University of Dundee

‘Role for Ubiquitin modification in Cancer Pathogenesis - the story of BAP1’

Event Date: 
Friday, May 11, 2018 - 16:00 to 17:00
Event Location: 
MSI Small Lecture Theatre
Professor Dario Alessi FRS FRSE
Event Speaker: 
Dr Vishva Dixit
Vice President and Staff Scientist in Physiological Chemistry at Genentech
Event Type: 

10th Scottish Institute for Cell Signalling Lecture


Vishva Dixit is recognized for his pioneering studies defining key components of the cell death and ubiquitylation machinery.


Apoptosis was a mysterious process in the early nineties and debate raged as to how the TNF receptor and its close homologue Fas engaged the suicide pathway.  The first breakthrough from the Dixit lab was the demonstration that a cysteine protease (now termed caspase) was a key component of the death receptor-induced apoptotic pathway (Tewari, JBC, 1995). 


These observations set the stage for the identification of caspase-3, as the key downstream executioner protease (Tewari, Cell, 1995).  Vishva next discovered the  adapter protein termed FADD worked to recruit and activate an initiating death protease called Caspase-8 (Chinnaiyan, Cell, 1995, Cell, 1996,).


Subsequently, his laboratory developed the “induced proximity model” for how caspase zymogens were activated (Muzio, JBC, 1998,). He showed that the FADD/caspase-8 pathway was indeed the central apoptotic conduit used by all death receptors (Pan, Science, 1997) and that TRAF3 functioned as a CD40 signaling adaptor (Hu, JBC, 1994;).


Vishva demonstrated that MyD88 was a key adaptor in IL-1 signaling (Muzio, Science,), discovered Paracaspases and Metacaspases, one of which plays a central role in MALT lymphoma (Uren, Mol Cell, 2000,), and established that NOD proteins possessing a death-fold are critical components of the inflammasome complex (Mariathasan, Nature, 2006,). 


Vishva discovered and characterised A20, an increasingly important negative regulator of NF-kappaB signaling that has been linked to human autoimmune disorders (Opipari, JBC, 1990, Krikos, JBC, 1992). Vishva work also suggested that A20 possesses ubiquitin editing activity (Wertz, Nature, 2004; Newton, Cell, 2008). 


Most recently, Vishva group has discovered a non-canonical Inflammasome pathway that responds to the presence of intracellular LPS independent of toll-like receptors (Kayagaki, Nature, 2011 and Kayagaki, Science, 2013).


Vishva group have also demonstrated that a deubiquitylase termed BAP1 acts as a tumor suppressor (Science 2012). In his SCILLS lecture, Vishva will discuss unpublished data on the signalling pathways that are controlled by BAP1 and their roles in cancer


For more information on many more of Vishva's Research achievements please see

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