Helen F. Ray-Jones

The paper investigates the chromosomal contacts of poised enhancers during the transition from naive to primed human pluripotency, revealing their dynamics and functional significance.

The paper combines natural and engineered genetic variation to identify 22 non-coding variants affecting haematological traits and shows how a CUX1 variant impacts megakaryopoiesis.

The paper identifies trimodal QTLs that jointly affect enhancer accessibility, promoter contacts, and gene expression in monocytes, revealing genetic links between enhancer activity and chromatin boundaries.

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.

The paper maps promoter interactions in human ILC3s using PCHi-C and links GWAS risk variants to target genes, identifying new autoimmune disease risk genes.

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

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.