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10.1016/j.clim.2016.12.011 http://scihub22266oqcxt.onion/10.1016/j.clim.2016.12.011 C5346332!5346332!28062222     free     free     free       Clin+Immunol 2017 ; 176 (ä): 42-8 Nephropedia Template TP {{tp|p=28062222|t=2017. Absent in Melanoma 2 proteins in SLE |pdf=|usr=}}{{28062222}} gab.com Text Absent in Melanoma 2 proteins in SLE JO: Clin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28062222 #FOAvip Type I interferons (IFN-?/?)-inducible PYRIN and HIN domain-containing protein family includes Absent in Melanoma 2 (murine Aim2 and human AIM2), murine p202, and human PYRIN-only protein 3 (POP3). The generation of Aim2-deficient mice indicated that the Aim2 protein is essential for inflammasome activation, resulting in the secretion of interleukin-1? (IL-1?) and IL-18 and cell death by pyroptosis. Further, Aim2-deficiency also increased constitutive expression of the IFN-? and expression of the p202 protein. Notably, an increased expression of p202 protein in female mice associated with the development of systemic lupus erythematosus (SLE). SLE in patients is characterized by a constitutive increase in serum levels of IFN-? and an increase in the expression IFN-stimulated genes. Recent studies indicate that p202 and POP3 proteins inhibit activation of the Aim2/AIM2 inflammasome and promote IFN-? expression. Therefore, we discuss the role of Aim2/AIM2 proteins in the suppression of type I IFNs production and lupus susceptibility. Twit Text FOAVip Absent in Melanoma 2 proteins in SLE ????Clin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28062222 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28062222 #FOAvip English Wikipedia <ref>{{Cite pmid|28062222}}</ref> Absent in Melanoma 2 proteins in SLE #MMPMID28062222 Choubey D; Panchanathan R Clin Immunol 2017[Mar]; 176 (ä): 42-8 PMID28062222show ga Type I interferons (IFN-?/?)-inducible PYRIN and HIN domain-containing protein family includes Absent in Melanoma 2 (murine Aim2 and human AIM2), murine p202, and human PYRIN-only protein 3 (POP3). The generation of Aim2-deficient mice indicated that the Aim2 protein is essential for inflammasome activation, resulting in the secretion of interleukin-1? (IL-1?) and IL-18 and cell death by pyroptosis. Further, Aim2-deficiency also increased constitutive expression of the IFN-? and expression of the p202 protein. Notably, an increased expression of p202 protein in female mice associated with the development of systemic lupus erythematosus (SLE). SLE in patients is characterized by a constitutive increase in serum levels of IFN-? and an increase in the expression IFN-stimulated genes. Recent studies indicate that p202 and POP3 proteins inhibit activation of the Aim2/AIM2 inflammasome and promote IFN-? expression. Therefore, we discuss the role of Aim2/AIM2 proteins in the suppression of type I IFNs production and lupus susceptibility. äAbsent in Melanoma 2 proteins in SLE (epmc).pdf DeepDyve Pubget Overpricing