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- W4313356667 abstract "Abstract Genetic variants near gene ETS1 have been associated with Systemic Lupus Erythematosus (SLE) in independent cohorts of Asian ancestry. ETS1 is a critical driver of immune cell function and differentiation, and mice deficient in ETS1 develop an SLE-like autoimmunity. We performed a fine-mapping study of 14,551 subjects using multi-ancestral cohorts, starting with genotyped variants and imputing to all common variants spanning the ETS1 locus. By constructing genetic models using frequentist and Bayesian association methods, we identified a set of 16 variants that are statistically most likely to be causal. We functionally assessed each of these variants based on their biological function predictions. Of the four variants that we experimentally examined, only rs6590330 differentially binds lysate from B cells. Using mass spectrometry, we found increased binding of the transcription factor signal transducer and activator of transcription 1 (STAT1) to DNA near the risk allele of rs6590330 compared to the non-risk allele. Western blot analysis and chromatin immunoprecipitation of pSTAT1 in B cells heterozygous for rs6590330 confirmed that the risk allele increased binding to the active form of STAT1. eQTL analysis indicates that the risk allele of rs6590330 is only associated with decreased ETS1 expression in Han Chinese. We propose a model in which the risk allele of rs6590330 increases SLE risk by enhancing the binding of pSTAT1, resulting in repression of the ETS1 expression." @default.
- W4313356667 created "2023-01-06" @default.
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- W4313356667 date "2015-05-01" @default.
- W4313356667 modified "2023-09-28" @default.
- W4313356667 title "Lupus risk-variant increases pSTAT1 binding and decreases ETS1 expression (BA4P.137)" @default.
- W4313356667 doi "https://doi.org/10.4049/jimmunol.194.supp.47.17" @default.
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