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10.1091/mbc.E16-05-0286 http://scihub22266oqcxt.onion/10.1091/mbc.E16-05-0286 C5007087!5007087 !27385336     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27385336 &cmd=llinks): Failed to open stream: HTTP request failed! 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AMPK activity regulates trafficking of mitochondria to the leading edge during cell migration and matrix invasion |pdf=|usr=}}{{27385336 }} gab.com Text AMPK activity regulates trafficking of mitochondria to the leading edge during cell migration and matrix invasion JO: Mol Biol Cell http://www.kidney.de/pget.php?&tw=1&pmid=27385336 #FOAvip Cell migration is a complex behavior involving many energy-expensive biochemical events that iteratively alter cell shape and location. Mitochondria, the principal producers of cellular ATP, are dynamic organelles that fuse, divide, and relocate to respond to cellular metabolic demands. Using ovarian cancer cells as a model, we show that mitochondria actively infiltrate leading edge lamellipodia, thereby increasing local mitochondrial mass and relative ATP concentration and supporting a localized reversal of the Warburg shift toward aerobic glycolysis. This correlates with increased pseudopodial activity of the AMP-activated protein kinase (AMPK), a critically important cellular energy sensor and metabolic regulator. Furthermore, localized pharmacological activation of AMPK increases leading edge mitochondrial flux, ATP content, and cytoskeletal dynamics, whereas optogenetic inhibition of AMPK halts mitochondrial trafficking during both migration and the invasion of three-dimensional extracellular matrix. These observations indicate that AMPK couples local energy demands to subcellular targeting of mitochondria during cell migration and invasion. Twit Text FOAVip AMPK activity regulates trafficking of mitochondria to the leading edge during cell migration and matrix invasion ????Mol Biol Cell http://www.kidney.de/pget.php?&tw=1&pmid=27385336 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27385336 #FOAvip English Wikipedia <ref>{{Cite pmid|27385336 }}</ref> AMPK activity regulates trafficking of mitochondria to the leading edge during cell migration and matrix invasion #MMPMID27385336 Cunniff B ; McKenzie AJ ; Heintz NH ; Howe AK Mol Biol Cell 2016[Sep]; 27 (17 ): 2662-74 PMID27385336 show ga Cell migration is a complex behavior involving many energy-expensive biochemical events that iteratively alter cell shape and location. Mitochondria, the principal producers of cellular ATP, are dynamic organelles that fuse, divide, and relocate to respond to cellular metabolic demands. Using ovarian cancer cells as a model, we show that mitochondria actively infiltrate leading edge lamellipodia, thereby increasing local mitochondrial mass and relative ATP concentration and supporting a localized reversal of the Warburg shift toward aerobic glycolysis. This correlates with increased pseudopodial activity of the AMP-activated protein kinase (AMPK), a critically important cellular energy sensor and metabolic regulator. Furthermore, localized pharmacological activation of AMPK increases leading edge mitochondrial flux, ATP content, and cytoskeletal dynamics, whereas optogenetic inhibition of AMPK halts mitochondrial trafficking during both migration and the invasion of three-dimensional extracellular matrix. These observations indicate that AMPK couples local energy demands to subcellular targeting of mitochondria during cell migration and invasion. |AMP-Activated Protein Kinases/metabolism [MESH] |Adenosine Triphosphate/metabolism [MESH] |Cell Line, Tumor [MESH] |Cell Movement/*physiology [MESH] |Cytoskeleton/metabolism [MESH] |Energy Metabolism [MESH] |Female [MESH] |Glycolysis [MESH] |Humans [MESH] |Mitochondria/metabolism/*physiology [MESH] |Ovarian Neoplasms [MESH] |Phosphorylation [MESH] |Protein Transport [MESH]AMPK activity regulates trafficking of mitochondria to the leading edg(epmc).pdf DeepDyve Pubget Overpricing