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Robert A. Seaborne

Researcher at Queen Mary University of London

Publications -  32
Citations -  832

Robert A. Seaborne is an academic researcher from Queen Mary University of London. The author has contributed to research in topics: Skeletal muscle & DNA methylation. The author has an hindex of 9, co-authored 28 publications receiving 525 citations. Previous affiliations of Robert A. Seaborne include Liverpool John Moores University & Keele University.

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Human Skeletal Muscle Possesses an Epigenetic Memory of Hypertrophy

TL;DR: GRIK2, TRAF1, BICC1, STAG1 were epigenetically sensitive to acute exercise demonstrating hypomethylation after a single bout of resistance exercise that was maintained 22 weeks later with the largest increase in gene expression and muscle mass after reloading.
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Does skeletal muscle have an ‘epi’-memory? The role of epigenetics in nutritional programming, metabolic disease, aging and exercise

TL;DR: It is believed that understanding the ‘epi’‐memory of skeletal muscle will enable the next generation of targeted therapies to promote muscle growth and reduce muscle loss to enable healthy aging.
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Comparative Transcriptome and Methylome Analysis in Human Skeletal Muscle Anabolism, Hypertrophy and Epigenetic Memory

TL;DR: For the first time across the transcriptome and epigenome combined, this study identifies novel differentially methylated genes associated with human skeletal muscle anabolism, hypertrophy and epigenetic memory.
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Methylome of human skeletal muscle after acute & chronic resistance exercise training, detraining & retraining

TL;DR: These valuable methylome data sets described in the present manuscript can now be shared and re-used to enable the identification of epigenetically regulated genes/networks that are modified after acute anabolic stimuli and hypertrophy, and further investigate the phenomenon of epigenetic memory in skeletal muscle.
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Transcriptomic and epigenetic regulation of disuse atrophy and the return to activity in skeletal muscle

TL;DR: This is the first study to demonstrate that skeletal muscle atrophy in response to disuse is accompanied by dynamic methylation modifications that are associated with alterations in gene expression, and that these epigenetic modifications and gene expression profiles are reversible after skeletal muscle returns to normal activity.