Douglas K. Bishop

RAD51 up-regulation bypasses BRCA1 function and is a common feature of BRCA1-deficient breast tumors.

Crossover interference in Saccharomyces cerevisiae requires a TID1/RDH54- and DMC1-dependent pathway.

Monitoring changes in the subcellular location of proteins in S. cerevisiae.

Early decision; meiotic crossover interference prior to stable strand exchange and synapsis.

A hot spot for RAD51C interactions revealed by a peptide that sensitizes cells to cisplatin.

Heterodimeric complexes of Hop2 and Mnd1 function with Dmc1 to promote meiotic homolog juxtaposition and strand assimilation.

Calcium ion promotes yeast Dmc1 activity via formation of long and fine helical filaments with single-stranded DNA.

Multiple repair pathways mediate tolerance to chemotherapeutic cross-linking agents in vertebrate cells.

Red-Hed regulation: recombinase Rad51, though capable of playing the leading role, may be relegated to supporting Dmc1 in budding yeast meiosis.

Tid1/Rdh54 promotes dissociation of Dmc1 from nonrecombinogenic sites on meiotic chromatin.

Multiple mechanisms of meiotic recombination.

Synthesis-dependent strand annealing in meiosis.

Brca1 in immunoglobulin gene conversion and somatic hypermutation.

Cells deficient in the FANC/BRCA pathway are hypersensitive to plasma levels of formaldehyde.

The Yin and Yang of treating BRCA-deficient tumors.

A comparative analysis of Dmc1 and Rad51 nucleoprotein filaments.

A chemical compound that stimulates the human homologous recombination protein RAD51.

The Mei5-Sae3 protein complex mediates Dmc1 activity in Saccharomyces cerevisiae.

Swi2/Snf2-related translocases prevent accumulation of toxic Rad51 complexes during mitotic growth.

The epistatic relationship between BRCA2 and the other RAD51 mediators in homologous recombination.

RecA homology search is promoted by mechanical stress along the scanned duplex DNA.

RI-1: a chemical inhibitor of RAD51 that disrupts homologous recombination in human cells.

Rad51 is an accessory factor for Dmc1-mediated joint molecule formation during meiosis.

Rad51, the lead in mitotic recombinational DNA repair, plays a supporting role in budding yeast meiosis.

Real-time solution measurement of RAD51- and RecA-mediated strand assimilation without background annealing.

Meiotic crossover control by concerted action of Rad51-Dmc1 in homolog template bias and robust homeostatic regulation.

The RAD51-stimulatory compound RS-1 can exploit the RAD51 overexpression that exists in cancer cells and tumors.

The third exon of the budding yeast meiotic recombination gene HOP2 is required for calcium-dependent and recombinase Dmc1-specific stimulation of homologous strand assimilation.

DNA strand exchange and RecA homologs in meiosis.

Gradual implementation of the meiotic recombination program via checkpoint pathways controlled by global DSB levels.

DNA damage response clamp 9-1-1 promotes assembly of ZMM proteins for formation of crossovers and synaptonemal complex.

RAD54 family translocases counter genotoxic effects of RAD51 in human tumor cells.

Caffeine inhibits gene conversion by displacing Rad51 from ssDNA.

Caffeine impairs resection during DNA break repair by reducing the levels of nucleases Sae2 and Dna2.