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Sherif F. El-Khamisy

Researcher at University of Sheffield

Publications -  95
Citations -  4760

Sherif F. El-Khamisy is an academic researcher from University of Sheffield. The author has contributed to research in topics: DNA repair & DNA damage. The author has an hindex of 33, co-authored 82 publications receiving 4056 citations. Previous affiliations of Sherif F. El-Khamisy include Ain Shams University & University of Bradford.

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A requirement for PARP‐1 for the assembly or stability of XRCC1 nuclear foci at sites of oxidative DNA damage

TL;DR: The data demonstrate that PARP-1 is required for the assembly or stability of XRCC1 nuclear foci after oxidative DNA damage and suggest that the formation of these foci is mediated via interaction with poly (ADP-ribose).
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Defective DNA single-strand break repair in spinocerebellar ataxia with axonal neuropathy-1

TL;DR: It is reported that TDP1 is sequestered into multi-protein single-strand break repair (SSBR) complexes by direct interaction with DNA ligase IIIα and that these complexes are catalytically inactive in SCAN1 cells, and implicate this process in the maintenance of genetic integrity in post-mitotic neurons.
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The neurodegenerative disease protein aprataxin resolves abortive DNA ligation intermediates

TL;DR: In this article, the authors show that aprataxin resolves abortive DNA ligation intermediates by catalyzing the nucleophilic release of adenylate groups covalently linked to 5'-phosphate termini at single-strand nicks and gaps.
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The Protein Kinase CK2 Facilitates Repair of Chromosomal DNA Single-Strand Breaks

TL;DR: It is shown that CK2 phosphorylates the scaffold protein XRCC1 and thereby enables the assembly and activity of DNA single-strand break repair protein complexes in vitro and at sites of chromosome breakage.
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TDP1 facilitates chromosomal single‐strand break repair in neurons and is neuroprotective in vivo

TL;DR: It is found that cerebellar neurons or primary astrocytes derived from Tdp1−/− mice display an inability to rapidly repair DNA SSBs associated with Top1–DNA complexes or oxidative damage, and a widespread requisite for TDP1 function in response to acutely elevated levels of Top1‐associated DNA strand breaks is revealed.