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10.1016/j.ceca.2017.03.004 http://scihub22266oqcxt.onion/10.1016/j.ceca.2017.03.004 28356194!ä!28356194 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Calcium 2017 ; 67 (ä): 166-173 Nephropedia Template TP {{tp|p=28356194|t=2017. Assessment of TRPM7 functions by drug-like small molecules |pdf=|usr=}}{{28356194}} gab.com Text Assessment of TRPM7 functions by drug-like small molecules JO: Cell Calcium http://www.kidney.de/pget.php?&tw=1&pmid=28356194 #FOAvip Transient receptor potential cation channel subfamily M member 7 (TRPM7) is a plasma membrane ion channel linked to a cytosolic protein kinase domain. Genetic inactivation of this bi-functional protein revealed its crucial role in Ca(2+) signalling, Mg(2+) metabolism, immune responses, cell motility, proliferation and differentiation. Malfunctions of TRPM7 are associated with anoxic neuronal death, cardiac fibrosis, tumour progression and macrothrombocytopenia. Recently, several groups have identified small organic compounds acting as inhibitors or activators of the TRPM7 channel. In follow-up studies, the identified TRPM7 modulators were successfully used to uncover new cellular functions of TRPM7 in situ including a crucial role of TRPM7 in Ca(2+) signaling and Ca(2+) dependent cellular processes. Hence, TRPM7 has been defined as a promising drug target. Here, we summarize the progress in this quickly developing field. Twit Text FOAVip Assessment of TRPM7 functions by drug-like small molecules ????Cell Calcium http://www.kidney.de/pget.php?&tw=1&pmid=28356194 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28356194 #FOAvip English Wikipedia <ref>{{Cite pmid|28356194}}</ref> Assessment of TRPM7 functions by drug-like small molecules #MMPMID28356194 Chubanov V; Ferioli S; Gudermann T Cell Calcium 2017[Nov]; 67 (ä): 166-173 PMID28356194show ga Transient receptor potential cation channel subfamily M member 7 (TRPM7) is a plasma membrane ion channel linked to a cytosolic protein kinase domain. Genetic inactivation of this bi-functional protein revealed its crucial role in Ca(2+) signalling, Mg(2+) metabolism, immune responses, cell motility, proliferation and differentiation. Malfunctions of TRPM7 are associated with anoxic neuronal death, cardiac fibrosis, tumour progression and macrothrombocytopenia. Recently, several groups have identified small organic compounds acting as inhibitors or activators of the TRPM7 channel. In follow-up studies, the identified TRPM7 modulators were successfully used to uncover new cellular functions of TRPM7 in situ including a crucial role of TRPM7 in Ca(2+) signaling and Ca(2+) dependent cellular processes. Hence, TRPM7 has been defined as a promising drug target. Here, we summarize the progress in this quickly developing field. |Animals[MESH] |Calcium Signaling[MESH] |Calcium/*metabolism[MESH] |Cell Death/drug effects[MESH] |Endomyocardial Fibrosis/drug therapy/*genetics/metabolism/pathology[MESH] |Gene Expression Regulation[MESH] |Genetic Diseases, X-Linked/drug therapy/genetics/metabolism/pathology[MESH] |Humans[MESH] |Hypoxia, Brain/drug therapy/*genetics/metabolism/pathology[MESH] |Magnesium/metabolism[MESH] |Mice[MESH] |Neoplasms/drug therapy/genetics/metabolism/pathology[MESH] |Neurons/cytology/metabolism/pathology[MESH] |Small Molecule Libraries/*pharmacology[MESH] |Structure-Activity Relationship[MESH] |TRPM Cation Channels/agonists/antagonists & inhibitors/*genetics/metabolism[MESH]Assessment of TRPM7 functions by drug-like small molecules (epmc).pdf DeepDyve Pubget Overpricing