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10.1007/112_2018_15

http://scihub22266oqcxt.onion/10.1007/112_2018_15
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30406297!ä!30406297

suck abstract from ncbi


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pmid30406297      Rev+Physiol+Biochem+Pharmacol 2019 ; 176 (ä): 65-105
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  • Magnesium Extravaganza: A Critical Compendium of Current Research into Cellular Mg(2+) Transporters Other than TRPM6/7 #MMPMID30406297
  • Kolisek M; Sponder G; Pilchova I; Cibulka M; Tatarkova Z; Werner T; Racay P
  • Rev Physiol Biochem Pharmacol 2019[]; 176 (ä): 65-105 PMID30406297show ga
  • Magnesium research has boomed within the last 20 years. The real breakthrough came at the start of the new millennium with the discovery of a plethora of possible Mg homeostatic factors that, in particular, included putative Mg(2+) transporters. Until that point, Mg research was limited to biochemical and physiological work, as no target molecular entities were known that could be used to explore the molecular biology of Mg homeostasis at the level of the cell, tissue, organ, or organism and to translate such knowledge into the field of clinical medicine and pharmacology. Because of the aforementioned, Mg(2+) and Mg homeostasis, both of which had been heavily marginalized within the biomedical field in the twentieth century, have become overnight a focal point of many studies ranging from primary biomedical research to translational medicine.The amount of literature concerning cellular Mg(2+) transport and cellular Mg homeostasis is increasing, together with a certain amount of confusion, especially about the function(s) of the newly discovered and, in the majority of instances, still only putative Mg(2+) transporters/Mg(2+) homeostatic factors. Newcomers to the field of Mg research will thus find it particularly difficult to orient themselves.Here, we briefly but critically summarize the status quo of the current understanding of the molecular entities behind cellular Mg(2+) homeostasis in mammalian/human cells other than TRPM6/7 chanzymes, which have been universally accepted as being unspecific cation channel kinases allowing the flux of Mg(2+) while constituting the major gateway for Mg(2+) to enter the cell.
  • |Animals[MESH]
  • |Homeostasis[MESH]
  • |Humans[MESH]
  • |Magnesium/*metabolism[MESH]
  • |Protein Serine-Threonine Kinases[MESH]


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