Michael Lagunoff, Ph.D.

Title
Professor
Department
Department of Microbiology
Institution
University of Washington
Address
1959 N.E. Pacific Street
Box 357735, J-287
City, State, Zip
Seattle, WA 98195
Phone
(206) 616-4285
E-mail
Lagunoff[at]uw.edu
Website
http://depts.washington.edu/micro/faculty/lagunoff.htm
Research Field
Virology
Award Year
2002

Research

The laboratory studies the molecular virology of Kaposi’s Sarcoma-associated herpesvirus (KSHV). KSHV is the infectious cause of Kaposi’s Sarcoma (KS). The laboratory is interested in how the virus alters the host cell to induce tumors. KSHV encodes over 80 genes and many are involved in altering host cell signal transduction. The laboratory focuses on how initiation of signal transduction pathways by viral genes leads to viral pathogenesis in endothelial and B-cells.

We are currently working on how KSHV induced signaling through the gp130 receptor induces persistent STAT3 activation and subsequent AKT activation, pathways commonly activated in tumors. This pathway is also involved in KSHV driven differentiation of blood endothelial cells to lymphatic endothelium and we are interested the role of differentiation in the biology of KSHV. We also have a major focus on viral induced angiogenesis. KS tumors are highly vascularized and KSHV induces many genes involved in angiogenesis. Ongoing studies in the lab examine the role of KSHV induced angiogenesis in KSHV biology. The laboratory studies the molecular virology of Kaposi’s Sarcoma-associated herpesvirus (KSHV). KSHV is the infectious cause of Kaposi’s Sarcoma (KS). The laboratory is interested in how the virus alters the host cell to induce tumors. KSHV encodes over 80 genes and many are involved in altering host cell signal transduction. The laboratory focuses on how initiation of signal transduction pathways by viral genes leads to viral pathogenesis in endothelial and B-cells.

We are currently working on how KSHV induced signaling through the gp130 receptor induces persistent STAT3 activation and subsequent AKT activation, pathways commonly activated in tumors. This pathway is also involved in KSHV driven differentiation of blood endothelial cells to lymphatic endothelium and we are interested the role of differentiation in the biology of KSHV. We also have a major focus on viral induced angiogenesis. KS tumors are highly vascularized and KSHV induces many genes involved in angiogenesis. Ongoing studies in the lab examine the role of KSHV induced angiogenesis in KSHV biology.