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SHR Neuro Krebs Kardio Lipid Stoffw Microb

Vishnu, N; Jadoon Khan, M; Karsten, F; Groschner, LN; Waldeck-Weiermair, M; Rost, R; Hallström, S; Imamura, H; Graier, WF; Malli, R.
ATP increases within the lumen of the endoplasmic reticulum upon intracellular Ca2+ release.
Mol Biol Cell. 2014; 25(3):368-379 Doi: 10.1091/mbc.E13-07-0433 [OPEN ACCESS]
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Führende Autor*innen der Med Uni Graz
Karsten Felix Daniel
Malli Roland
Vishnu Neelanjan
Co-Autor*innen der Med Uni Graz
Graier Wolfgang
Groschner Lukas
Hallström Seth
Khan Muhammad Jadoon
Rost René
Waldeck-Weiermair Markus
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Abstract:
Multiple functions of the endoplasmic reticulum (ER) essentially depend on ATP within this organelle. However, little is known about ER ATP dynamics and the regulation of ER ATP import. Here we describe real-time recordings of ER ATP fluxes in single cells using an ER-targeted, genetically encoded ATP sensor. In vitro experiments prove that the ATP sensor is both Ca(2+) and redox insensitive, which makes it possible to monitor Ca(2+)-coupled ER ATP dynamics specifically. The approach uncovers a cell type-specific regulation of ER ATP homeostasis in different cell types. Moreover, we show that intracellular Ca(2+) release is coupled to an increase of ATP within the ER. The Ca(2+)-coupled ER ATP increase is independent of the mode of Ca(2+) mobilization and controlled by the rate of ATP biosynthesis. Furthermore, the energy stress sensor, AMP-activated protein kinase, is essential for the ATP increase that occurs in response to Ca(2+) depletion of the organelle. Our data highlight a novel Ca(2+)-controlled process that supplies the ER with additional energy upon cell stimulation.
Find related publications in this database (using NLM MeSH Indexing)
AMP-Activated Protein Kinases - metabolism
Adenosine Triphosphate - biosynthesis
Adenosine Triphosphate - metabolism
Animals -
Biological Transport -
Calcium - metabolism
Cell Line, Tumor -
Endoplasmic Reticulum - metabolism
Glucose - metabolism
Glycolysis - physiology
HEK293 Cells -
HeLa Cells -
Human Umbilical Vein Endothelial Cells -
Humans -
Oxidation-Reduction -
RNA Interference -
RNA, Small Interfering -
Rats -

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