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10.1172/JCI90699 http://scihub22266oqcxt.onion/10.1172/JCI90699 C5707143!5707143!29130929     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 269.2 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\29130929.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Clin+Invest ä ; 127 (12): 4488-97 Nephropedia Template TP {{tp|p=29130929|t=ä. TNF regulates transcription of NLRP3 inflammasome components and inflammatory molecules in cryopyrinopathies |pdf=|usr=}}{{29130929}} gab.com Text TNF regulates transcription of NLRP3 inflammasome components and inflammatory molecules in cryopyrinopathies JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=29130929 #FOAvip The NLRP3 inflammasome is a protein complex responsible for caspase-1?dependent maturation of the proinflammatory cytokines IL-1? and IL-18. Gain-of-function missense mutations in NLRP3 cause the disease spectrum known as the cryopyrin-associated periodic syndromes (CAPS). In this study, we generated Nlrp3-knockin mice on various KO backgrounds including Il1b/Il18-, caspase-1?, caspase-11? (Casp1/11-), and Tnf-deficient strains. The Nlrp3L351PIl1b?/?Il18?/? mutant mice survived and grew normally until adulthood and, at 6 months of age, exhibited marked splenomegaly and leukophilia. Injection of these mice with low-dose LPS resulted in elevated serum TNF levels compared with Nlrp3L351PCasp1/11?/? mice and Il1b?/?Il18?/? littermates. Treatment of Nlrp3A350V mice with the TNF inhibitor etanercept resulted in all pups surviving to adulthood, with normal body and spleen/body weight ratios. Nlrp3A350VTnf?/? mice showed a similar phenotypic rescue, with marked reductions in serum IL-1? and IL-18, reduced myeloid inflammatory infiltrate in the skin and spleen, and substantial decreases in splenic mRNA expression of both inflammasome components (Nlrp3, Pycard, pro-Casp1) and pro-cytokines (Il1b, Il18). Likewise, we observed a reduction in the expression of both pro-Casp1 and pro-Il1b in cultured Nlrp3A350VTnf?/? BM-derived DCs. Our data show that TNF is an important transcriptional regulator of NLRP3 inflammasome components in murine inflammasomopathies. Moreover, these results may have therapeutic implications for CAPS patients with partial responses to IL-1?targeted therapies. Twit Text FOAVip TNF regulates transcription of NLRP3 inflammasome components and inflammatory molecules in cryopyrinopathies ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=29130929 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29130929 #FOAvip English Wikipedia <ref>{{Cite pmid|29130929}}</ref> TNF regulates transcription of NLRP3 inflammasome components and inflammatory molecules in cryopyrinopathies #MMPMID29130929 McGeough MD; Wree A; Inzaugarat ME; Haimovich A; Johnson CD; Peña CA; Goldbach-Mansky R; Broderick L; Feldstein AE; Hoffman HM J Clin Invest ä[]; 127 (12): 4488-97 PMID29130929show ga The NLRP3 inflammasome is a protein complex responsible for caspase-1?dependent maturation of the proinflammatory cytokines IL-1? and IL-18. Gain-of-function missense mutations in NLRP3 cause the disease spectrum known as the cryopyrin-associated periodic syndromes (CAPS). In this study, we generated Nlrp3-knockin mice on various KO backgrounds including Il1b/Il18-, caspase-1?, caspase-11? (Casp1/11-), and Tnf-deficient strains. The Nlrp3L351PIl1b?/?Il18?/? mutant mice survived and grew normally until adulthood and, at 6 months of age, exhibited marked splenomegaly and leukophilia. Injection of these mice with low-dose LPS resulted in elevated serum TNF levels compared with Nlrp3L351PCasp1/11?/? mice and Il1b?/?Il18?/? littermates. Treatment of Nlrp3A350V mice with the TNF inhibitor etanercept resulted in all pups surviving to adulthood, with normal body and spleen/body weight ratios. Nlrp3A350VTnf?/? mice showed a similar phenotypic rescue, with marked reductions in serum IL-1? and IL-18, reduced myeloid inflammatory infiltrate in the skin and spleen, and substantial decreases in splenic mRNA expression of both inflammasome components (Nlrp3, Pycard, pro-Casp1) and pro-cytokines (Il1b, Il18). Likewise, we observed a reduction in the expression of both pro-Casp1 and pro-Il1b in cultured Nlrp3A350VTnf?/? BM-derived DCs. Our data show that TNF is an important transcriptional regulator of NLRP3 inflammasome components in murine inflammasomopathies. Moreover, these results may have therapeutic implications for CAPS patients with partial responses to IL-1?targeted therapies. äTNF regulates transcription of NLRP3 inflammasome components and infla(epmc).pdf DeepDyve Pubget Overpricing