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Mark Isalan

Researcher at Imperial College London

Publications -  102
Citations -  3964

Mark Isalan is an academic researcher from Imperial College London. The author has contributed to research in topics: Zinc finger & Gene. The author has an hindex of 31, co-authored 89 publications receiving 3540 citations. Previous affiliations of Mark Isalan include University of Cambridge & European Bioinformatics Institute.

Papers
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Journal ArticleDOI

A rapid, generally applicable method to engineer zinc fingers illustrated by targeting the HIV-1 promoter.

TL;DR: A rapid and convenient method that can be used to design zinc finger proteins against a variety of DNA-binding sites and yields proteins that bind sequence-specifically to DNA with Kd values in the nanomolar range is presented.
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Evolvability and hierarchy in rewired bacterial gene networks

TL;DR: It is shown that ∼95% of new networks are tolerated by the bacteria, that very few alter growth, and that expression level correlates with factor position in the wild-type network hierarchy, and therefore new links in the network are rarely a barrier for evolution and can even confer a fitness advantage.
Patent

Nucleic acid binding polypeptide library

TL;DR: In this article, the authors describe a set of zinc finger polypeptide libraries which encode overlapping zinc fingers, with each polypide comprising more than one zinc finger which has been at least partially randomised.
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Synthetic zinc finger repressors reduce mutant huntingtin expression in the brain of R6/2 mice.

TL;DR: Zinc finger repression was tested at several levels, resulting in protein aggregate reduction, reduced decline in rotarod performance, and alleviation of clasping in R6/2 mice, establishing a proof-of-principle for synthetic transcription factor repressors in the brain.
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Zinc-finger protein-targeted gene regulation: Genomewide single-gene specificity

TL;DR: It is reported that a ZFP TF can repress target gene expression with single-gene specificity within the human genome and was sufficient to generate a functional phenotype, as demonstrated by the loss of DNA damage-induced CHK2-dependent p53 phosphorylation.