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10.1074/jbc.M116.738138 http://scihub22266oqcxt.onion/10.1074/jbc.M116.738138 C5122777!5122777 !27758856     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27758856 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Biol+Chem 2016 ; 291 (48 ): 25096-25105 Nephropedia Template TP {{tp|p=27758856 |t=2016. Novel Antibody for the Treatment of Transthyretin Amyloidosis |pdf=|usr=}}{{27758856 }} gab.com Text Novel Antibody for the Treatment of Transthyretin Amyloidosis JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27758856 #FOAvip Familial amyloidotic polyneuropathy (FAP) is a systemic amyloidosis mainly caused by amyloidogenic transthyretin (ATTR). This incurable disease causes death ?10 years after onset. Although it has been widely accepted that conformational change of the monomeric form of transthyretin (TTR) is very important for amyloid formation and deposition in the organs, no effective therapy targeting this step is available. In this study, we generated a mouse monoclonal antibody, T24, that recognized the cryptic epitope of conformationally changed TTR. T24 inhibited TTR accumulation in FAP model rats, which expressed human ATTR V30M in various tissues and exhibited non-fibrillar deposits of ATTR in the gastrointestinal tracts. Additionally, humanized T24 (RT24) inhibited TTR fibrillation and promoted macrophage phagocytosis of aggregated TTR. This antibody did not recognize normal serum TTR functioning properly in the blood. These results demonstrate that RT24 would be an effective novel therapeutic antibody for FAP. Twit Text FOAVip Novel Antibody for the Treatment of Transthyretin Amyloidosis ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27758856 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27758856 #FOAvip English Wikipedia <ref>{{Cite pmid|27758856 }}</ref> Novel Antibody for the Treatment of Transthyretin Amyloidosis #MMPMID27758856 Hosoi A ; Su Y ; Torikai M ; Jono H ; Ishikawa D ; Soejima K ; Higuchi H ; Guo J ; Ueda M ; Suenaga G ; Motokawa H ; Ikeda T ; Senju S ; Nakashima T ; Ando Y J Biol Chem 2016[Nov]; 291 (48 ): 25096-25105 PMID27758856 show ga Familial amyloidotic polyneuropathy (FAP) is a systemic amyloidosis mainly caused by amyloidogenic transthyretin (ATTR). This incurable disease causes death ?10 years after onset. Although it has been widely accepted that conformational change of the monomeric form of transthyretin (TTR) is very important for amyloid formation and deposition in the organs, no effective therapy targeting this step is available. In this study, we generated a mouse monoclonal antibody, T24, that recognized the cryptic epitope of conformationally changed TTR. T24 inhibited TTR accumulation in FAP model rats, which expressed human ATTR V30M in various tissues and exhibited non-fibrillar deposits of ATTR in the gastrointestinal tracts. Additionally, humanized T24 (RT24) inhibited TTR fibrillation and promoted macrophage phagocytosis of aggregated TTR. This antibody did not recognize normal serum TTR functioning properly in the blood. These results demonstrate that RT24 would be an effective novel therapeutic antibody for FAP. |Amyloid Neuropathies, Familial/*drug therapy/*immunology/pathology [MESH] |Animals [MESH] |Antibodies, Monoclonal, Murine-Derived/*immunology/therapeutic use [MESH] |Female [MESH] |Humans [MESH] |Macrophages/*immunology/pathology [MESH] |Male [MESH] |Mice [MESH] |Phagocytosis/*drug effects [MESH] |Prealbumin/*immunology [MESH]Novel Antibody for the Treatment of Transthyretin Amyloidosis (epmc).pdf DeepDyve Pubget Overpricing