Dr Wayne Grant Carter completed a BSc (Hons) degree in Biochemistry with Nutrition and then a PhD in Biochemistry at the University of Southampton. He subsequently undertook post-doctoral research posts at The Babraham Institute, Cambridge; Imperial College, London; University of California at Irvine, USA, and then at the University of Oxford. Additionally, Dr Carter has worked for a global reagent supplier, Sigma, a SME company, Mobious Genomics, and has been employed as a consultant for Syngenta. Dr Carter is currently an Associate Professor and Group Leader within the School of Medicine, University of Nottingham. Dr Carter's research interests are varied and include detection and utilisation of novel biomarkers of toxicological exposure.
Understanding the molecular mechanisms that underpin disease provides the basis for targeted therapeutics. The research in my lab is concerned with understanding protein changes and modifications that can trigger pathology. In recent years we have focussed upon hepato- and neuro- toxicological mechanisms. We employ cell and animal models and human postmortem tissue to understand pathological changes, and utilise a broad range of biological and biochemical techniques to study disease. Current projects include an examination of biological targets of environmental pesticides in brain, hepato- and neuro-pathology of alcohol abuse, and protein aggregation in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease.
My research expertise includes methods utilized to detect and quantify post-translational modifications, and examine tissue, cell, and protein damage and repair mechanisms;
- 1D and 2D proteomic separation techniques; mass spectrometry; and autoradiographic imaging.
- Immuno-detection methods. animal dosing and toxicokinetics.
- Protein and peptide purification techniques, including FPLC and Smart system IEC, SEC, HIC, affinity-ligand, and RP-HPLC.
- Gene cloning, recombinant protein production and purification.
- Biophysical methods such as surface plasmon resonance.
- Synthetic methods such as solid phase peptide and phosphopeptide synthesis.
- Cell monolayer and suspension culturing.
- Small animal surgery, and toxicokinetic measurements.
BSc (Hons) Medical Physiology & Therapeutics, course code B121.
Year 1: A11 Body Structure & Function (teaching protein structure/function, cell cycle & genetics, & alimentary physiology).
Year 1: A11 Infection & Defense (teaching immunology).
Year 2: A12 Cancer Biology (teaching all elements of cancer cell biology, cellular signalling, genetics, radiotherapy, chemotherapy, etc).
Year 3: A13 Cellular Basis of Disease (teaching microbiological & neurodegenerative diseases & treatments).
Year 1: A11 Supply & Demand I (teaching nutrition & metabolism). A11 MVT Movement (teaching the motor system in health & disease).
Year 2: A12 Neuroscience (teaching neurodegeneration); A12 Pharmacology & Therapeutics (teaching drug use & toxicity); A12 Respiratory Disease (teaching lung cancer).
Year 3: A13 Final Year Research Project (Supervisor for lab-based research & systematic reviews & meta-analysis based research projects).
Bachelor of Medicine Bachelor of Surgery (BMBS), course code A100:
Year 2: A12 Clinical Toxicology Studies (teaching clinical toxicology with case studies).
Year 1: A12 Structure, Function & Defense (teaching protein structure/function, bacteria & viral immunology); A12 Alimentary System (teaching liver structure, function, & pathology); A12 Respiratory Sciences (teaching respiratory inflammation, & oncogenesis).
Year 2: A12 Neuroscience (teaching neuroscience & neurodegeneration).
Year 1 & Year 2 problem based learning (PBL) facilitation.
My research & development career has been concerned with understanding cellular signaling and the protein changes and modifications that can trigger pathology, and how therapeutics can limit… read more
My research & development career has been concerned with understanding cellular signaling and the protein changes and modifications that can trigger pathology, and how therapeutics can limit disease progression. Many extracellular signals bind to specific trans-membranous receptors to initiate a cellular signaling pathway. Signal transduction invariably requires protein post-translational modifications (PTMs) to propagate intracellular signaling events. Additionally, PTMs arise from extracellular xenobiotic agents that cross cell membranes. An example is environmental pesticides that can adduct cellular proteins including a number of specific neuronal targets. Other toxic agents such as alcohol trigger protein PTMs and damage to tissues and cellular proteins.
By utilizing proteomic strategies we have characterised the cellular damage that arises from these agents, and their specific cellular and nuclear (epigenetic) protein targets. One such protein target is protein isoaspartyl methyltransferase (PIMT), an enzyme that normally repairs age-related protein damage, and whose activity is impaired by alcohol consumption.
My current laboratory studies include an examination of the targets and consequences of environmental pesticide exposures; hepato- and neuro-pathology of alcohol abuse; and studies of the protein PTMs and protein aggregation in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease.