Yukiko的其他文献

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{{ truncateString('YOSHIDA Yukiko', 18)}}的其他基金

Elucidation of the molecular mechanism how deficiency of deglycosylation in the cytosol causes abnormalities in organism.
阐明细胞质中去糖基化缺陷如何导致生物体异常的分子机制。
  • 批准号:
    19H02926
  • 财政年份:
    2019
  • 资助金额:
    $ 3.16万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Analysis of the mechanism how glycosylation of proteins functions as a signal for ubiquitination
蛋白质糖基化作为泛素化信号的机制分析
  • 批准号:
    16K07705
  • 财政年份:
    2016
  • 资助金额:
    $ 3.16万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Identification of target substrates of uncharacterized F-box proteins.
鉴定未表征的 F-box 蛋白的靶底物。
  • 批准号:
    24580152
  • 财政年份:
    2012
  • 资助金额:
    $ 3.16万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Screening for the targets of F-box proteins by using dominant-negative mutants
使用显性失活突变体筛选 F-box 蛋白的靶标
  • 批准号:
    19044049
  • 财政年份:
    2007
  • 资助金额:
    $ 3.16万
  • 项目类别:
    Grant-in-Aid for Scientific Research on Priority Areas
Elucidation of novel roles of F-box protein that recognizes sugar chain.
阐明识别糖链的 F-box 蛋白的新作用。
  • 批准号:
    19580114
  • 财政年份:
    2007
  • 资助金额:
    $ 3.16万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Molecular mechanism of substrate recognition of the ubiquitin-ligases that recognize sugar chain
识别糖链的泛素连接酶底物识别的分子机制
  • 批准号:
    15580085
  • 财政年份:
    2003
  • 资助金额:
    $ 3.16万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Experimental study on the effect of Pd-Co dental casting ferro-magnetic alloys in the bone tissue.
Pd-Co牙科铸造铁磁合金对骨组织影响的实验研究。
  • 批准号:
    63570939
  • 财政年份:
    1988
  • 资助金额:
    $ 3.16万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)

相似海外基金

Elucidation of the molecular mechanism how deficiency of deglycosylation in the cytosol causes abnormalities in organism.
阐明细胞质中去糖基化缺陷如何导致生物体异常的分子机制。
  • 批准号:
    19H02926
  • 财政年份:
    2019
  • 资助金额:
    $ 3.16万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Analysis of the mechanism how glycosylation of proteins functions as a signal for ubiquitination
蛋白质糖基化作为泛素化信号的机制分析
  • 批准号:
    16K07705
  • 财政年份:
    2016
  • 资助金额:
    $ 3.16万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Elucidating the molecular mechanisms of selective mitochondrial degradation
阐明选择性线粒体降解的分子机制
  • 批准号:
    16H04784
  • 财政年份:
    2016
  • 资助金额:
    $ 3.16万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Study on the protein quality control mechanism in the endoplasmic reticulum
内质网蛋白质质量控​​制机制研究
  • 批准号:
    26440096
  • 财政年份:
    2014
  • 资助金额:
    $ 3.16万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
小胞体ストレス応答性ユビキチンリガーゼの分子機構解析と神経変性疾患治療への応用
内质网应激反应性泛素连接酶分子机制分析及其在神经退行性疾病治疗中的应用
  • 批准号:
    13J09807
  • 财政年份:
    2013
  • 资助金额:
    $ 3.16万
  • 项目类别:
    Grant-in-Aid for JSPS Fellows
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