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Andrew D. Paterson

Researcher at University of Dundee

Publications -  9
Citations -  1402

Andrew D. Paterson is an academic researcher from University of Dundee. The author has contributed to research in topics: MAP2K7 & Type 1 diabetes. The author has an hindex of 8, co-authored 9 publications receiving 1334 citations. Previous affiliations of Andrew D. Paterson include Hospital for Sick Children.

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Journal ArticleDOI

PDK1 acquires PDK2 activity in the presence of a synthetic peptide derived from the carboxyl terminus of PRK2

TL;DR: PDK1 and PDK2 might be the same enzyme, the substrate specificity and activity of PDK1 being regulated through its interaction with another protein(s), and PRK2 is a probable substrate for PDK 1.
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Activation of protein kinase B beta and gamma isoforms by insulin in vivo and by 3-phosphoinositide-dependent protein kinase-1 in vitro: comparison with protein kinase B alpha.

TL;DR: PKBgamma which had been activated by PDK1 possessed a substrate specificity identical with that of PKBalpha and PKBbeta towards a range of peptides, and was the major isoform activated by insulin in rat L6 myotubes (a skeletal-muscle cell line).
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Synergistic activation of stress-activated protein kinase 1/c-Jun N-terminal kinase (SAPK1/JNK) isoforms by mitogen-activated protein kinase kinase 4 (MKK4) and MKK7.

TL;DR: It is reported that MKK3, MKK4 and MKK6 all show a strong preference for phosphorylation of the tyrosine residue of the Thr-Gly-Tyr motifs in their known substrates SAPK2a/p38, SAPK3/ p38 gamma and SAPK4/p 38 delta, demonstrating that Mkk7 is intrinsically a 'dual-specific' protein kinase.
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The Genetic Landscape of Renal Complications in Type 1 Diabetes.

Niina Sandholm, +61 more
TL;DR: Examining a more comprehensive set of genetic variants in larger numbers of subjects with type 1 diabetes characterized for a wider range of cross-sectional diabetic kidney disease phenotypes provides further evidence for the role of genetic factors influencing diabetic kidneys disease in those with type 2 diabetes and highlights some key pathways that may be responsible.