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10.1002/dneu.22001 http://scihub22266oqcxt.onion/10.1002/dneu.22001 C3727165!3727165!22102510     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Dev+Neurobiol 2012 ; 72 (6): 865-77 Nephropedia Template TP {{tp|p=22102510|t=2012. Modulation of Transient Receptor Potential Melastatin Related 7 (TRPM7) Channel by Presenilins |pdf=|usr=}}{{22102510}} gab.com Text Modulation of Transient Receptor Potential Melastatin Related 7 (TRPM7) Channel by Presenilins JO: Dev Neurobiol http://www.kidney.de/pget.php?&tw=1&pmid=22102510 #FOAvip Presenilins (PS1 and PS2) are multi-functional proteins involved in a diverse array of molecular and cellular functions, including proteolysis, development, neurogenesis, synaptic plasticity, ion channel regulation and phospholipid metabolism. Mutations in presenilin genes are responsible for the majority of Familial Alzheimer disease (FAD). Consequently, FAD-associated mutations in genes encoding PS1 or PS2 lead to several key cellular phenotypes, including alterations in proteolysis of ?-amyloid precursor protein (APP) and Ca2+ entry. The mechanism underlying presenilin (PS)-mediated modulation of Ca2+ entry remains to be determined. Our previous studies showed that the PS-dependent down-regulation of phosphatidylinositol-4,5-bisphosphate (PIP2) is attributable to the observed Ca2+ deficits. In this study, we attempted to identify the ion channel that is subject to the PIP2 and PS-dependent modulation. We found that Ca2+ or Zn2+ entry via the transient receptor potential melastatin 7 (TRPM7) channel was attenuated by the presence of FAD-associated PS1 mutants, such as ?E9 and L286V. TRPM7 has been implicated in Mg2+ homeostasis and embryonic development. The intracellular delivery of PIP2 restored TRPM7-mediated Ca2+ influx, indicating that the observed deficits in Ca2+ entry are due to down-regulation of PIP2. Conversely, PS1 and PS2 deficiency, previously shown to up-regulate PIP2 levels, potentiated TRPM7-mediated Ca2+ influx. PS-dependent changes in Ca2+ influx could be neutralized by a TRPM7 channel blocker. Collectively, these results indicate that TRPM7 may underlie the Ca2+ entry deficits observed in FAD-associated PS mutants and suggest that the normal function of PS involves regulation of TRPM7 through a PIP2-dependent mechanism. Twit Text FOAVip Modulation of Transient Receptor Potential Melastatin Related 7 (TRPM7) Channel by Presenilins ????Dev Neurobiol http://www.kidney.de/pget.php?&tw=1&pmid=22102510 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22102510 #FOAvip English Wikipedia <ref>{{Cite pmid|22102510}}</ref> Modulation of Transient Receptor Potential Melastatin Related 7 (TRPM7) Channel by Presenilins #MMPMID22102510 Oh HG; Chun YS; Kim Y; Youn SH; Shin S; Park MK; Kim TW; Chung S Dev Neurobiol 2012[Jun]; 72 (6): 865-77 PMID22102510show ga Presenilins (PS1 and PS2) are multi-functional proteins involved in a diverse array of molecular and cellular functions, including proteolysis, development, neurogenesis, synaptic plasticity, ion channel regulation and phospholipid metabolism. Mutations in presenilin genes are responsible for the majority of Familial Alzheimer disease (FAD). Consequently, FAD-associated mutations in genes encoding PS1 or PS2 lead to several key cellular phenotypes, including alterations in proteolysis of ?-amyloid precursor protein (APP) and Ca2+ entry. The mechanism underlying presenilin (PS)-mediated modulation of Ca2+ entry remains to be determined. Our previous studies showed that the PS-dependent down-regulation of phosphatidylinositol-4,5-bisphosphate (PIP2) is attributable to the observed Ca2+ deficits. In this study, we attempted to identify the ion channel that is subject to the PIP2 and PS-dependent modulation. We found that Ca2+ or Zn2+ entry via the transient receptor potential melastatin 7 (TRPM7) channel was attenuated by the presence of FAD-associated PS1 mutants, such as ?E9 and L286V. TRPM7 has been implicated in Mg2+ homeostasis and embryonic development. The intracellular delivery of PIP2 restored TRPM7-mediated Ca2+ influx, indicating that the observed deficits in Ca2+ entry are due to down-regulation of PIP2. Conversely, PS1 and PS2 deficiency, previously shown to up-regulate PIP2 levels, potentiated TRPM7-mediated Ca2+ influx. PS-dependent changes in Ca2+ influx could be neutralized by a TRPM7 channel blocker. Collectively, these results indicate that TRPM7 may underlie the Ca2+ entry deficits observed in FAD-associated PS mutants and suggest that the normal function of PS involves regulation of TRPM7 through a PIP2-dependent mechanism. äModulation of Transient Receptor Potential Melastatin Related 7 (TRPM7(epmc).pdf DeepDyve Pubget Overpricing