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
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Czech description
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Classification
Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
CE - Biochemistry
OECD FORD branch
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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
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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