susceptibility

[키워드] 3′ UTR 3′UTR activate affecting African Americans allelic Americans Antigen Asian Asians association Author Autoimmune Autoimmune disease binding binding site C allele C-allele carriers conducted contributed Control copy number correlated debilitating autoimmune disease decrease Degradation dose-dependent downregulated driven by duplication elevated Epigenetic European Evidence exhibited exhibiting expression functional G allele G-allele genomic greater HEK-293 HEK-293 cell HEK-293 cells Human identify IFN IFN-α pathway increased risk independent individual innate immune activation lack led to luciferase luciferase activity Lupus lupus erythematosus lupus-like disease mechanism microRNA microRNA-3148 microRNA–gene miR-3148 modulation mononuclear cell mononuclear cells mRNA murine model non-risk allele non-risk C allele nuclear nucleotide Odds ratio overexpression Pathways PBMC PBMCs Peripheral blood Peripheral blood mononuclear cells polymorphism predicted promote Protein protein level provide R 2 reduction regulate Regulatory reported reporter reporter gene respond resulting risk sequence signaling pathways significantly increased single nucleotide Single nucleotide polymorphism SLE SLE patient SLE patients SNP subject susceptibility systemic systemic lupus erythematosus the strongest These data TLR7 TLR7 gene TLR7 mRNA TLR7-TLR8 region TLR7/8/9 TLRs Toll-like receptor toll-like receptor 7 Toll-like receptors transcript transcript level transcripts transfected cells type I interferon UTR variant Variation while
[DOI] 10.1371/journal.pgen.1003336 PMC 바로가기 [Article Type] Research Article