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Bortree Lecture Series - Edward Harhaj - Talk Title: “Regulation of Inflammatory Signaling Pathways By the Autophagy Receptor TAX1BP1” on November 30, 2022

Bortree Lecture Series - Edward Harhaj - Talk Title: “Regulation of Inflammatory Signaling Pathways By the Autophagy Receptor TAX1BP1”.

Edward Harhaj, PhD Professor, Department of Microbiology and Immunology Penn State Cancer Institute Cancer Institute, Mechanisms of Carcinogenesis

Bortree Lecture Series - Edward Harhaj -  Talk Title:  “Regulation of Inflammatory Signaling Pathways By the Autophagy Receptor TAX1BP1”.

https://vbs.psu.edu/events/bortree-lecture-series-edward-harhaj-talk-title-to-be-announced

Bortree Lecture Series - Edward Harhaj - Talk Title: “Regulation of Inflammatory Signaling Pathways By the Autophagy Receptor TAX1BP1”.

2022-11-30T11:00:00-05:00

2022-11-30T12:00:00-05:00

Edward Harhaj, PhD Professor, Department of Microbiology and Immunology Penn State Cancer Institute Cancer Institute, Mechanisms of Carcinogenesis

When

November 30, 2022, 11:00 AM - 12:00 PM

Where

106 AVBS Building

Contact

Margaret Weber

Contact Phone

814-865-7697

Web

Visit external website

Dr. Edward Harhaj’s research interests focus on the mechanisms of viral-induced malignancy by the human T-cell leukemia virus type 1 (HTLV-1). HTLV-1 is a retrovirus that primarily infects CD4+ T lymphocytes and is etiologically linked to adult T-cell leukemia (ATL) and an inflammatory autoimmune-like neurological disorder known as HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Tax is a trans-activating protein encoded by the HTLV-1 genome that regulates viral and cellular gene expression. The underlying mechanisms of Tax-mediated oncogenesis are unclear and are the primary focus of research in this laboratory. One of the main cellular targets of Tax is the NF-kB/Rel transcription factor family, an important regulator of cell growth, survival and innate and adaptive immunity. NF-kB is constitutively activated in Tax-expressing cells, HTLV-1 transformed cell lines and ATL cells. Tax requires NF-kB for the immortalization of primary T cells and ATL cells are dependent on NF-kB for their survival. Thus, determining the mechanisms of Tax-mediated activation of NF-kB as well as Tax-independent NF-kB activation in ATL is a major focus in the laboratory. Dr. Harhaj’s laboratory is currently investigating the role of autophagy and ubiquitin pathway components in Tax activation of NF-kB.

Original source can be found here.

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