SLE non-coding genetic risk variant determines the epigenetic dysfunction of an immune cell specific enhancer that controls disease-critical microRNA expression - Hou, Guojun; Harley, Isaac T. W.; Lu, Xiaoming; Zhou, Tian; Xu, Ning; Yao, Chao; Qin, Yuting; Ouyang, Ye; Ma, Jianyang; Zhu, Xinyi; Yu, Xiang; Xu, Hong; et al. (Nature communications, 2021)
Keywords: 38/23; 38/39; 38/43; 38/47; 631/208/177; 631/208/199; 631/208/4041/3196; 631/250/38; 631/337/384/331; Animals; Autoimmune diseases; Case-Control Studies; Cell Line, Tumor; Chromatin; Chronic conditions; CRISPR; CRISPR-Cas Systems; Disease control; Enhancers; Epigenesis, Genetic - immunology; Epigenetics; Etiology; Female; Gene expression; Genetic diversity; Genetic Predisposition to Disease; Genetic variance; Genome editing; Genomes; Genomic analysis; Genomics; Genotyping Techniques; Health risk assessment; Health risks; Healthy Volunteers; HEK293 Cells; Humanities and Social Sciences; Humans; Immune system; Immunoregulation; Interferon; Interferon Type I - metabolism; Leukocytes, Mononuclear - transplantation; Lupus Erythematosus, Systemic - blood; Lupus Erythematosus, Systemic - genetics; Lupus Erythematosus, Systemic - immunology; Mice; MicroRNAs; MicroRNAs - genetics; MicroRNAs - metabolism; miRNA; multidisciplinary; NF-kappa B - metabolism; NF-κB protein; Non-coding RNA; Pathogenesis; Phenotypes; Polymorphism, Single Nucleotide; Primary Cell Culture; Promoter Regions, Genetic; Regulatory sequences; Regulatory Sequences, Nucleic Acid - genetics; Ribonucleic acid; Risk; RNA; RNA-Seq; Science; Science (multidisciplinary); Signal Transduction - genetics; Signal Transduction - immunology; Structural analysis; Systemic lupus erythematosus