scispace - formally typeset
J

Jonathan G. Moggs

Researcher at Novartis

Publications -  90
Citations -  6523

Jonathan G. Moggs is an academic researcher from Novartis. The author has contributed to research in topics: Nucleotide excision repair & DNA methylation. The author has an hindex of 37, co-authored 87 publications receiving 6165 citations. Previous affiliations of Jonathan G. Moggs include University of Cambridge & University of Dundee.

Papers
More filters
Journal ArticleDOI

Xeroderma pigmentosum group F caused by a defect in a structure-specific DNA repair endonuclease

TL;DR: Results demonstrate that the XPF, ERCC4, and ERCC11 genes are equivalent, complete the isolation of the XP genes that form the core nucleotide excision repair system, and solve the catalytic function of theXPF-containing complex.
Journal ArticleDOI

Mechanism of open complex and dual incision formation by human nucleotide excision repair factors.

TL;DR: Analysis of mechanism of open complex formation finds that mutations in XPB or XPD, the DNA helicase subunits of the transcription and repair factor TFIIH, can completely prevent opening and dual incision in cell‐free extracts, and supports a mechanism in whichTFIIH‐associated helicase activity and XPC protein catalyze initial formation of the key open intermediate.
Journal ArticleDOI

XPG endonuclease makes the 3' incision in human DNA nucleotide excision repair.

TL;DR: It is shown that XPG makes a structure-specific endonucleolytic incision in a synthetic DNA substrate containing a duplex region and single-stranded arms, by cleaving 3' to DNA damage during nucleotide excision repair.
Journal ArticleDOI

Circulating microRNAs as potential markers of human drug‐induced liver injury

TL;DR: This work provides the first evidence for the potential use of miRNAs as biomarkers of human drug‐induced liver injury by examining these molecules, for the first time, in humans with APAP poisoning.
Journal ArticleDOI

Mechanistic biomarkers provide early and sensitive detection of acetaminophen-induced acute liver injury at first presentation to hospital.

TL;DR: Elevations in plasma miR‐122, HMGB1, and necrosis K18 identified subsequent ALI development in patients on admission to the hospital, soon after acetaminophen overdose, and in patients with ALTs in the normal range.