Control of protein translation by IP3R-mediated Ca(2+) release in Drosophila neuroendocrine cells.
|Title||Control of protein translation by IP3R-mediated Ca(2+) release in Drosophila neuroendocrine cells.|
|Publication Type||Journal Article|
|Year of Publication||2017|
|Date Published||2017 Sep 26|
The inositol 1,4,5-trisphosphate receptor (IP3R) is one of two Ca(2+) channels that gates Ca(2+) release from ER-stores. The ligand IP3, generated upon specific G-protein coupled receptor activation, binds to IP3R to release Ca(2+) into the cytosol. IP3R also mediates ER-store Ca(2+) release into the mitochondria, under basal as well as stimulatory conditions; an activity that influences cellular bioenergetics and thus, cellular growth and proliferation. In Drosophila neuroendocrine cells expressing a hypomorphic mutant of IP3R, we observed reduced protein translation levels. Here, we discuss the possible molecular mechanism for this observation. We hypothesise that the cellular energy sensor, AMPK connects IP3R mediated Ca(2+) release into the mitochondria, to protein translation, via the TOR pathway.
|Alternate Journal||Fly (Austin)|