Skip to main content

Myotonic dystrophy CTG repeat expansion alters Ca2+ channel functional expression in PC12 cells

9Citations
Citations of this article
23Readers
Mendeley users who have this article in their library.

This artice is free to access.

Abstract

We previously reported that expression of myotonic dystrophy (DM1) expanded CUG repeats impedes NGF-induced differentiation in a PC12 clone (CTG90 cells). Here, we present evidence for changes in the fractional contribution of distinct voltage-gated Ca2+ channels, key elements in neurotrophin-promoted differentiation, to the total Ca2+ current in the CTG90 cells. Patch-clamp recordings showed that the relative proportion of pharmacologically isolated Ca2+ channel types differed between control and CTG90 cells. Particularly, the functional expression of N-type channels was significantly reduced. Though quantitative real-time RT-PCR revealed that transcripts for the pore-forming subunit encoding the N-type channels remained unchanged, the protein level analyzed by semi-quantitative Western blotting was down-regulated in the CTG90 cells. These data suggest modifications in the processing of N-type Ca2+ channels in PC12 cells expressing the DM1 mutation. © 2007 Federation of European Biochemical Societies.

Cite

CITATION STYLE

APA

Andrade, A., de León, M. B., Hernández-Hernández, O., Cisneros, B., & Felix, R. (2007). Myotonic dystrophy CTG repeat expansion alters Ca2+ channel functional expression in PC12 cells. FEBS Letters, 581(23), 4430–4438. https://doi.org/10.1016/j.febslet.2007.08.020

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free