@misc{10481/69345,
year = {2016},
url = {http://hdl.handle.net/10481/69345},
abstract = {OBJECTIVES: It is believed that tumor cells expressing
Kv10.1 channel acquire selective advantages that allow
them to maintain chronic proliferation. The ciliary
disassembly is a prerequisite to enter into the cell
cycle, therefore our objective was to find correlations
between primary cilium disassembly and the Kv10.1
channel through the Kv10.1 cortactin binding site.
Methods: Wild type Kv10.1, as well as the mutant form
lacking the binding site to the cytoskeleton protein
cortactin, were overexpressed in RPE-TERT cell line. The
effect on ciliary disassembly of such overexpression
forms was imaging using confocal microscopy.
Results: Kv10.1 wild type overexpression induced
disassembly of the primary cilium and alteration of the
cytoskeleton, which corresponded to overproduction
of filament structures positive to α-tubulin acetylated
in the cytoplasm. Overexpression of mutated Kv10.1
did not show this pattern, nor the untreated cells.
ConclusionS: This data suggests that Kv10.1
channel could be interfering with the cilium
formation, and thus influences the cell cycle in
a way that cortactine binding site is not involved.
That should be furtherly studied because due
to its possible implications in cancer.},
publisher = {Archivos de Medicina Universitaria},
keywords = {Kv10.1 channel},
keywords = {Primary cilium},
keywords = {Cortactin},
keywords = {Acetylated alpha-tubulin},
keywords = {Canal Kv10.1},
keywords = {Cilio primario},
keywords = {Cortactina},
keywords = {Alfa-tubulina acetilada},
title = {Primary cilium, cortactine, and Kv10.1 dynamics under confocal microscopy},
author = {Sánchez, José Manuel and Carretero, Irene and González, Jorge and Urrego, Diana and Stühmer, Walter and Pardo, Luis A.},
}