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Articles by Alan E. Tomkinson
End processing in NHEJ by Polymerase λ and PNKP is coordinated during short-range synapsis
Abstract Non-homologous end joining (NHEJ) is a major pathway of DNA double strand break (DSB) repair, capable of directly joining both damaged strands of DNA through the coordinated activities of repair factors that detect the termini, physically bridge them together, and perform the chemistry necessary to complete repair.
Molecular basis of nick ligation in the nucleosome by DNA Ligase IIIα
Abstract Genomic DNA is packaged into chromatin through a fundamental repeating unit known as the nucleosome core particle. Chromatinized genomic DNA is constantly exposed to endogenous and exogenous stresses that result in DNA damage, which must be repaired to maintain genome stability. Single-strand breaks (SSBs) are a prevalent form of DNA damage that arise via the oxidation-induced disintegration of the sugar-phosphate backbone or as repair intermediates during base excision repair.
UV damage mapping reveals different impacts of yeast XPD mutations on global genomic and transcription-coupled DNA repair
Introduction: NER consists of two intertwined subpathways, global genomic NER (GG-NER) and transcription-coupled NER (TC-NER)1,2. Notably, inherited defects in GG-NER and TC-NER have been identified as the causative factors in xeroderma pigmentosum (XP) and Cockayne syndrome (CS), respectively3,4.
The zinc finger of DNA ligase 3α binds to nucleosomes via an arginine anchor - Nature Communications
Abstract Ligation of DNA single strand breaks is critical for maintaining genome integrity during DNA replication and repair. DNA Ligase III (LIG3α) forms an important complex with X-ray cross complementing protein 1 (XRCC1) during single strand break and base excision repair. We utilize a real time single molecule approach to quantify DNA binding kinetics of HaloTag-LIG3α and XRCC1-YFP from nuclear extracts on long DNA substrates containing nicks, nucleosomes or nicks embedded in nucleosomes.
"Mechanistic Study of DNA Ligase IV-Mediated Double-Strand Break Repair" by Tasmin Naila and Alan E. Tomkinson
DNA repair, DNA Ligase IV, NHEJ, double-strand break repair, Ligation Dissertation Biomedical Sciences Biomedical Sciences Graduate Program Hua-Ying Fan Alan E. Tomkinson David Lee Laurie G. Hudson Naila, Tasmin and Alan E. Tomkinson. "Mechanistic Study of DNA Ligase IV-Mediated Double-Strand Break Repair in Non-Homologous End Joining." (2024). https://digitalrepository.unm.edu/biom_etds/270
Cryo-EM structures and biochemical insights into heterotrimeric PCNA regulation of DNA ligase
Highlights • Cryo-EM structures of archaeal DNA ligase with heterotrimeric PCNA and nicked DNA • DNA ligase contacts two subunits of the PCNA sliding clamp ring • PCNA and DNA ligase form a continuous DNA-binding surface to support an arched DNA shape • Cryo-EM structures and biochemistry provide insight into PCNA stimulation of ligation Summary DNA ligases act in the final step of many DNA repair pathways and are commonly regulated by the DNA sliding clamp proliferating cell nuclear antigen...
Repair of DNA double-strand breaks by mammalian alternative end-joining pathways
Alternative end-joining (a-EJ) pathways, which repair DNA double-strand breaks (DSBs), are initiated by end resection that generates 3′ single strands. This reaction is shared, at least in part, with homologous recombination but distinguishes a-EJ from the major nonhomologous end-joining pathway.
Repair of DNA double-strand breaks by mammalian alternative end-joining pathways
Alternative end-joining (alt-EJ) pathways, which repair DNA double-strand breaks (DSBs), are initiated by end resection that generates 3’ single strands. This reaction is shared, at least in part, with homologous recombination but distinguishes alt-EJ from the major nonhomologous end-joining pathway.
The Human Ligase IIIα-XRCC1 Protein Complex Performs DNA Nick Repair after Transient Unwrapping of Nucleosomal DNA
Reactive oxygen species generate potentially cytotoxic and mutagenic lesions in DNA, both between and within the nucleosomes that package DNA in chromatin. The vast majority of these lesions are subject to base excision repair (BER). Enzymes that catalyze the first three steps in BER can act at many sites in nucleosomes without the aid of chromatin-remodeling agents and without irreversibly disrupting the host nucleosome.
The Human DNA Ligase IIIα-X-ray Repair Cross-complementing Protein 1 Complex Performs DNA Nick Repair after Transient Unwrapping of Nucleosomal DNA
Reactive oxygen species generate potentially cytotoxic and mutagenic lesions in DNA, both between and within the nucleosomes that package DNA in chromatin. The vast majority of these lesions are subject to base excision repair (BER). Enzymes that catalyze the first three steps in BER can act at many sites in nucleosomes without the aid of chromatin-remodeling agents, and without irreversibly disrupting the host nucleosome.
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