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首页> 外文期刊>Biochemistry >Assembly with the Na,K-ATPase α1 Subunit Is Required for Export of β1 and β2 Subunits from the Endoplasmic Reticulum
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Assembly with the Na,K-ATPase α1 Subunit Is Required for Export of β1 and β2 Subunits from the Endoplasmic Reticulum

机译：从内质网输出β1和β2亚基需要与Na，K-ATPaseα1亚基组装

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摘要

The level of the heterodimericNa,K-ATPase is tightly controlled in epithelia tomaintain appropriatentransport function. The catalytic Na,K-ATPase R subunit is not able to exit the ER or catalyze ion transportnunless assembled with the β subunit. However, requirements for the ER exit of the Na,K-ATPase β subunit thatnplays an additional, ion-transport-independent, role in intercellular adhesion are not clear. Exogenous β1 or β2nsubunits expressed in renal MDCK cells replace endogenous β1 subunits in the R-β complexes in the ER,nresulting in a decrease in the amount of the R1-bound endogenous β1 subunits by 47-61%withnochangeinthenamount of R1 subunits. Disruption of the R1-β association by mutations in defined R1-interacting regions ofneither β1 or β2 subunits results in the ERretention and rapid degradation of unassembledmutants.Hence, the ERnquality control system allows export only of assembled R-β complexes to the Golgi, thereby maintaining annequimolar ratio of R and β subunits in the plasma membrane, whereas the number of R1 subunits in the ERndetermines the amount of the R-β complexes.
机译：上皮细胞中异源二聚Na，K-ATP酶的水平受到严格控制，以维持适当的转运功能。催化的Na，K-ATPase R亚基不能离开ER或催化与β亚基组装在一起的离子转运。然而，尚不清楚Na，K-ATPaseβ亚基的ER出口在细胞间粘附中起额外的，不依赖离子迁移的作用的要求。肾脏MDCK细胞中表达的外源β1或β2n亚基取代了ER中R-β复合物中的内源性β1亚基，导致R1结合的内源性β1亚基的量减少了47-61％，而R1亚基的含量没有变化。由于β1或β2亚基的既定R1相互作用区域中的突变导致的R1-β缔合破坏，导致ER保留并导致未装配的突变体快速降解。因此，ERnquality控制系统仅允许将装配的R-β配合物输出至高尔基体，从而维持质膜中R和β亚基的摩尔比，而ERnd中R1亚基的数量决定了R-β络合物的数量。

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  • 来源
    《Biochemistry》 |2009年第48期|p.11421-11431|共11页
  • 作者

    Elmira Tokhtaeva George Sachs and Olga Vagin;

  • 作者单位

    Department of Physiology, School of Medicine, UCLA and Veterans Administration Greater Los Angeles Health Care System,Los Angeles, VAGLAHS/West LA, Building 113, Room 324, 11301 Wilshire Boulevard, Los Angeles, California 90073;

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