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10.1074/jbc.RA120.013277 http://scihub22266oqcxt.onion/10.1074/jbc.RA120.013277 32439805!7380176!32439805     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Biol+Chem 2020 ; 295 (29): 9879-9892 Nephropedia Template TP {{tp|p=32439805|t=2020. The magnesium transporter NIPAL1 is a pancreatic islet-expressed protein that conditionally impacts insulin secretion |pdf=|usr=}}{{32439805}} gab.com Text The magnesium transporter NIPAL1 is a pancreatic islet-expressed protein that conditionally impacts insulin secretion JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=32439805 #FOAvip Type 2 diabetes is a chronic metabolic disease characterized by pancreatic beta-cell dysfunction and peripheral insulin resistance. Among individuals with type 2 diabetes, approximately 30% exhibit hypomagnesemia. Hypomagnesemia has been linked to insulin resistance through reduced tyrosine kinase activity of the insulin receptor; however, its impact on pancreatic beta-cell function is unknown. In this study, through analysis of several single-cell RNA-sequencing data sets in tandem with quantitative PCR validation in both murine and human islets, we identified NIPAL1 (NIPA-like domain containing 1), encoding a magnesium influx transporter, as an islet-enriched gene. A series of immunofluorescence experiments confirmed NIPAL1's magnesium-dependent expression and that it specifically localizes to the Golgi in Min6-K8 cells, a pancreatic beta-cell-like cell line (mouse insulinoma 6 clone K8). Under varying magnesium concentrations, NIPAL1 knockdown decreased both basal insulin secretion and total insulin content; in contrast, its overexpression increased total insulin content. Although the expression, distribution, and magnesium responsiveness of NIPAL1 in alpha-TC6 glucagonoma cells (a pancreatic alpha-cell line) were similar to the observations in Min6-K8 cells, no effect was observed on glucagon secretion in alpha-TC6 cells under the conditions studied. Overall, these results suggest that NIPAL1 expression is regulated by extracellular magnesium and that down-regulation of this transporter decreases glucose-stimulated insulin secretion and intracellular insulin content, particularly under conditions of hypomagnesemia. Twit Text FOAVip The magnesium transporter NIPAL1 is a pancreatic islet-expressed protein that conditionally impacts insulin secretion ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=32439805 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32439805 #FOAvip English Wikipedia <ref>{{Cite pmid|32439805}}</ref> The magnesium transporter NIPAL1 is a pancreatic islet-expressed protein that conditionally impacts insulin secretion #MMPMID32439805 Manialawy Y; Khan SR; Bhattacharjee A; Wheeler MB J Biol Chem 2020[Jul]; 295 (29): 9879-9892 PMID32439805show ga Type 2 diabetes is a chronic metabolic disease characterized by pancreatic beta-cell dysfunction and peripheral insulin resistance. Among individuals with type 2 diabetes, approximately 30% exhibit hypomagnesemia. Hypomagnesemia has been linked to insulin resistance through reduced tyrosine kinase activity of the insulin receptor; however, its impact on pancreatic beta-cell function is unknown. In this study, through analysis of several single-cell RNA-sequencing data sets in tandem with quantitative PCR validation in both murine and human islets, we identified NIPAL1 (NIPA-like domain containing 1), encoding a magnesium influx transporter, as an islet-enriched gene. A series of immunofluorescence experiments confirmed NIPAL1's magnesium-dependent expression and that it specifically localizes to the Golgi in Min6-K8 cells, a pancreatic beta-cell-like cell line (mouse insulinoma 6 clone K8). Under varying magnesium concentrations, NIPAL1 knockdown decreased both basal insulin secretion and total insulin content; in contrast, its overexpression increased total insulin content. Although the expression, distribution, and magnesium responsiveness of NIPAL1 in alpha-TC6 glucagonoma cells (a pancreatic alpha-cell line) were similar to the observations in Min6-K8 cells, no effect was observed on glucagon secretion in alpha-TC6 cells under the conditions studied. Overall, these results suggest that NIPAL1 expression is regulated by extracellular magnesium and that down-regulation of this transporter decreases glucose-stimulated insulin secretion and intracellular insulin content, particularly under conditions of hypomagnesemia. |*Insulin Secretion[MESH] |Animals[MESH] |Cation Transport Proteins/*biosynthesis/genetics[MESH] |Cell Line, Tumor[MESH] |Gene Expression Regulation[MESH] |Glucagon-Secreting Cells/cytology/metabolism[MESH] |Insulin-Secreting Cells/cytology/*metabolism[MESH] |Magnesium/*metabolism[MESH] |Male[MESH]The magnesium transporter NIPAL1 is a pancreatic islet-expressed prote(epmc).pdf DeepDyve Pubget Overpricing