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10.1073/pnas.1815361116 http://scihub22266oqcxt.onion/10.1073/pnas.1815361116 30718434!6386685!30718434     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Proc+Natl+Acad+Sci+U+S+A 2019 ; 116 (8): 2925-2934 Nephropedia Template TP {{tp|p=30718434|t=2019. Magnesium-sensitive upstream ORF controls PRL phosphatase expression to mediate energy metabolism |pdf=|usr=}}{{30718434}} gab.com Text Magnesium-sensitive upstream ORF controls PRL phosphatase expression to mediate energy metabolism JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=30718434 #FOAvip Phosphatases of regenerating liver (PRL-1, PRL-2, and PRL-3, also known as PTP4A1, PTP4A2, and PTP4A3) control magnesium homeostasis through an association with the CNNM magnesium transport regulators. Although high PRL levels have been linked to cancer progression, regulation of their expression is poorly understood. Here we show that modulating intracellular magnesium levels correlates with a rapid change of PRL expression by a mechanism involving its 5'UTR mRNA region. Mutations or CRISPR-Cas9 targeting of the conserved upstream ORF present in the mRNA leader derepress PRL protein synthesis and attenuate the translational response to magnesium levels. Mechanistically, magnesium depletion reduces intracellular ATP but up-regulates PRL protein expression via activation of the AMPK/mTORC2 pathway, which controls cellular energy status. Hence, altered PRL-2 expression leads to metabolic reprogramming of the cells. These findings uncover a magnesium-sensitive mechanism controlling PRL expression, which plays a role in cellular bioenergetics. Twit Text FOAVip Magnesium-sensitive upstream ORF controls PRL phosphatase expression to mediate energy metabolism ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=30718434 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30718434 #FOAvip English Wikipedia <ref>{{Cite pmid|30718434}}</ref> Magnesium-sensitive upstream ORF controls PRL phosphatase expression to mediate energy metabolism #MMPMID30718434 Hardy S; Kostantin E; Wang SJ; Hristova T; Galicia-Vazquez G; Baranov PV; Pelletier J; Tremblay ML Proc Natl Acad Sci U S A 2019[Feb]; 116 (8): 2925-2934 PMID30718434show ga Phosphatases of regenerating liver (PRL-1, PRL-2, and PRL-3, also known as PTP4A1, PTP4A2, and PTP4A3) control magnesium homeostasis through an association with the CNNM magnesium transport regulators. Although high PRL levels have been linked to cancer progression, regulation of their expression is poorly understood. Here we show that modulating intracellular magnesium levels correlates with a rapid change of PRL expression by a mechanism involving its 5'UTR mRNA region. Mutations or CRISPR-Cas9 targeting of the conserved upstream ORF present in the mRNA leader derepress PRL protein synthesis and attenuate the translational response to magnesium levels. Mechanistically, magnesium depletion reduces intracellular ATP but up-regulates PRL protein expression via activation of the AMPK/mTORC2 pathway, which controls cellular energy status. Hence, altered PRL-2 expression leads to metabolic reprogramming of the cells. These findings uncover a magnesium-sensitive mechanism controlling PRL expression, which plays a role in cellular bioenergetics. |AMP-Activated Protein Kinase Kinases[MESH] |CRISPR-Cas Systems[MESH] |Cation Transport Proteins[MESH] |Cell Cycle Proteins/genetics[MESH] |Cellular Reprogramming/*genetics[MESH] |Cyclins/genetics[MESH] |Energy Metabolism/*genetics[MESH] |Gene Expression Regulation, Neoplastic[MESH] |Humans[MESH] |Liver Regeneration/genetics[MESH] |MCF-7 Cells[MESH] |Magnesium/metabolism[MESH] |Mechanistic Target of Rapamycin Complex 2/genetics[MESH] |Membrane Proteins/genetics[MESH] |Neoplasm Proteins/genetics[MESH] |Neoplasms/*genetics/pathology[MESH] |Protein Kinases/genetics[MESH]Magnesium-sensitive upstream ORF controls PRL phosphatase expression t(epmc).pdf DeepDyve Pubget Overpricing