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10.1152/ajpendo.00289.2015 http://scihub22266oqcxt.onion/10.1152/ajpendo.00289.2015 C4835944!4835944!26884383     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 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       Am+J+Physiol+Endocrinol+Metab 2016 ; 310 (8): E612-23 Nephropedia Template TP {{tp|p=26884383|t=2016. Direct regulation of IGF-binding protein 1 promoter by interleukin-1? via an insulin- and FoxO-1-independent mechanism |pdf=|usr=}}{{26884383}} gab.com Text Direct regulation of IGF-binding protein 1 promoter by interleukin-1 via an insulin- and FoxO-1-independent mechanism JO: Am J Physiol Endocrinol Metab http://www.kidney.de/pget.php?&tw=1&pmid=26884383 #FOAvip The level of insulin-like growth factor-binding protein 1 (IGFBP1), a liver-produced serum protein that regulates insulin-like growth factor-I bioactivity, glucose homeostasis, and tissue regeneration, increases during inflammation. This manuscript describes a novel pathway for the regulation of hepatic IGFBP1 mRNA and protein levels by interleukin (IL)-1?. Experiments with the luciferase reporter system show that IL-1? stimulates transcriptional activity from the 1-kb promoter region of IGFBP1. Although IL-1? stimulation suppresses the insulin activation of protein kinase B, the major upstream regulator of IGFBP1 mRNA transcription, the induction of IGFBP1 by IL-1? did not require an intact insulin response element. Furthermore, neither overexpression nor silencing of FoxO-1 had any effect on the IL-1?-induced increase in IGFBP1 mRNA levels and promoter activity. However, inhibition of the ERK MAP kinases effectively prevented the IL-1? effects. Inhibition of neutral sphingomyelinase, a key player in the IL-1? signaling cascade that acts upstream of ERK, also suppressed the IL-1? effects, while increasing the ceramide, through the addition of C2-ceramide or via treatment with exogenous sphingomyelinase, was sufficient to induce IGFBP1 promoter-driven luciferase activity. Studies in primary rat hepatocytes where the levels of neutral sphingomyelinase were either elevated or suppressed using adenoviral constructs affirmed the key role of neutral sphingomyelinase and ceramide (exerted likely through ERK activation) in the IL-1?-induced IGFBP1 production. Finally, the IL-1? effects on IGFBP1 mRNA production and protein secretion could be abolished by the addition of insulin, either at very late time points or at very high doses. Twit Text FOAVip Direct regulation of IGF-binding protein 1 promoter by interleukin-1 via an insulin- and FoxO-1-independent mechanism ????Am J Physiol Endocrinol Metab http://www.kidney.de/pget.php?&tw=1&pmid=26884383 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26884383 #FOAvip English Wikipedia <ref>{{Cite pmid|26884383}}</ref> Direct regulation of IGF-binding protein 1 promoter by interleukin-1? via an insulin- and FoxO-1-independent mechanism #MMPMID26884383 Shi L; Banerjee D; Dobierzewska A; Sathishkumar S; Karakashian AA; Giltiay NV; Nikolova-Karakashian MN Am J Physiol Endocrinol Metab 2016[Apr]; 310 (8): E612-23 PMID26884383show ga The level of insulin-like growth factor-binding protein 1 (IGFBP1), a liver-produced serum protein that regulates insulin-like growth factor-I bioactivity, glucose homeostasis, and tissue regeneration, increases during inflammation. This manuscript describes a novel pathway for the regulation of hepatic IGFBP1 mRNA and protein levels by interleukin (IL)-1?. Experiments with the luciferase reporter system show that IL-1? stimulates transcriptional activity from the 1-kb promoter region of IGFBP1. Although IL-1? stimulation suppresses the insulin activation of protein kinase B, the major upstream regulator of IGFBP1 mRNA transcription, the induction of IGFBP1 by IL-1? did not require an intact insulin response element. Furthermore, neither overexpression nor silencing of FoxO-1 had any effect on the IL-1?-induced increase in IGFBP1 mRNA levels and promoter activity. However, inhibition of the ERK MAP kinases effectively prevented the IL-1? effects. Inhibition of neutral sphingomyelinase, a key player in the IL-1? signaling cascade that acts upstream of ERK, also suppressed the IL-1? effects, while increasing the ceramide, through the addition of C2-ceramide or via treatment with exogenous sphingomyelinase, was sufficient to induce IGFBP1 promoter-driven luciferase activity. Studies in primary rat hepatocytes where the levels of neutral sphingomyelinase were either elevated or suppressed using adenoviral constructs affirmed the key role of neutral sphingomyelinase and ceramide (exerted likely through ERK activation) in the IL-1?-induced IGFBP1 production. Finally, the IL-1? effects on IGFBP1 mRNA production and protein secretion could be abolished by the addition of insulin, either at very late time points or at very high doses. äDirect regulation of IGF-binding protein 1 promoter by interleukin-1? (epmc).pdf DeepDyve Pubget Overpricing