Physiology of apoptosis

Citation
E. Gulbins et al., Physiology of apoptosis, AM J P-REN, 279(4), 2000, pp. F605-F615
Citations number
113
Categorie Soggetti
da verificare
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
ISSN journal
03636127 → ACNP
Volume
279
Issue
4
Year of publication
2000
Pages
F605 - F615
Database
ISI
SICI code
0363-6127(200010)279:4<F605:POA>2.0.ZU;2-9
Abstract
Ion fluxes and volume changes of the whole cell as well as of organelles be long to the hallmarks of apoptosis; however, the molecular mechanism regula ting these changes is only poorly characterized. Several ion channels in th e plasma membrane, in particular the N-type K+ channel, the chloride channe l cystic fibrosis conductance regulator, and an outward rectifying chloride channel, as well as the mitochondrial permeability transition pore, have b een implicated to be involved in signal transduction cascades regulating ap optosis. Furthermore, Bcl-2-like proteins have been suggested to function, at least in part, as ion channels, because they display some homology to ba cterial pore-forming toxins. In contrast to the demonstration of the involv ement of these different ion channels in apoptosis, the molecular consequen ces regulated by these ion channels, and finally triggering apoptosis, are almost completely unknown.