Jachen A. Solinger
University of California, Davis
24 Papers
162 Citations
Jachen A. Solinger is an academic researcher from University of California, Davis. The author has contributed to research in topics: RAD51 & DNA. The author has an hindex of 15, co-authored 18 publications. Previous affiliations of Jachen A. Solinger include Kaiserslautern University of Technology & University of Virginia.
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Papers
Rad54, a Swi2/Snf2-like Recombinational Repair Protein, Disassembles Rad51:dsDNA Filaments
TL;DR: Rad54 protein is a member of the Swi2/Snf2-like family of DNA-dependent/stimulated ATPases that dissociate and remodel protein complexes on dsDNA as mentioned in this paper.
294
Holliday junctions in the eukaryotic nucleus: resolution in sight?
TL;DR: The endonucleases Mus81/Mms4-Eme1 and XPF-MEI-9/MUS312 are structurally related to the archaeal resolvase Hjc and were found to be involved in crossover formation in budding yeast and flies, respectively and open up the possibility that junctions other than classical Holliday junctions might contribute to crossovers.
106
Terminal association of Rad54 protein with the Rad51-dsDNA filament.
TL;DR: The authors' data support a mechanism of processive dsDNA-Rad51 filament dissociation by the translocating Rad54 protein, and show that an oligomeric form of Rad54 associates preferentially with termini of the Rad51-dsDNA filament.
70
Rad54 Protein Exerts Diverse Modes of ATPase Activity on Duplex DNA Partially and Fully Covered with Rad51 Protein
TL;DR: It is suggested that the interaction of Rad54 with dsDNA-Rad51 complexes is of functional importance in homologous recombination in DNA strand exchange.
56
Spontaneous and double-strand break-induced recombination, and gene conversion tract lengths, are differentially affected by overexpression of wild-type or ATPase-defective yeast Rad54.
TL;DR: It is found that overexpression of ATPase(-) Rad54 reduced spontaneous direct repeat gene conversion and increased both spontaneous direct Repeat deletion and spontaneous allelic conversion, which contributes to genome stability by promoting high-fidelity DSB repair and suppressing spontaneous deletions.