Oxford Events, the new replacement for OxTalks, will launch on 16th March. From now until the launch of Oxford Events, new events cannot be published or edited on OxTalks while all existing records are migrated to the new platform. The existing OxTalks site will remain available to view during this period.
From 16th, Oxford Events will launch on a new website: events.ox.ac.uk, and event submissions will resume. You will need a Halo login to submit events. Full details are available on the Staff Gateway.
Autophagy is a highly regulated cellular degradation system that engulfs cytosol, organelles, protein aggregates and invading microorganisms into a double-membrane vesicle termed the autophagosome, then delivers cargo to endolysosomes for degradation. Autophagy dysfunction has been implicated in a broad spectrum of human diseases, including cancers, neurodegeneration, infectious diseases, metabolic diseases and aging. My lab focuses on the biochemical mechanisms of autophagosome biogenesis, substrate recruitments and autophagosome fusion with lysosomes. We have identified and characterized novel protein factors (ATG14, NRBF2, TECPR1, OFD1 etc.,) essential for autophagy initiation, cargo recruitment and autophagosome-lysosome fusion (PNAS 2008,2010, 2012, Nature 2013, 2015, Mol Cell 2012).
