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Our research team focuses on genetic approaches to understanding the biology of damage-sensing neurons (nociceptors), somatosensation, pain and touch.
The past two decades have seen a revolution in our understanding of the receptor systems and regulatory pathways that underlie the responses of these specialised cells to the occurrence of tissue damage. This has important implications for human health and disease. Pain is still an enormous clinical problem, and new drugs are urgently required for a range of chronic pain syndromes.
Our group combines recombinant DNA technology, electrophysiology, gene targeting and behavioural approaches to explore the channels, receptors, transcription factors and regulatory pathways that control nociceptor excitability. We collaborate closely with human geneticists and clinicians, using mouse models to unravel molecular mechanisms that underlie pain disorders. We also take part in early-stage drug discovery programmes based on targets we identify in the lab.
We collaborate with research groups in Europe, the United States, Korea, Japan and Australia, using transgenic mouse models, natural products and cloned genes to explore the physiology of pain perception. As well as providing information about pain pathways, the systems we study have a broad relevance to understanding how the nervous system works, in terms of synaptic plasticity, responses to environmental stimuli, sensation and behaviour.
- 2001-present Professor, UCL
- Wellcome foundation and Sandoz Institute – Group Leader
- Visiting Professor Harvard, Seoul National University
- 2009 FMedSci, FRS
- 1976-1979 The Pasteur Institute, Paris
- 1976 PhD University of Warwick
- 1972 MSc University of Warwick
- 1971 BSc University of Leeds
Cho H, Yang YD, Lee J, Lee B, Kim T, Jang Y, Back SK, Na HS, Harfe BD, Wang F, Raouf R, Wood JN, Oh U. The calcium-activated chloride channel anoctamin 1 acts as a heat sensor in nociceptive neurons. Nature Neurosci. 2012 May 27;15(7):1015-21.
Minett MS, Nassar MA, Clark AK, Passmore G, Dickenson AH, Wang F, Malcangio M Wood JN. Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons. Nature Comm. 2012, 3:791
Vetter I, Touska F, Hess A, Hinsbey R, Sattler S, Lampert A, Sergejeva M, Sharov A, Collins LS, Eberhardt M, Engel M, Cabot PJ, Wood JN, Vlachova V, Reeh PW, Lewis RJ, Zimmermann K. Ciguatoxins activate specific cold pain pathways to elicit burning pain from cooling. EMBO J. 2012 31(19):3795-808.
Chambers JC, Zhao J, Terracciano CM, Bezzina CR, Zhang W, Kaba R, Navaratnarajah M, Lotlikar A, Sehmi JS, Kooner MK, Deng G, Siedlecka U, Parasramka S, El-Hamamsy I, Wass MN, Dekker LR, de Jong JS, Sternberg MJ, McKenna W, Severs NJ, de Silva R, Wilde AA, Anand P, Yacoub M, Scott J, Elliott P, Wood JN, Kooner JS. Genetic variation in SCN10A influences cardiac conduction. Nat Genet. 2010 Jan 10
Abrahamsen, B., Zhao J, Asante C, Cendan C, Marsh S, Martinez-Barbera J , Nassar, MA, Dickenson AS and J. N. Wood The cell and molecular basis of mechanical, cold and inflammatory pain. Science 321(5889):702-52007 Zimmermann K, Leffler A, Babes A, Cendan CM, Carr RW, Kobayashi J, Nau C, Wood JN, Reeh PW. Sensory neuron sodium channel Nav1.8 is essential for pain at low temperatures. Nature. 2007 Jun 14;447(7146):855-8.
Further publication information can be viewed at https://iris.ucl.ac.uk/iris/browse/profile?upi=JNWOO78