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Daniel Lockshon

Researcher at University of Washington

Publications -  12
Citations -  5933

Daniel Lockshon is an academic researcher from University of Washington. The author has contributed to research in topics: Saccharomyces cerevisiae & Gene. The author has an hindex of 11, co-authored 12 publications receiving 5806 citations. Previous affiliations of Daniel Lockshon include Buck Institute for Research on Aging.

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A comprehensive analysis of protein–protein interactions in Saccharomyces cerevisiae

TL;DR: Examination of large-scale yeast two-hybrid screens reveals interactions that place functionally unclassified proteins in a biological context, interactions between proteins involved in the same biological function, and interactions that link biological functions together into larger cellular processes.
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The arrest of replication forks in the rDNA of yeast occurs independently of transcription

TL;DR: It is proposed that replication forks are arrested in a directional manner through the binding of one or more proteins to two closely spaced sites in the RFB.
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A role for recombination junctions in the segregation of mitochondrial DNA in yeast.

TL;DR: It is shown here that resolvase deficiency causes a larger proportion of molecules to be linked together by recombination junctions, resulting in the aggregation of mtDNA into a small number of cytological structures, which can account for the increased mitotic loss of mt DNA and the altered pattern of mitochondrial segregation from zygotes.
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The Complete Set of Predicted Genes from Saccharomyces cerevisiae in a Readily Usable Form

TL;DR: Cloning by genetic recombination obviates the need for ligations or bacterial manipulations and should permit convenient global approaches to gene function that require the assay of each putative yeast gene.
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The sensitivity of yeast mutants to oleic acid implicates the peroxisome and other processes in membrane function.

TL;DR: It is proposed that yeast deficient in peroxisomal and other functions are sensitive to oleate perhaps because of an inability to effectively control the fatty acid composition of membrane phospholipids.