M
Mark E. Cooper
Researcher at University of Queensland
Publications - 1514
Citations - 141899
Mark E. Cooper is an academic researcher from University of Queensland. The author has contributed to research in topics: Diabetes mellitus & Diabetic nephropathy. The author has an hindex of 158, co-authored 1463 publications receiving 124887 citations. Previous affiliations of Mark E. Cooper include University of Cambridge & University of Adelaide.
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Receptor for advanced glycation end-products (RAGE) provides a link between genetic susceptibility and environmental factors in type 1 diabetes
Josephine M. Forbes,Josephine M. Forbes,Jenny Söderlund,Jenny Söderlund,Felicia Y. T. Yap,Mikael Knip,Sofianos Andrikopoulos,Jorma Ilonen,Jorma Ilonen,Olli Simell,Riitta Veijola,Karly C. Sourris,Melinda T. Coughlan,Carol Forsblom,Carol Forsblom,Robyn Maree Slattery,Shane T. Grey,Maija Wessman,Hiroshi Yamamoto,Angelika Bierhaus,Mark E. Cooper,Mark E. Cooper,Per-Henrik Groop,Per-Henrik Groop,Per-Henrik Groop +24 more
TL;DR: These studies suggest that inherited AGER gene polymorphisms may confer susceptibility to environmental insults, and declining circulating levels of soluble RAGE, before the development of overt diabetes, may also be predictive of clinical disease in children with high to medium risk HLA II backgrounds.
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Amylin as a growth factor during fetal and postnatal development of the rat kidney
TL;DR: It is suggested that amylin peptide is biosynthesized in the developing proximal tubules, acts in an autocrine fashion to promote the proliferation and differentiation of brush border epithelial cells and hence plays an important role as a growth factor in the development of the kidney.
Journal ArticleDOI
Drug-likeness and increased hydrophobicity of commercially available compound libraries for drug screening.
Johannes Zuegg,Mark E. Cooper +1 more
TL;DR: A 'right shift' of chemical properties has been found in the majority of the compounds with significant biological activity in ChEMBL, reflecting a common trend in current drug discovery, towards larger, more hydrophobic compounds and fewer drug-like compounds.
Journal ArticleDOI
Deficiency in Mitochondrial Complex I Activity Due to Ndufs6 Gene Trap Insertion Induces Renal Disease
Josephine M. Forbes,Bi-Xia Ke,Tuong-Vi Nguyen,Darren C. Henstridge,Sally A. Penfold,Adrienne Laskowski,Karly C. Sourris,Lukas N. Groschner,Mark E. Cooper,David R. Thorburn,Melinda T. Coughlan +10 more
TL;DR: In this paper, mice with a knockdown of the complex I gene, Ndufs6 were studied to determine whether an abnormality in mitochondrial complex I per se is associated with development of renal disease.