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Dr Adam Piers
CardioRegen will embed a framework for discovery through to translation encompassing three major research programs in 1 - Diagnostics, 2 - Discovery and 3 – Translation. Collectively, these programs will establish key resources and technology platforms that will feed into a broader research program across the cardiovascular space including the establishment of a large biobank including cardiac tissues, DNA and patient-matched stem cells for disease modeling and development of new personalised regenerative medicine approaches.
Borovikov YS, Rysev NA, Karpicheva OE, Sirenko VV, Avrova SV, Piers A, Redwood CS (2017). Molecular mechanisms of dysfunction of muscle fibres associated with Glu139 deletion in TPM2 gene. Sci Rep. 7(1):16797
Borovikov YS, Simonyan AO, Karpicheva OE, Avrova SV, Rysev NA, Sirenko VV, Piers A, Redwood CS (2017). The reason for a high Ca2+-sensitivity associated with Arg91Gly substitution in TPM2 gene is the abnormal behavior and high flexibility of tropomyosin during the ATPase cycle. Biochem Biophys Res Commun. 494(3-4):681-686.
Borovikov YS, Avrova SV, Rysev NA, Sirenko VV, Simonyan AO, Chernev AA, Karpicheva OE, Piers A, Redwood CS (2015). Aberrant movement of β-tropomyosin associated with congenital myopathies causes defective response of myosin heads and actin during the ATPase cycle. Archives of Biochemistry and Biophysics. 577: 11-23.
Karpicheva OE, Robinson P, Piers A, Borovikov YS, Redwood CS (2013). The Nemaline myopathy-causing E117 mutation in β-tropomyosin reduces thin filament activation. Archives of Biochemistry and Biophysics. 536 (1): 25-30.
Piers AT, Lavin T, Radley-Crabb HG, Bakker AJ, Grounds MD, Pinniger GJ (2011). Blockade of TNF in vivo using cV1q antibody reduces contractile dysfunction of skeletal muscle in response to eccentric exercise in dystrophic mdx and normal mice. Neuromuscular Disorders. 21:132–141.
The Royal Children's Hospital Foundation