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• Lecturer for Biomedical Science BSc (Hons) and Medical Science BSc (Hons)
  
  
• Active researcher investigating mast cells in asthma
  
  
• Previous research interests:

-        MicroRNAs in cancer

-        Clinical trials in cardiac surgery

-        Premature aging disorders

Smallwood, D.T., Apollonio, B., Willimott, S., Ambrose, A., Alharthi, A., Ramsay, A.G., Wagner, S.D. (2016) Extracellular vesicles released by CD40/IL-4 stimulated chronic lymphocytic leukemia cells confer altered functional properties to CD4+ T cells. Blood. 2016 Jul 28;128(4):542-52 

Duffy, S.M., Ashmole, I., Smallwood, D.T., Leyland, M. L., Bradding, P. (2015) Orai/CRACM1 and K_Ca3.1 ion channels interact in the human lung mast cell plasma membrane. Cell Commun Signal., Jul 16; 13:32

Smallwood, D.T., Shackleton, S. (2010) Lamin A-linked progerias: is farnesylation the be all and end all? Biochem Soc Trans., Feb, 281-286

Haque, F., Mazzeo, D., Patel, J.T., Smallwood, D.T., Ellis, J.A., Shanahan, C.M., Shackleton, S. (2010) Mammalian SUN protein interaction networks at the inner nuclear membrane and their role in laminopathy disease processes. J Biol Chem., 285, 3487-3498

Mazereeuw-Hautier, J., Wilson, L., Mohammed, S., Smallwood, D., Shackleton, S., Atherton, D.J., Harper, J.I. (2007) Hutchinson-Gilford progeria syndrome: clinical findings in three patients carrying the G608G mutation in LMNA and review of the literature. Br J Dermatol., 156, 1308-1314

Haque, F., Lloyd, D., Smallwood, D.T., Dent, C.L., Shanahan, C.M., Fry, A.M., Trembath, R.C., Shackleton, S. (2006) SUN1 interacts with nuclear lamin A and cytoplasmic nesprins to provide a physical connection between the nuclear lamina and the cytoskeleton. Mol Cell Biol., 26, 3738-3751

Shackleton, S., Smallwood, D.T., Clayton, P., Wilson, L.C., Agarwal, A.K., Garg, A., Trembath, R.C. (2005) Compound heterozygous ZMPSTE24 mutations reduce prelamin A processing and result in a severe progeroid phenotype. J Med Genet., 42, e36 

Evidence suggests that mast cells play a central role in the pathophysiology of asthma. Mast cells act as sensors of the environment to defend against damage and infection. They are activated by tissue insult and respond by secreting biological mediators to initiate inflammatory responses and repair. In asthma, damage to the airway epithelium allows chronic mast cell activation and harmful chronic inflammatory responses which cause permanent damage to airways. We are investigating mast cells activators and the inhibition of mast cell activation.

• Biomedical Science
• Medical Science