Molecular Nociception Group

Professor John Wood FRS
Professor of Molecular Neurobiology and Head of the Molecular Nociception Group
Tel: +44 (0) 207 679 6954
Fax: +44 (0)207 679 7096
Molecular Nociception Group web page

John Wood is Professor of Molecular Neurobiology and Head of the Molecular Nociception group at University College London , where he has worked since 1994. Dr Wood completed a Ph.D. in virology in 1975 at Warwick University and carried out post-doctoral research with Luc Montagnier at The Pasteur Institute in Paris from 1976-1979. He then moved into Neuroscience, working with Brian Anderton and Tom Jessell at St Georges Hospital London, before spending 12 years in industry, first at the Wellcome Foundation, and later at the Sandoz (now Novartis) Institute for Medical Research in London. In 2002, he co-founded Ionix pharmaceuticals, a start-up biotechnology company comprising 46 scientists based in Cambridge UK, which is developing analgesic drugs directed against new targets defined by genetic research. Dr Wood is the author of more than a hundred research publications, and several books and patents. 

The Molecular Nociception Group focuses on genetic approaches to understanding the biology of damage-sensing neurons. The past decade has 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.

By combining electrophysiological studies of specific ion channel types in damage-sensing neurons with the characterisation of cloned receptor genes in heterologous expression systems, an understanding of the fundamental responses of these neurons to chemical, mechanical and thermal stimuli can be obtained.

Our group combines recombinant DNA technology, electrophysiology and gene targeting and behavioural approaches to explore the channels, receptors transcription factors and regulatory pathways that control nociceptor excitability.

Prof. John N Wood is head of the Molecular Nociception Group and a member of the London Pain Consortium.

Selected publications:

  • Zhao J, Lee MC, Momin A, Cendan CM, Shepherd ST, Baker MD, Asante C, Bee L, Bethry A, Perkins JR, Nassar MA, Abrahamsen B, Dickenson A, Cobb BS, Merkenschlager M, Wood JN. Small RNAs control sodium channel expression, nociceptor excitability, and pain thresholds. J Neurosci. 2010 Aug 11;30(32):10860-71.
  • Kremeyer B, Lopera F, Cox JJ, Momin A, Rugiero F, Marsh S, Woods CG, Jones NG, Paterson KJ, Fricker FR, Villegas A, Acosta N, Pineda-Trujillo NG, Ramírez JD, Zea J, Burley MW, Bedoya G, Bennett DL, Wood JN, Ruiz-Linares A. A gain-of-function mutation in TRPA1 causes familial episodic pain syndrome. Neuron. 2010 Jun 10;66(5):671-80.
  • 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 Feb;42(2):149-52.
  • Abrahamsen B, Zhao J, Asante CO, Cendan CM, Marsh S, Martinez-Barbera JP, Nassar MA, Dickenson AH, Wood JN. The cell and molecular basis of mechanical, cold, and inflammatory pain. Science. 2008 Aug 1;321(5889):702-5.
  • 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. Drew LJ, Rugiero F, Cesare P, Gale JE, Abrahamsen B, Bowden S, Heinzmann S, Robinson M, Brust A, Colless B, Lewis RJ, Wood JN. High-threshold mechanosensitive ion channels blocked by a novel conopeptide mediate pressure-evoked pain. PLoS One. 2007 Jun 13;2(6):e515.
  • Nassar MA, Stirling LC, Forlani G, Baker MD, Matthews EA, Dickenson AH, Wood JN. Nociceptor-specific gene deletion reveals a major role for Nav1.7 (PN1) in acute and inflammatory pain. Proc Natl Acad Sci U S A. 2004 Aug 24;101(34):12706-11.