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Mani P Grover

Researcher at Deakin University

Publications -  5
Citations -  425

Mani P Grover is an academic researcher from Deakin University. The author has contributed to research in topics: Candidate gene & Drug repositioning. The author has an hindex of 4, co-authored 5 publications receiving 412 citations.

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Potential role of glutathione in evolution of thiol-based redox signaling sites in proteins.

TL;DR: A redox-active disulfide may be introduced into a protein structure by stepwise mutation of two residues in the native sequence to Cys, which is likely to be the cysteine of the CSD which undergoes nucleophilic attack by thioredoxin.
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Identification of novel therapeutics for complex diseases from genome-wide association data

TL;DR: In this paper, the authors integrate drug-target data with candidate gene prediction systems to identify novel phenotypes which may benefit from current therapeutics, which can save valuable time and money spent on preclinical studies and phase I clinical trials.

Novel therapeutics for complex diseases from genome-wide association data

Mani P Grover
TL;DR: It is demonstrated that currently available drugs may be repositioned as novel therapeutics for the seven diseases studied here, quickly taking advantage of prior work in pharmaceutics to translate ground-breaking results in genetics to clinical treatments.
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Novel therapeutics for coronary artery disease from genome-wide association study data.

TL;DR: It is demonstrated that available drugs may potentially be repositioned as novel therapeutics for the treatment of CAD and drug repositioning can save valuable time and money spent on preclinical and phase I clinical studies.
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Mapping genotype-phenotype associations of nsSNPs in coiled-coil oligomerization domains of the human proteome

TL;DR: The impact of disease mutations (DMs) versus polymorphisms (PYs) in coiled‐coil domains in UniProt is assessed by modeling the structural and functional impact of variants in silico with the CC prediction program Multicoil and testing the association of CC variants with multiple phenotypes, that is, pleiotropy.