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Laboratory of Skin Biology
The skin functions as a barrier that protects the body from the external environment and excessive water loss. Barrier function is established through a multi-stage differentiation program of keratinocytes in the epidermis. Recent studies indicate that genetic mutations are linked to barrier dysfunction in skin disorders: ichthyosis vulgaris, atopic dermatitis and psoriasis. Most inflammatory skin disorders exhibit abnormal keratinocyte differentiation, disrupted barrier function and/or abnormalities of immunocytes.
The Laboratory of Skin Biology utilizes a systematic approach to understand the function of specific regulators and pathways, and a combination of mouse models, toward elucidating the molecular processes that contribute to epidermal differentiation and barrier formation, appendage development and the mechanisms underlying the pathologies of Ectodermal Dysplasias (EDs).
- Developmental Skin Biology Section — Chief, Maria Morasso, Ph.D.
Duverger O, Isaac J, Zah A, Hwang J, Berdal A, Lian JB, Morasso MI. In vivo impact of Dlx3 conditional inactivation in neural crest-derived craniofacial bones. J Cell Physiol. 2012 Aug 9. doi: 10.1002/jcp.24175.
Okano J , Lichti U, Mamiya S, Aronova M, Zhang G, Yuspa S.H, Hamada H, Sakai Y and Morasso MI. Increased retinoic acid levels through ablation of Cyp26b1 determine the processes of embryonic skin barrier formation and peridermal development. Journal of Cell Science . 2012 Feb 24. [Epub ahead of print]
Duverger O, Zah A, Isaac J, Sun HW, Bartels AK, Lian JB, Berdal A, Hwang J, Morasso MI. Neural crest deletion of Dlx3 leads to Major Dentin defects through downregulation of Dspp. J Biol Chem. 2012 Feb 20. [Epub ahead of print]See extended list of publications
Updated October 13, 2011