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About us


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Dept. of Dermatology
Center for Health & Healing
Located on the 16th
and 5th floors
3303 SW Bond Ave.
Portland, Ore. 97239

Appointments: 503-418-3376
Administration: 503-494-4713
Toll-free: 888-482-7546

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Yuangang Liu, Ph.D.
Yuangang Liu, Ph.D.
Research Assistant Professor of Dermatology

Dermatology Research Division


Overview
Ph.D. Biochemistry, University of Buffalo (SUNY), 1998

Yuangang Liu's project:

Psoriasis is an inflammatory disease involving many genes and multiple cell types including immune cells and keratinocytes, the major cell type in the skin. Although it is believed that keratinocytes are affected by the immune cells' behavior in psoriasis, there is much evidence to suggest that keratinocytes play an important role in triggering psoriasis. We found that Trim32 changes keratinocyte production of CCL20, a chemokine that attracts immune cells to psoriatic skin where they worsen the psoriasis symptoms. In so doing, Trim32 control of CCL20 levels provides a mechanism whereby keratinocytes can act as active players with immune cells creating a cycle that maintains the disease. My research is mainly focused on defining 1) the functional role of CCL20 chemokine in skin inflammation; 2) CCL20 regulation by Trim32, a bi-functional protein with E3 ubiquitin ligase and microRNA enhancement activities; 3) mechanism of ubiquitynation and microRNA coordination in the regulation of cytokine and chemokines. The study of CCL20 control by Trim32 in psoriasis will not only help us understand how psoriasis can be triggered by keratinocytes, but also provide therapies that target keratinocytes, and should be less toxic than drugs which affect the entire immune system.
Yuangang Liu, Ph.D.
Selected publications:

Liu, Y., Lagowski, J.P., Sunberg, A., and Kulesz-Martin, M.F. Microtubule disruption and tumor suppression by mitogen activated protein kinase phosphatase 4. Cancer Res, 67:10711-9, 2007

Liu, Y., Lagowski, J.P., Vanderbeek, G.E., and Kulesz-Martin, M.F. Facilitated search for specific genomic targets by p53 C-terminal basic DNA binding domain. Cancer Biology & Therapy, 3(11) 2004.

Horn, E.J., Albor, A., Liu, Y., El-Hizawi, S., Babcock, M., Bowden, G.T., Hennings, H., Lozano, G., Weinberg, W.C. and Kulesz-Martin. M. RING domain protein Trim32 associated with anti-apoptotic and E3-ubiquitin ligase properties in skin carcinogenesis. Carcinogenesis, 25: 157-167, 2004.

More publications