Irwin McLean

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Irwin McLean
Born
William Henry Irwin McLean

(1963-01-09) 9 January 1963 (age 61)[3]
Ballymoney, County Antrim[3]
Alma materQueen's University of Belfast (BSc, PhD, DSc)
Awards
Scientific career
Fields
InstitutionsUniversity of Dundee
ThesisElectrophoretic and immunological analysis of proteins in the muscular dystrophies (1988)
Websitelifesci.dundee.ac.uk/people/irwin-mclean

(William Henry) Irwin McLean (born 1963) FRS[1] FRSE FMedSci[2] is Emeritus Professor of Genetic Medicine, at the School of Life Sciences, University of Dundee.[4][5][6][7][8][9][10]

Education[edit]

McLean was educated at Queen's University of Belfast where he was awarded a Bachelor of Science degree with honours in microbiology in 1985 followed by a PhD in 1988 for electrophoretic and immunological analysis of proteins involved in muscular dystrophy.[11]

Research[edit]

The McLean Lab investigates genetic disorders that affect the cells and tissues of the epithelium[12][13][14][15][16][17] and is funded by the Medical Research Council (MRC)[18] and the Wellcome Trust.[19]

Awards and honours[edit]

McLean was elected a fellow of the Royal Society in 2014. His nomination reads:

Irwin McLean is distinguished his major contributions to our understanding of the genetic basis of heritable skin diseases. Of particular note is his discovery that null mutations in filaggrin, which are carried by 10% of the population, not only cause the dry, flaky skin condition ichthyosis vulgaris but also strongly predispose individuals to the most common skin disorder, atopic eczema, and the associated phenotypes of atopic asthma, allergy and hay fever. This research has revolutionised the field by showing that a skin barrier defect, rather than an immunological defect, is the primary cause of eczema and focused attention on improving barrier function to treat these common diseases. He was also the first to map and identify the causative genes for a number of monogenic cell fragility disorders affecting the epidermis, its appendages and other epithelial tissues, including pachyonychia congenita, muscular dystrophy with epidermolysis bullosa simplex and Meesmann corneal dystrophy. His work has established that a primary function of the intermediate filament cytoskeleton, its attachment structures and modifying proteins is to provide epithelial tissues with mechanical strength.[1]

References[edit]

