Nicastrin knockdown in keratinocytes induces expression profiles for decreased expression of cell cycle genes and increases gene expression related to type I interferon response

Knockdown of nicastrin (NCSTN) in human keratinocytes (HEK001) and embryonic kidney cells (HEK293) resulted in exacerbated response to proinflammatory stimulus. Confirmed with genome editing NCSTN. Suggests that haploinsufficiency of NCSTN in familial hidradenitis suppurativa has an inflammatory etiology rather than being the result of recurrent bacterial infection.