Judith L. Campbell

Publications103
h-index41
Citations4,915
Highly Influential Citations316
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BLM-DNA2-RPA-MRN and EXO1-BLM-RPA-MRN constitute two DNA end resection machineries for human DNA break repair.
TLDR
Two of the core machineries that initiate recombinational DNA repair in human cells are established: Bloom helicase and DNA2 nuclease, and the complex comprising MRE11, RAD50, and NBS1 (MRN).
DNA end resection by Dna2-Sgs1-RPA and its stimulation by Top3-Rmi1 and Mre11-Rad50-Xrs2
TLDR
It is established that Dna2, Sgs1 and RPA constitute a minimal protein complex capable of DNA resection in vitro and that both the topoisomerase 3 and Rmi1 complex and the Mre11–Rad50–Xrs2 complex (MRX) have important roles as stimulatory components.
Mrc1 and DNA polymerase epsilon function together in linking DNA replication and the S phase checkpoint.
Evidence Suggesting that Pif1 Helicase Functions in DNA Replication with the Dna2 Helicase/Nuclease and DNA Polymerase δ
TLDR
It is shown that deletion of PIF1 suppresses the lethality of a DNA2-null mutant and the high rate of formation of gross chromosomal rearrangements in pif1Δ mutants, suggesting a role for Dna2 in telomere elongation in the absence of Pif1.
Human Dna2 Is a Nuclear and Mitochondrial DNA Maintenance Protein
TLDR
The data indicate that hDna2 is similar to its yeast counterpart and is a new addition to the growing list of proteins that participate in both nuclear and mitochondrial DNA maintenance.
Dna2 Helicase/Nuclease Causes Replicative Fork Stalling and Double-strand Breaks in the Ribosomal DNA of Saccharomyces cerevisiae*
TLDR
It is shown directly that DNA replication pausing at the ribosomal DNA replication fork barrier (RFB) is accompanied by the occurrence of double-strand breaks near the RFB, which is symbolic of similar events occurring either stochastically throughout the genome or at other regions where replication forks move slowly or stall, such as telomeres, centromeres, or replication slow zones.
The human Bloom syndrome gene suppresses the DNA replication and repair defects of yeast dna2 mutants
TLDR
It is shown that hBLM can suppress both the temperature-sensitive growth defect and the DNA damage sensitivity of the yeast DNA replication mutant dna2-1, suggesting that human BLM participates in the same steps of DNA replication or repair as scFEN1 and scDna2.
Preventing over-resection by DNA2 helicase/nuclease suppresses repair defects in Fanconi anemia cells
TLDR
This work demonstrates that excessive resection can lead to genome instability and shows that strict regulatory processes have evolved to inhibit resection nucleases, and is deleterious to crosslink repair.
Mammalian DNA2 helicase/nuclease cleaves G‐quadruplex DNA and is required for telomere integrity
TLDR
The genetic, cytological, and biochemical results suggest that mammalian DNA2 reduces replication stress at telomeres, thereby preserving genome stability and suppressing cancer development, and that this may involve, at least in part, nucleolytic processing of telomeric G4.
On the Roles of Saccharomyces cerevisiae Dna2p and Flap Endonuclease 1 in Okazaki Fragment Processing*
TLDR
Dna2p has a role in a pathway for processing structured flaps, in which it aids F EN1 using both its nuclease and helicase activities, and substantially stimulated FEN1 cleavage of tailed-foldback flaps and also 30-nucleotide unstructured flaps.
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