Dr Richard Billington

Qualifications

Degree:
1996-1999 Biochemistry, University of Bristol
PhD: 
1999-2002 Department of Pharmacology, University of Cambridge
Postdoc:
2002-2003 Department of Pharmacology, University of Cambridge (Biotechnology and Biological Sciences Research Council) 2003-2005 Università degli Studi del Piemonte Orientale. 
Teaching
2006-2008 “Ricercatore” at the Università degli Studi del Piemonte Orientale, Novara, Italy.

Professional membership

FLS

Teaching interests

I teach on a wide variety of modules from biochemistry, cell biology and pharmacology right up to field biology.

As a naturalist at heart, I attend a number of field courses both in the UK and abroad.

Research interests

Pyridine nucleotides and their roles in basic metabolism and signalling

NAD(P) has long been thought of as a simple redox co-factor involved in basic metabolism but recent findings show that it is also involved in cell signalling pathways. These pathways include fundamental processes such as gene expression (via the Sirtuin enzymes), DNA repair (via PARP; poly ADP-ribose polymerase), posttranslational protein modification (via PARP and ADP-ribosyl tranferases; ART) and Ca2+-signalling (via CD38 metabolites). Furthermore, it has been shown that the maintenance of high intracellular NAD levels can prolong the lifespan of cells probably in a Sirtuin-dependent manner. Many of these roles have been elucidated only recently and we are still only beginning to understand the wide-ranging implications that pyridine nucleotide signalling may have in the cell. My research is aimed at elucidating some of the fundamental processes which control and are controlled by pyridine nucleotides and their derivatives.

Pyridine nucleotide homeostasis as a pharmacological target

The widespread involvement of NAD(P) in signalling pathways has also led to the hypothesis that such NAD(P)-mediated processes and NAD(P) homeostasis pathways could be promising drug targets for a wide range of diseases, in particular cancer and diabetes but also neurodegeneration, obesity and psoriasis to name a few. Although we are still some way off the clinical use of such drugs, my research aims to highlight novel targets and mechanisms that could provide therapeutics in the future.

Ca2+-signalling with particular respect to pyridine nucleotide second messengers.

The enzyme CD38 is a multifunctional cell surface enzyme and receptor. Two of its enzymatic products, cADPR and NAADP (metabolites of NAD and NADP), have been shown to be potent releasers of intracellular Ca2+ via the Ryanodine receptor and Two Pore Channels (TPC) respectively. Little is know still about the mechanisms that control the actions of these two messengers and my research is aimed at elucidating these mechanisms.

The generation of specificity/complexity and its decoding in signalling pathways.

Cell signalling pathways must specifically control only selected target proteins. Indeed, many disease states are caused by the inappropriate or dysregulated activation of non target proteins. In order to acheive this, cellular signals must necessarily include a certain level of complexity (for instance variation of the spatial and temporal parameters). There is still much to understand about how levels of complexity are both encoded and decoded such that only specific targets respond.

Immune function in invertebrates

Invertebrates lack an adaptive immune system such as that found in mammals and must rely on their innate mechanisms for combatting pathogens and parasites. I am interested in the biochemistry of the mechanisms applied by invertebrates to achieve this and linking immune function to ecology and rarity.