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10.1093/hmg/ddp392 http://scihub22266oqcxt.onion/10.1093/hmg/ddp392 C2766295!2766295!19692351     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hum+Mol+Genet 2009 ; 18 (22): 4367-75 Nephropedia Template TP {{tp|p=19692351|t=2009. Mice defective in Trpm6 show embryonic mortality and neural tube defects |pdf=|usr=}}{{19692351}} gab.com Text Mice defective in Trpm6 show embryonic mortality and neural tube defects JO: Hum Mol Genet http://www.kidney.de/pget.php?&tw=1&pmid=19692351 #FOAvip The syndrome of hypomagnesemia with secondary hypocalcemia is caused by defective TRPM6. This protein is an ion channel that also contains a kinase in its C-terminus. It is usually diagnosed in childhood and, without treatment with supplemental Mg, affected children suffer from mental retardation, seizures and retarded development. We developed a mouse lacking Trpm6 in order to understand in greater detail the function of this protein. In contrast to our expectations, Trpm6?/? mice almost never survived to weaning. Many mice died by embryonic day 12.5. Most that survived to term had neural tube defects consisting of both exencephaly and spina bifida occulta, an unusual combination. Feeding dams a high Mg diet marginally improved offspring survival to weaning. The few Trpm6?/? mice that survived were fertile but matings between Trpm6?/? mice produced no viable pregnancies. Trpm6+/? mice had normal electrolytes except for modestly low plasma [Mg]. In addition, some Trpm6+/? mice died prematurely. Absence of Trpm6 produces an apparently different phenotype in mice than in humans. The presence of neural tube defects identifies a previously unsuspected role of Trpm6 in effecting neural tube closure. This genetic defect produces one of very few mouse models of spina bifida occulta. These results point to a critical role of Trpm6 in development and suggest an important role in neural tube closure. Twit Text FOAVip Mice defective in Trpm6 show embryonic mortality and neural tube defects ????Hum Mol Genet http://www.kidney.de/pget.php?&tw=1&pmid=19692351 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19692351 #FOAvip English Wikipedia <ref>{{Cite pmid|19692351}}</ref> Mice defective in Trpm6 show embryonic mortality and neural tube defects #MMPMID19692351 Walder RY; Yang B; Stokes JB; Kirby PA; Cao X; Shi P; Searby CC; Husted RF; Sheffield VC Hum Mol Genet 2009[Nov]; 18 (22): 4367-75 PMID19692351show ga The syndrome of hypomagnesemia with secondary hypocalcemia is caused by defective TRPM6. This protein is an ion channel that also contains a kinase in its C-terminus. It is usually diagnosed in childhood and, without treatment with supplemental Mg, affected children suffer from mental retardation, seizures and retarded development. We developed a mouse lacking Trpm6 in order to understand in greater detail the function of this protein. In contrast to our expectations, Trpm6?/? mice almost never survived to weaning. Many mice died by embryonic day 12.5. Most that survived to term had neural tube defects consisting of both exencephaly and spina bifida occulta, an unusual combination. Feeding dams a high Mg diet marginally improved offspring survival to weaning. The few Trpm6?/? mice that survived were fertile but matings between Trpm6?/? mice produced no viable pregnancies. Trpm6+/? mice had normal electrolytes except for modestly low plasma [Mg]. In addition, some Trpm6+/? mice died prematurely. Absence of Trpm6 produces an apparently different phenotype in mice than in humans. The presence of neural tube defects identifies a previously unsuspected role of Trpm6 in effecting neural tube closure. This genetic defect produces one of very few mouse models of spina bifida occulta. These results point to a critical role of Trpm6 in development and suggest an important role in neural tube closure. äMice defective in Trpm6 show embryonic mortality and neural tube defec(epmc).pdf DeepDyve Pubget Overpricing