マツイ　タケシ   Takeshi Matsui   松井　毅    所属   応用生物学部 応用生物学科    職種   教授
言語種別	英語
発行・発表の年月	2012
形態種別	学術論文
査読	査読あり
標題	Mutations in the SASPase gene (ASPRV1) are not associated with atopic eczema or clinically dry skin
執筆形態	共著
掲載誌名	Journal of Investigative Dermatology
掲載区分	国外
巻・号・頁	132,pp.1507-1510
担当区分	最終著者
国際共著	国際共著
著者・共著者	Aileen Sandilands, Sara J. Brown, Christabelle S. Goh, Elizabeth Pohler, Neil J. Wilson, Linda E. Campbell, Kenichi Miyamoto, Akiharu Kubo, Alan D. Irvine, Fatema Thawer-Esmail, Colin S. Munro, W.H. Irwin McLean, Jun Kudoh, Masayuki Amagai, Takeshi Matsui
概要	A key event during epidermal differentiation is the proteolytic breakdown of profilaggrin into “free” filaggrin monomers. A recent study has shown that the skin specific retroviral-like aspartic protease (SASPase) plays a key role in profilaggrin-filaggrin processing. SASPase cleaves the linker peptide between the individual filaggrin monomers of profilaggrin and on a hairless mouse background, loss of SASPase leads to dry, scaly skin with reduced stratum corneum hydration accompanied by accumulations of profilaggrin-filaggrin intermediates but an absence of filaggrin monomers. In this same study several missense mutations in the SASPase gene in atopic eczema patients and controls were identified, some of which were shown to have a detrimental effect on the ability of SASPase to cleave the profilaggrin linker peptide. Given the important role of filaggrin in skin barrier function and maintaining stratum corneum hydration, these results prompted us to question whether aberrant profilaggrin-filaggrin processing due to altered SASPase activity could provide an alternative pathogenic mechanism for atopic eczema or clinically dry skin.