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Maureen Higgins

Researcher at University of Dundee

Publications -  53
Citations -  2741

Maureen Higgins is an academic researcher from University of Dundee. The author has contributed to research in topics: Quinone oxidoreductase & KEAP1. The author has an hindex of 20, co-authored 48 publications receiving 2037 citations. Previous affiliations of Maureen Higgins include University of St Andrews.

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Discovery, in vivo activity, and mechanism of action of a small-molecule p53 activator

TL;DR: It is shown that tenovins act through inhibition of the protein-deacetylating activities of SirT1 and SirT2, two important members of the sirtuin family, and underscores the utility of these compounds as biological tools for the study of sIRTuin function as well as their potential therapeutic interest.
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Ribosomal protein S3: A multi-functional protein that interacts with both p53 and MDM2 through its KH domain.

TL;DR: DNA pull-down assays using a 7,8-dihydro-8-oxoguanine duplex oligonucleotide as a substrate found that RPS3 acted as a scaffold for the additional binding of MDM2 and p53, suggesting that R PS3 interacts with important proteins involved in maintaining genomic integrity.
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Novel Cambinol Analogs as Sirtuin Inhibitors: Synthesis, Biological Evaluation, and Rationalization of Activity

TL;DR: Modifications to the core structure of cambinol are described by incorporation of substituents at the N1-position, which lead to increased potency and modified selectivity, which has been rationalized using molecular modeling techniques.
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KEAP1-modifying small molecule reveals muted NRF2 signaling responses in neural stem cells from Huntington's disease patients

TL;DR: The use of a unique chemical scaffold revealed that NRF2 activation responses were muted in HD patient-derived neural stem cells, suggesting increased susceptibility of this critical renewable cell population to oxidative stress in HD brain, and a muted NRf2 activation response in human HD Neural stem cells was discovered, which was restored by genetic correction of the disease-causing mutation.