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10.1371/journal.pone.0209563 http://scihub22266oqcxt.onion/10.1371/journal.pone.0209563 30615643!6322742!30615643     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2019 ; 14 (1): e0209563 Nephropedia Template TP {{tp|p=30615643|t=2019. TRPM7 residue S1269 mediates cAMP dependence of Ca2+ influx |pdf=|usr=}}{{30615643}} gab.com Text TRPM7 residue S1269 mediates cAMP dependence of Ca2+ influx JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=30615643 #FOAvip The nonspecific divalent cation channel TRPM7 (transient receptor potential-melastatin-like 7) is involved in many Ca2+ and Mg2+-dependent cellular processes, including survival, proliferation and migration. TRPM7 expression predicts metastasis and recurrence in breast cancer and several other cancers. In cultured cells, it can induce an invasive phenotype by promoting Ca2+-mediated epithelial-mesenchymal transition. We previously showed that in neuroblastoma cells that overexpress TRPM7 moderately, stimulation with Ca2+-mobilizing agonists leads to a characteristic sustained influx of Ca2+. Here we report that sustained influx through TRPM7 is abruptly abrogated by elevating intracellular levels of cyclic adenosine monophosphate (cAMP). Using pharmacological inhibitors and overexpression studies we show that this blockage is mediated by the cAMP effector Protein Kinase A (PKA). Mutational analysis demonstrates that the Serine residue S1269, which is present proximal to the coiled-coil domain within the protein c-terminus, is responsible for sensitivity to cAMP. Twit Text FOAVip TRPM7 residue S1269 mediates cAMP dependence of Ca2+ influx ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=30615643 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30615643 #FOAvip English Wikipedia <ref>{{Cite pmid|30615643}}</ref> TRPM7 residue S1269 mediates cAMP dependence of Ca2+ influx #MMPMID30615643 Broertjes J; Klarenbeek J; Habani Y; Langeslag M; Jalink K PLoS One 2019[]; 14 (1): e0209563 PMID30615643show ga The nonspecific divalent cation channel TRPM7 (transient receptor potential-melastatin-like 7) is involved in many Ca2+ and Mg2+-dependent cellular processes, including survival, proliferation and migration. TRPM7 expression predicts metastasis and recurrence in breast cancer and several other cancers. In cultured cells, it can induce an invasive phenotype by promoting Ca2+-mediated epithelial-mesenchymal transition. We previously showed that in neuroblastoma cells that overexpress TRPM7 moderately, stimulation with Ca2+-mobilizing agonists leads to a characteristic sustained influx of Ca2+. Here we report that sustained influx through TRPM7 is abruptly abrogated by elevating intracellular levels of cyclic adenosine monophosphate (cAMP). Using pharmacological inhibitors and overexpression studies we show that this blockage is mediated by the cAMP effector Protein Kinase A (PKA). Mutational analysis demonstrates that the Serine residue S1269, which is present proximal to the coiled-coil domain within the protein c-terminus, is responsible for sensitivity to cAMP. |Animals[MESH] |Calcium Signaling/drug effects[MESH] |Calcium/*metabolism[MESH] |Cell Line, Tumor[MESH] |Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/*metabolism[MESH] |Cyclic AMP/*metabolism[MESH] |Isoquinolines/pharmacology[MESH] |Mice[MESH] |Neurons/drug effects/*metabolism[MESH] |Phosphorylation/drug effects[MESH] |Protein Kinase Inhibitors/pharmacology[MESH] |Sulfonamides/pharmacology[MESH]TRPM7 residue S1269 mediates cAMP dependence of Ca2+ influx (epmc).pdf DeepDyve Pubget Overpricing