scispace - formally typeset
E

Eva Alés

Researcher at University of Seville

Publications -  27
Citations -  1096

Eva Alés is an academic researcher from University of Seville. The author has contributed to research in topics: Exocytosis & Vesicle fusion. The author has an hindex of 14, co-authored 26 publications receiving 1038 citations. Previous affiliations of Eva Alés include Autonomous University of Madrid.

Papers
More filters
Journal ArticleDOI

High calcium concentrations shift the mode of exocytosis to the kiss-and-run mechanism.

TL;DR: In this paper, the authors investigate the fate of single secretory vesicles after fusion with the plasma membrane by measuring capacitance changes and transmitter release in rat chromaffin cells using the cell-attached patch-amperometry technique.
Journal ArticleDOI

Galantamine prevents apoptosis induced by β-amyloid and thapsigargin: involvement of nicotinic acetylcholine receptors

TL;DR: Results strongly suggest that galantamine can prevent apoptotic cell death by inducing neuroprotection through a mechanism related to that described for nicotine, i.e. activation of nAChRs and upregulation of Bcl-2.
Journal ArticleDOI

Myosin II contributes to fusion pore expansion during exocytosis.

TL;DR: It is demonstrated that the fusion pore is of critical importance to control the release of catecholamines during single vesicle secretion in chromaffin cells and it is proved that myosin II acts as a molecular motor on the fuse pore expansion by hindering its dilation when it lacks the phosphorylation sites.
Journal ArticleDOI

Push-and-pull regulation of the fusion pore by synaptotagmin-7

TL;DR: It is shown that, surprisingly, Ca2+ binding to the C2A domain suffices to trigger fusion pore opening but that the resulting fusion pores are unstable and collapse, causing a dramatic increase in kiss-and-run fusion events.
Journal ArticleDOI

ERG K+ channel blockade enhances firing and epinephrine secretion in rat chromaffin cells: the missing link to LQT2-related sudden death?

TL;DR: It is concluded that, in addition to being crucial in regulating the QT period in the heart, ERG channels play a role in modulating epinephrine, a fundamental neurotransmitter shaping cardiac function.