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Control of protein translation by IP(3)R-mediated Ca(2+) release in Drosophila neuroendocrine cells
The inositol 1,4,5-trisphosphate receptor (IP(3)R) is one of two Ca(2+) channels that gates Ca(2+) release from ER-stores. The ligand IP(3), generated upon specific G-protein coupled receptor activation, binds to IP(3)R to release Ca(2+) into the cytosol. IP(3)R also mediates ER-store Ca(2+) release...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5721944/ https://www.ncbi.nlm.nih.gov/pubmed/28949794 http://dx.doi.org/10.1080/19336934.2017.1384103 |
Sumario: | The inositol 1,4,5-trisphosphate receptor (IP(3)R) is one of two Ca(2+) channels that gates Ca(2+) release from ER-stores. The ligand IP(3), generated upon specific G-protein coupled receptor activation, binds to IP(3)R to release Ca(2+) into the cytosol. IP(3)R 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 IP(3)R, we observed reduced protein translation levels. Here, we discuss the possible molecular mechanism for this observation. We hypothesize that the cellular energy sensor, AMPK connects IP(3)R mediated Ca(2+) release into the mitochondria, to protein translation, via the TOR pathway. |
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