1. Insight from the Air–Skin Interface
Ryan F.L. O'Shaughnessy, Sara J. Brown 
Journal of Investigative Dermatology 
Volume 135, Issue 2, Pages (February 2015)
DOI: /jid
Copyright © 2015 The Society for Investigative Dermatology, Inc Terms and Conditions

2. Figure 1
Simplified schematic of the hypoxia-inducible factor (HIF) pathway. In normoxic conditions, oxygen (O2) permeates the tissues and activates prolyl hydroxylases (PHDs) to hydroxylate HIF-1α. This allows recognition of HIF-1α by the Von Hippel–Lindau tumor suppressor (VHL), a ubiquitin ligase, which targets HIF-1α for degradation. In hypoxic conditions, such as those experienced by the epidermis, HIF-1α is free to enter the nucleus, where it associates with HIF-2α and the aryl hydrocarbon receptor nuclear translocator protein (ARNT). This transcription complex, the hypoxia-induced factor, then activates transcription by binding to hypoxia response elements (HREs), in the promoters of genes related to controlling oxygen transport, such as erythropoietin (EPO) and the vascular endothelial growth factor (VEGF). In keratinocytes, the complex activates transcription of filaggrin (FLG) and potentially other genes involved in epidermal terminal differentiation and barrier function.
Journal of Investigative Dermatology  , DOI: ( /jid )
Copyright © 2015 The Society for Investigative Dermatology, Inc Terms and Conditions

3. Journal of Investigative Dermatology 2015 135, 331-333DOI: (10
Journal of Investigative Dermatology  , DOI: ( /jid )
Copyright © 2015 The Society for Investigative Dermatology, Inc Terms and Conditions