September 23, 2016-Regulation of NF-kappaB signaling in cancer and immunity: from bench to“BET”side
Title: Regulation of NF-kappaB signaling in cancer and immunity: from bench to "BET" side
Lecturer: Linfeng Chen Ph.D.
Tenured associate professor,
Department of biochemistry,
University of Illinois.
Time: AM 10:30-11:30, September 23, 2016 (Friday).
Venue: G405, School of Life Sciences.
Invitor: Prof. Ruichuan Chen
Abstract: The transcription factor NF-kappaB plays a key role in regulating immune and inflammatory responses, apoptosis, cell proliferation and differentiation, and tumorigenesis. Constitutively active NF-kappaB is frequently encountered in a wide variety of tumors and inflammatroy diseases. The strength and duration of the transcriptional activity of NF-kappaB is dictated by a variety of posttranslational modifications, including phosphorylation, acetylation and ubiquitination.
Our lab has identified bromodomain and extra terminal (BET) family protein Brd4 as a key regulator of NF-kappaB via its binding to acetylated RelA subunit of NF-kappaB. In this seminar, I will discuss our most recent findings on how binding of Brd4 to acetylated RelA contributes to NF-kappaB-dependent inflammatory gene expression and to maintaining the constitutively active NF-kappaB in cancer cells.
While Brd4 has emerged as a key epigenetic regulator in the inflammatory response and cancer, the potential in vivo functions of Brd4 in NF-kappaB-mediated immune response remains unknown. I will also discuss some of our recent studies on understanding the pathophysiological functions of Brd4 by using Brd4 knockout animals in different disease models.
Finally, I will discuss whether targeting Brd4 would be an approach with therapeutic potentials for the treatment of NF-kappaB-dependent inflammatory diseases and cancer.