Chenfu Shi

Identification of causal genes and mechanisms by which genetic variation mediates juvenile idiopathic arthritis susceptibility using functional genomics and CRISPR-Cas9

This study identifies causal genes and mechanisms for juvenile idiopathic arthritis by integrating GWAS, PCHi-C, ATAC-seq, and CRISPRa/i in CD4+ T cells from JIA patients.

Dissection of a non-coding risk locus at 1p36.23 identifies ERRFI1 as a novel gene in the pathogenesis of psoriasis and psoriatic arthritis

The paper identifies ERRFI1 as a novel gene involved in psoriasis and psoriatic arthritis by showing its regulation by a non-coding risk variant at 1p36.23 through enhancer activity in keratinocytes.

Germline intergenic duplications at Xq26.1 underlie Bazex-Dupre-Christol syndrome, an inherited basal cell carcinoma susceptibility condition

The paper identifies intergenic duplications at Xq26.1 as the genetic cause of Bazex-Dupre-Christol syndrome, linking them to ARHGAP36 dysregulation and BCC susceptibility.

An active chromatin interactome in relevant cell lines elucidates biological mechanisms at genetic risk loci for dermatological traits

The paper identifies gene targets at risk loci for skin-related disorders by integrating HiChIP data from relevant cell lines and public datasets.

Exploring the overlap between rheumatoid arthritis susceptibility loci and long non-coding RNA annotations

The paper investigates the overlap between RA susceptibility loci and lncRNA annotations, finding that immune-enriched lncRNA show a small but significant enrichment among RA variants.

HiChIP-Peaks: A HiChIP peak calling algorithm

HiChIP-Peaks improves HiChIP peak calling by focusing on re-ligation sites, enhancing reliability and enabling differential peak analysis across samples.

Chromatin-based techniques map DNA interaction landscapes in psoriasis susceptibility loci and highlight KLF4 as a target gene in 9q31

This study uses Capture Hi-C and CRISPR activation to identify KLF4 as a target gene in the 9q31 psoriasis risk locus, linking GWAS variants to functional interactions.