Jonathan Dyer

Department of Dermatology, University of Missouri School of Medicine, United States of America

Any competing interests declared are displayed with individual evaluations.

Faculty Member: Dermatology > Pediatric Skin Diseases (inc. Genetic Diseases) (since 25 May 2006)

All recent recommendations

• 3.0
  Oncostatin M receptor-beta mutations underlie familial primary localized cutaneous amyloidosis.
  Recommended by Jonathan Dyer
  
• 6.7
  Impaired T(H)17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome.
  Recommended by Joseph Mizgerd, Lars Rogge, Jonathan Dyer, Michelle Lowes with Kristine E Nograles
  
• 3.0
  Fabry disease and the skin: data from FOS, the Fabry outcome survey.
  Recommended by Jonathan Dyer
  
• 3.0
  Mutations in X-linked PORCN, a putative regulator of Wnt signaling, cause focal dermal hypoplasia.
  Recommended by Jonathan Dyer
  
• 3.0
  Deficiency of PORCN, a regulator of Wnt signaling, is associated with focal dermal hypoplasia.
  Recommended by Jonathan Dyer
  
• 3.0
  Mosaicism of activating FGFR3 mutations in human skin causes epidermal nevi.
  Recommended by Jonathan Dyer