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10.1007/s00726-010-0773-2 http://scihub22266oqcxt.onion/10.1007/s00726-010-0773-2 20957395!3062728!20957395     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Amino+Acids 2012 ; 42 (4): 1151-61 Nephropedia Template TP {{tp|p=20957395|t=2012. Advanced glycation endproducts: from precursors to RAGE: round and round we go |pdf=|usr=}}{{20957395}} gab.com Text Advanced glycation endproducts: from precursors to RAGE: round and round we go JO: Amino Acids http://www.kidney.de/pget.php?&tw=1&pmid=20957395 #FOAvip The formation of advanced glycation endproducts (AGEs) occurs in diverse settings such as diabetes, aging, renal failure, inflammation and hypoxia. The chief cellular receptor for AGEs, RAGE, transduces the effects of AGEs via signal transduction, at least in part via processes requiring the RAGE cytoplasmic domain binding partner, diaphanous-1 or mDia1. Data suggest that RAGE perpetuates the inflammatory signals initiated by AGEs via multiple mechanisms. AGE-RAGE interaction stimulates generation of reactive oxygen species and inflammation--mechanisms which enhance AGE formation. Further, recent data in type 1 diabetic kidney reveal that deletion of RAGE prevents methylglyoxal accumulation, at least in part via RAGE-dependent regulation of glyoxalase-1, a major enzyme involved in methylglyoxal detoxification. Taken together, these considerations place RAGE in the center of biochemical and molecular stresses that characterize the complications of diabetes and chronic disease. Stopping RAGE-dependent signaling may hold the key to interrupting cycles of cellular perturbation and tissue damage in these disorders. Twit Text FOAVip Advanced glycation endproducts: from precursors to RAGE: round and round we go ????Amino Acids http://www.kidney.de/pget.php?&tw=1&pmid=20957395 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20957395 #FOAvip English Wikipedia <ref>{{Cite pmid|20957395}}</ref> Advanced glycation endproducts: from precursors to RAGE: round and round we go #MMPMID20957395 Ramasamy R; Yan SF; Schmidt AM Amino Acids 2012[Apr]; 42 (4): 1151-61 PMID20957395show ga The formation of advanced glycation endproducts (AGEs) occurs in diverse settings such as diabetes, aging, renal failure, inflammation and hypoxia. The chief cellular receptor for AGEs, RAGE, transduces the effects of AGEs via signal transduction, at least in part via processes requiring the RAGE cytoplasmic domain binding partner, diaphanous-1 or mDia1. Data suggest that RAGE perpetuates the inflammatory signals initiated by AGEs via multiple mechanisms. AGE-RAGE interaction stimulates generation of reactive oxygen species and inflammation--mechanisms which enhance AGE formation. Further, recent data in type 1 diabetic kidney reveal that deletion of RAGE prevents methylglyoxal accumulation, at least in part via RAGE-dependent regulation of glyoxalase-1, a major enzyme involved in methylglyoxal detoxification. Taken together, these considerations place RAGE in the center of biochemical and molecular stresses that characterize the complications of diabetes and chronic disease. Stopping RAGE-dependent signaling may hold the key to interrupting cycles of cellular perturbation and tissue damage in these disorders. |Animals[MESH] |Disease/etiology[MESH] |Glycation End Products, Advanced/*metabolism[MESH] |Glycosylation[MESH] |Humans[MESH] |Receptor for Advanced Glycation End Products[MESH] |Receptors, Immunologic/*metabolism[MESH]Advanced glycation endproducts: from precursors to RAGE: round and rou(epmc).pdf DeepDyve Pubget Overpricing