The WEISS Lab

Pathophysiology of Ion Channels

Secretory carrier-associated membrane protein 5 regulates cell-surface targeting of T-type calcium channels


Journal article


E. R. Mustafá, Konstantin Weiss, N. Weiss
Channels, 2023

Semantic Scholar DOI PubMedCentral PubMed
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Cite

APA   Click to copy
Mustafá, E. R., Weiss, K., & Weiss, N. (2023). Secretory carrier-associated membrane protein 5 regulates cell-surface targeting of T-type calcium channels. Channels.


Chicago/Turabian   Click to copy
Mustafá, E. R., Konstantin Weiss, and N. Weiss. “Secretory Carrier-Associated Membrane Protein 5 Regulates Cell-Surface Targeting of T-Type Calcium Channels.” Channels (2023).


MLA   Click to copy
Mustafá, E. R., et al. “Secretory Carrier-Associated Membrane Protein 5 Regulates Cell-Surface Targeting of T-Type Calcium Channels.” Channels, 2023.


BibTeX   Click to copy

@article{e2023a,
  title = {Secretory carrier-associated membrane protein 5 regulates cell-surface targeting of T-type calcium channels},
  year = {2023},
  journal = {Channels},
  author = {Mustafá, E. R. and Weiss, Konstantin and Weiss, N.}
}

Abstract

ABSTRACT Missense mutations in the human secretary carrier-associated membrane protein 5 (SCAMP5) cause a variety of neurological disorders including neurodevelopmental delay, epilepsy, and Parkinson’s disease. We recently documented the importance of SCAMP2 in the regulation of T-type calcium channel expression in the plasma membrane. Here, we show that similar to SCAMP2, the co-expression of SCAMP5 in tsA-201 cells expressing recombinant Cav3.1, Cav3.2, and Cav3.3 channels nearly abolished whole-cell T-type currents. Recording of intramembrane charge movements revealed that SCAMP5-induced inhibition of T-type currents is primarily caused by the reduced expression of functional channels in the plasma membrane. Moreover, we show that SCAMP5-mediated downregulation of Cav3.2 channels is essentially preserved with disease-causing SCAMP5 R91W and G180W mutations. Hence, this study extends our previous findings with SCAMP2 and indicates that SCAMP5 also contributes to repressing the expression of T-type channels in the plasma membrane.


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