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Cooperative roles of glucose and asparagine-linked glycosylation in T-type calcium channel expression

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388963%3A_____%2F16%3A00469487" target="_blank" >RIV/61388963:_____/16:00469487 - isvavai.cz</a>

  • Result on the web

    <a href="http://dx.doi.org/10.1007/s00424-016-1881-y" target="_blank" >http://dx.doi.org/10.1007/s00424-016-1881-y</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1007/s00424-016-1881-y" target="_blank" >10.1007/s00424-016-1881-y</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Cooperative roles of glucose and asparagine-linked glycosylation in T-type calcium channel expression

  • Original language description

    T-type calcium channels are key contributors to neuronal physiology where they shape electrical activity of nerve cells and contribute to the release of neurotransmitters. Enhanced T-type channel expression has been causally linked to a number of pathological conditions including peripheral painful diabetic neuropathy. Recently, it was demonstrated that asparagine-linked glycosylation not only plays an essential role in regulating cell surface expression of Ca(v)3.2 channels, but may also support glucose-dependent potentiation of T-type currents. However, the underlying mechanisms by which N-glycosylation and glucose levels modulate the expression of T-type channels remain elusive. In the present study, we show that site-specific N-glycosylation of Ca(v)3.2 is essential to stabilize expression of the channel at the plasma membrane. In contrast, elevated external glucose concentration appears to potentiate intracellular forward trafficking of the channel to the cell surface, resulting in an increased steady-state expression of the channel protein at the plasma membrane. Collectively, our study indicates that glucose and N-glycosylation act in concert to control the expression of Ca(v)3.2 channels, and that alteration of these mechanisms may contribute to the altered expression of T-type channels in pathological conditions.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    CE - Biochemistry

  • OECD FORD branch

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2016

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Pflugers Archiv - European Journal of Physiology

  • ISSN

    0031-6768

  • e-ISSN

  • Volume of the periodical

    468

  • Issue of the periodical within the volume

    11/12

  • Country of publishing house

    DE - GERMANY

  • Number of pages

    15

  • Pages from-to

    1837-1851

  • UT code for WoS article

    000389834100005

  • EID of the result in the Scopus database

    2-s2.0-84988723398