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10.1016/j.heliyon.2015.e00046 http://scihub22266oqcxt.onion/10.1016/j.heliyon.2015.e00046 26705539!4685751!26705539     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26705539&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Heliyon 2015 ; 1 (4): e00046 Nephropedia Template TP {{tp|p=26705539|t=2015. Mesendogen, a novel inhibitor of TRPM6, promotes mesoderm and definitive endoderm differentiation of human embryonic stem cells through alteration of magnesium homeostasis |pdf=|usr=}}{{26705539}} gab.com Text Mesendogen, a novel inhibitor of TRPM6, promotes mesoderm and definitive endoderm differentiation of human embryonic stem cells through alteration of magnesium homeostasis JO: Heliyon http://www.kidney.de/pget.php?&tw=1&pmid=26705539 #FOAvip The homo- and hetero-tetrameric channel complexes formed by transient receptor potential cation channel, subfamily M, member 6 (TRPM6) and 7 (TRPM7) (collectively referred to as TRPM6/TRPM7 channels in this study) are the major regulators of cellular magnesium uptake, yet the exact roles of TRPM6/TRPM7 channels and cellular magnesium homeostasis during development are poorly understood. Here, we report a novel small molecule Mesendogen (MEG) which robustly induces nearly homogeneous (>/=85%) mesoderm and definitive endoderm (DE) differentiations of human embryonic stem cells (hESCs) in combination with growth factors. A kinome screen followed by loss-of-function experiments identified TRPM6 as the biological target of MEG. We demonstrated that MEG functions by inhibiting TRPM6/TRPM7 magnesium channel activity, as MEG reduced intracellular magnesium level, while TRPM6/TRPM7 channel modulation and magnesium-withdrawal phenocopied MEG at enhancing mesoderm and DE differentiations. This study discovers a robust chemical enhancer of hESC directed differentiation, and uncovers a novel regulatory role of cellular magnesium homeostasis during early embryonic cell fate specification. Twit Text FOAVip Mesendogen, a novel inhibitor of TRPM6, promotes mesoderm and definitive endoderm differentiation of human embryonic stem cells through alteration of magnesium homeostasis ????Heliyon http://www.kidney.de/pget.php?&tw=1&pmid=26705539 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26705539 #FOAvip English Wikipedia <ref>{{Cite pmid|26705539}}</ref> Mesendogen, a novel inhibitor of TRPM6, promotes mesoderm and definitive endoderm differentiation of human embryonic stem cells through alteration of magnesium homeostasis #MMPMID26705539 Geng Y; Feng B Heliyon 2015[Dec]; 1 (4): e00046 PMID26705539show ga The homo- and hetero-tetrameric channel complexes formed by transient receptor potential cation channel, subfamily M, member 6 (TRPM6) and 7 (TRPM7) (collectively referred to as TRPM6/TRPM7 channels in this study) are the major regulators of cellular magnesium uptake, yet the exact roles of TRPM6/TRPM7 channels and cellular magnesium homeostasis during development are poorly understood. Here, we report a novel small molecule Mesendogen (MEG) which robustly induces nearly homogeneous (>/=85%) mesoderm and definitive endoderm (DE) differentiations of human embryonic stem cells (hESCs) in combination with growth factors. A kinome screen followed by loss-of-function experiments identified TRPM6 as the biological target of MEG. We demonstrated that MEG functions by inhibiting TRPM6/TRPM7 magnesium channel activity, as MEG reduced intracellular magnesium level, while TRPM6/TRPM7 channel modulation and magnesium-withdrawal phenocopied MEG at enhancing mesoderm and DE differentiations. This study discovers a robust chemical enhancer of hESC directed differentiation, and uncovers a novel regulatory role of cellular magnesium homeostasis during early embryonic cell fate specification. ?Mesendogen, a novel inhibitor of TRPM6, promotes mesoderm and definiti(epmc).pdf DeepDyve Pubget Overpricing