Dye, Danielle - Curtin University - School of Biomedical Sciences

研究领域

Melanoma This project investigates the role of melanoma cell adhesion molecule (MCAM), a cell surface protein that is important in the metastatic progression of melanoma cells. MCAM is highly expressed on the surface of most melanoma cells but little is know about where it is located inside the cell, what proteins it interacts with, how it cycles to and from the cell surface and the mechanism behind it’s pro-metastatic effects. This project aims to investigate the synthesis, recycling and degradation of MCAM within the cell and how this relates to directional cell migration. This will provide further information about how MCAM contributes to the proliferation, invasion and metastasis of melanoma cells Muscle regeneration in aging Healthy, young skeletal muscle is able to quickly regenerate following injury or overuse. This capacity decreases with age, and loss of muscle mass in the elderly leads to an increased risk of impaired mobility and loss of functional autonomy. Muscle maintenance and regeneration is stimulated by the connective tissue surrounding each muscle fibre. The aim of our work is to identify factors that differ between old and young muscle. This knowledge will be used to engineer muscle-specific scaffolds to stimulate new muscle formation, the long-term goal being to improve the treatment of muscle injury, diseased muscle and age-related muscle loss.

近期论文

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Chaturvedi, V., D. E. Dye, B. F. Kinnear, T. Van Kuppevelt, M. Grounds, and D. R. Coombe. 2015.“Interactions between skeletal muscle myoblasts and their extracellular matrix revealed by a serum free culture system.”PLoS One 10 (6): 1-27. Jackaman, C., D. E. Dye, and D. J. Nelson. 2014.“IL-2/CD40-activated macrophages rescue age and tumor-induced T cell dysfunction in elderly mice.”Age 36: 1315-1328. Brameld, K. J., D. E. Dye, S. J. Maxwell, J. M. Brisbane, E. Glasson, J. Goldblatt, and P. O'Leary. 2014.“The Western Australian Family Connections Genealogical Project: Detection of familial occurrences of single gene and chromosomal disorders.”Genetic Testing and Molecular Biomarkers 18 (2): 77-82. Gardner, J., C. D. Mamotte, T. McGonigle, D. E. Dye, C. Jackaman, and D. J. Nelson. 2014.“Lipid-laden partially-activated plasmacytoid and CD4-CD8[alpha]+ dendritic cells accumulate in tissues in elderly mice.”Immunity & Ageing 11 (1). Glasson, E. J., D. E. Dye, and A. H. Bittles. 2014.“The triple challenges associated with age-related comorbidities in Down syndrome.”Journal of Intellectual Disability Research 58: 393-398. Dye, D. E., S. medic, M. Ziman, and D. R. Coombe. 2013.“Melanoma Biomolecules: Independently Identified but Functionally Intertwined.”Frontiers in Oncology 3 (252). Fyfe, G., S. D. Fyfe, D. E. Dye, and H. G. Radley-Crabb. 2013.“Use of Anatomage tables in a large first year core unit.” In 30th ascilite Conference 2013, Dec 1, 2013, Macquarie University, Sydney: Macquarie University. Wong, C. W., D. E. Dye, and D. R. Coombe. 2012.“The Role of Immunoglobulin Superfamily Cell Adhesion Molecules in Cancer Metastasis.”International Journal of Cell Biology 2012. Dye, D. E., K. J. Brameld, S. J. Maxwell, J. Goldblatt, and P. O'Leary. 2011.“The impact of single gene and chromosomal disorders on hospital admissions in an adult population.”Journal of Community Genetics 2: 81-90. Dye, D. E., K. J. Brameld, S. J. Maxwell, J. Goldblatt, C. Bower, H. Leonard, J. Bourke, E. J. Glasson, and P. O'Leary. 2011.“The Impact of Single Gene and Chromosomal Disorders on Hospital Admissions of Children and Adolescents: A Population-Based Study.”Public Health Genomics 14 (3): 153-161. Dye, D. E., L. Youngs, B. McNamara, J. Goldblatt, and P. O'Leary. 2010.“The disclosure of genetic information: A human research ethics perspective.”Journal of Bioethical Inquiry 7 (1): 103-109. Dye, D. E., S. Karlen, B. Rohrbach, O. Staub, L. R. Braathen, K. A. Eidne, and D. R. Coombe. 2009.“hShroom1 links a membrane bound protein to the actin cytoskeleton.”Cellular and Molecular Life Sciences 66: 681-696. Clarke, N., H. Kolski, D. E. Dye, E. Lim, R. Smith, R. Patel, M. Fahey, R. Bellance, N. Romero, E. Johnson et al. 2008.“Mutations in TPM3 are a common cause of congenital fiber type disproportion.”Annals of Neurology 63 (3): 329-337. Shingde, M., P. Spring, A. Maxwell, E. Wills, C. Harper, D. E. Dye, N. Laing, and K. North. 2006.“Myosin storage (hyaline body) myopathy: A case report.”Neuromuscular Disorders 16 (12): 882-886. Dye, D. E., B. Azzarelli, H. Goebel, and N. Laing. 2006.“Novel slow-skeletal myosin (MYH7) mutation in the original myosin storage myopathy kindred.”Neuromuscular Disorders 16 (6): 357-360. Laing, N., C. Ceuterick-de Groote, D. E. Dye, K. Liyanage, R. Duff, B. Dubois, W. Robberecht, R. Sciot, J. Martin, and H. Goebel. 2005.“Myosin storage myopathy: Slow skeletal myosin (MYH7) mutation in two isolated cases.”Neurology 64 (3): 527-529. Meredith, C., R. Herrmann, C. Parry, K. Liyanage, D. E. Dye, H. Durling, R. Duff, K. Beckman, M. De Visser, M. Van Der Graaff et al. 2004.“Mutations in the slow skeletal muscle fiber myosin heavy chain gene (MYH7) cause Laing early-onset distal myopathy (MPD1).”American Journal of Human Genetics 75 (4): 703-708. Laing, N., N. Clarke, D. E. Dye, K. Liyanage, K. Walker, Y. Kobayashi, S. Shimakawa, T. Hagiwara, R. Ouvrier, J. Sparrow et al. 2004.“Actin mutations are one cause of congenital fibre type disproportion.”Annals of Neurology 56 (5): 689-694.