[New aspects of the mechanism of Ca2+ entry in non-excitable cells].
The capacitative Ca2+ entry has been accepted to play a crucial role in Ca2+ signaling in non-excitable cells, and the mechanisms linking the depletion of intracellular Ca2+ stores to the activation of Ca2+ entry are presently the subject of intensive investigation. There are two hypotheses to explain the molecular mechanism of capacitative Ca2+ entry. One is that a diffusible second messenger released from intracellular Ca2+ stores may activate a Ca2+ channel at the plasma membrane. Numerous molecules, including CIF, cGMP, arachidonic acid, and a small G-protein, are proposed as the candidates for the diffusible messenger. In addition, the capacitative Ca2+ entry has been suggested to be modulated by protein phosphorylation/dephosphorylation. Another hypothesis is termed the "conformational coupling model". This model suggests that information between the IP3 receptor and a plasma membrane Ca2+ channel may be transferred directly through conformational protein-protein interactions. The plasma membrane Ca2+ channel involved in the capacitative Ca2+ entry is still neither purified nor cloned, but recent studies suggest that the mammalian homologue of the Drosophila protein Trp may function as a capacitative Ca2+ entry channel.
Tojyo
Y
Y
Department of Dental Pharmacology, School of Dentistry, Health Sciences University of Hokkaido, Japan.
Tanimura
A
A
Matsumoto
Y
Y
D000818:Animals; D001685:Biological Factors / Q000502:physiology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism / Q000502:physiology; D002462:Cell Membrane / Q000378:metabolism; D006801:Humans; D010766:Phosphorylation; D011506:Proteins / Q000378:metabolism; D015290:Second Messenger Systems / Q000502:physiology; D050052:TRPC Cation Channels
D001685:Biological Factors; D015220:Calcium Channels; D011506:Proteins; D050052:TRPC Cation Channels; C096351:transient receptor potential cation channel, subfamily C, member 1; D002118:Calcium