  1. ^ a b c "Professor Irwin McLean FMedSci FRS". London: The Royal Society.
  2. ^ a b c Professor Irwin McLean FRS FRSE FMedSci, The Academy of Medical Sciences
  3. ^ a b "McLEAN, Prof. (William Henry) Irwin". Who's Who. Vol. 2015 (online Oxford University Press ed.). A & C Black. (Subscription or UK public library membership required.)
  4. ^ Irwin McLean's publications indexed by the Scopus bibliographic database. (subscription required)
  5. ^ Irwin McLean publications indexed by Microsoft Academic
  6. ^ Palmer, C. N.; Irvine, A. D.; Terron-Kwiatkowski, A; Zhao, Y; Liao, H; Lee, S. P.; Goudie, D. R.; Sandilands, A; Campbell, L. E.; Smith, F. J.; O'Regan, G. M.; Watson, R. M.; Cecil, J. E.; Bale, S. J.; Compton, J. G.; Digiovanna, J. J.; Fleckman, P; Lewis-Jones, S; Arseculeratne, G; Sergeant, A; Munro, C. S.; El Houate, B; McElreavey, K; Halkjaer, L. B.; Bisgaard, H; Mukhopadhyay, S; McLean, W. H. (2006). "Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis". Nature Genetics. 38 (4): 441–446. doi:10.1038/ng1767. PMID 16550169. S2CID 2500278.
  7. ^ Smith, F. J.; Irvine, A. D.; Terron-Kwiatkowski, A; Sandilands, A; Campbell, L. E.; Zhao, Y; Liao, H; Evans, A. T.; Goudie, D. R.; Lewis-Jones, S; Arseculeratne, G; Munro, C. S.; Sergeant, A; O'Regan, G; Bale, S. J.; Compton, J. G.; Digiovanna, J. J.; Presland, R. B.; Fleckman, P; McLean, W. H. (2006). "Loss-of-function mutations in the gene encoding filaggrin cause ichthyosis vulgaris". Nature Genetics. 38 (3): 337–342. doi:10.1038/ng1743. PMID 16444271. S2CID 21948747.
  8. ^ McLean, W. H.; Irvine, A. D. (2012). "Heritable filaggrin disorders: The paradigm of atopic dermatitis". The Journal of Investigative Dermatology. 132 (E1): E20–E21. doi:10.1038/skinbio.2012.6. hdl:2262/74868. PMID 23154627.
  9. ^ Weidinger, S; Illig, T; Baurecht, H; Irvine, A. D.; Rodriguez, E; Diaz-Lacava, A; Klopp, N; Wagenpfeil, S; Zhao, Y; Liao, H; Lee, S. P.; Palmer, C. N.; Jenneck, C; Maintz, L; Hagemann, T; Behrendt, H; Ring, J; Nothen, M. M.; McLean, W. H.; Novak, N (2006). "Loss-of-function variations within the filaggrin gene predispose for atopic dermatitis with allergic sensitizations". The Journal of Allergy and Clinical Immunology. 118 (1): 214–219. doi:10.1016/j.jaci.2006.05.004. PMID 16815158.
  10. ^ Has, Cristina; Sitaru, Cassian (2013). Molecular Dermatology: Methods and Protocols. Methods in Molecular Biology. Vol. 961. doi:10.1007/978-1-62703-227-8. ISBN 9781627032261. S2CID 21781092.
  11. ^ McLean, William Henry Irwin (1988). Electrophoretic and immunological analysis of proteins in the muscular dystrophies (PhD thesis). Queen's University of Belfast.
  12. ^ Research in the McLean Lab, University of Dundee
  13. ^ Nomura, T; Sandilands, A; Akiyama, M; Liao, H; Evans, A. T.; Sakai, K; Ota, M; Sugiura, H; Yamamoto, K; Sato, H; Palmer, C. N.; Smith, F. J.; McLean, W. H.; Shimizu, H (2007). "Unique mutations in the filaggrin gene in Japanese patients with ichthyosis vulgaris and atopic dermatitis". The Journal of Allergy and Clinical Immunology. 119 (2): 434–440. doi:10.1016/j.jaci.2006.12.646. PMID 17291859.
  14. ^ Basu, K; Palmer, C. N.; Lipworth, B. J.; Irwin Mclean, W. H.; Terron-Kwiatkowski, A; Zhao, Y; Liao, H; Smith, F. J.; Mitra, A; Mukhopadhyay, S (2008). "Filaggrin null mutations are associated with increased asthma exacerbations in children and young adults" (PDF). Allergy. 63 (9): 1211–1217. doi:10.1111/j.1398-9995.2008.01660.x. PMID 18307574. S2CID 8105444.
  15. ^ Palmer, C. N.; Ismail, T; Lee, S. P.; Terron-Kwiatkowski, A; Zhao, Y; Liao, H; Smith, F. J.; McLean, W. H.; Mukhopadhyay, S (2007). "Filaggrin null mutations are associated with increased asthma severity in children and young adults". The Journal of Allergy and Clinical Immunology. 120 (1): 64–68. doi:10.1016/j.jaci.2007.04.001. PMID 17531295.
  16. ^ Henderson, J; Northstone, K; Lee, S. P.; Liao, H; Zhao, Y; Pembrey, M; Mukhopadhyay, S; Smith, G. D.; Palmer, C. N.; McLean, W. H.; Irvine, A. D. (2008). "The burden of disease associated with filaggrin mutations: A population-based, longitudinal birth cohort study". The Journal of Allergy and Clinical Immunology. 121 (4): 872–877.e9. doi:10.1016/j.jaci.2008.01.026. PMID 18325573.
  17. ^ Bisgaard, H; Simpson, A; Palmer, C. N.; Bønnelykke, K; McLean, I; Mukhopadhyay, S; Pipper, C. B.; Halkjaer, L. B.; Lipworth, B; Hankinson, J; Woodcock, A; Custovic, A (2008). "Gene-environment interaction in the onset of eczema in infancy: Filaggrin loss-of-function mutations enhanced by neonatal cat exposure". PLOS Medicine. 5 (6): e131. doi:10.1371/journal.pmed.0050131. PMC 2504043. PMID 18578563.
  18. ^ UK Government research grants awarded to Irwin McLean, via Research Councils UK
  19. ^ Wellcome Trust strategic awards 2013
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