Lab master unit
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CNE 621 mapped within a psoriasis copy number variant (LCE3C_LCE3Bdel) suggesting loss of regulatory activity in psoriasis. Two CNEs, 621 and 923, exhibited epidermal-specific enhancer activity in transgenic reporter mice. We have previously identified a group of conserved noncoding elements (CNEs) in the EDC that demonstrate dynamic regulatory activity.
#Lab master unit skin
How are genes in the EDC coordinated? On a genomic scale, how does a proliferating epidermal cell evolve to a terminally differentiated cell and form the essential unit of the skin barrier? Why is the EDC genetically implicated in common inflammatory skin diseases, atopic dermatitis and psoriasis, that are barrier-impaired? What are the genetic variants in the EDC in these diseases? How do they contribute to the pathophysiology? We are currently addressing these basic science and translational research questions using experimental and computational approaches in mice and men. To date, very little is known about the molecular mechanisms to regulate the EDC. The Epidermal Differentiation Complex locus (EDC) encodes many proteins that are cross-linked together to form one of the essential components of the skin epidermal barrier. These investigations will enable us to understand how these mechanisms are perturbed in common skin diseases. We use the mammalian skin as a model system to explore the molecular mechanisms governing protective barrier formation. Perturbations in this complex biological process often lead to inflammation and opportunistic infections. The long-term goal of the Strong laboratory is to understand the morphogenesis and homeostasis of functional tissue barriers. Principal investigator bio Lab overview Regulation of skin barrier formation: Development and disease