Featured Publications
A cell-penetrating antibody inhibits human RAD51 via direct binding
Turchick A, Hegan DC, Jensen RB, Glazer PM. A cell-penetrating antibody inhibits human RAD51 via direct binding. Nucleic Acids Research 2017, 45: 11782-11799. PMID: 29036688, PMCID: PMC5714174, DOI: 10.1093/nar/gkx871.Peer-Reviewed Original ResearchConceptsHomology-directed repairMolecular basisDirect bindingSynthetic lethal killingPre-clinical developmentBRCA2-deficient cancer cellsCell-penetrating antibodiesAnti-cancer agentsLupus autoantibodiesHuman Rad51DNA repairDNA bindingRAD51N-terminusCancer cellsSilico molecular modelingFunction mutationsCancer therapySpecific inhibitorDNANovel inhibitorsAttractive targetComplementarity-determining regionsMolecular modelingCell penetrationBRCA2 is epistatic to the RAD51 paralogs in response to DNA damage
Jensen RB, Ozes A, Kim T, Estep A, Kowalczykowski SC. BRCA2 is epistatic to the RAD51 paralogs in response to DNA damage. DNA Repair 2013, 12: 306-311. PMID: 23384538, PMCID: PMC3602134, DOI: 10.1016/j.dnarep.2012.12.007.Peer-Reviewed Original ResearchConceptsRAD51 paralogsHomologous recombinationDNA double-strand breaksDNA damage responseDNA DSB repairDonor DNA moleculesDouble-strand breaksHigh-fidelity repairLoss of BRCA2SiRNA-mediated knockdownHuman BRCA2 proteinCell cycle arrestGenetic interactionsSister chromatidsDamage responseDSB repairMammalian cellsParalogsRegulated eventDNA breaksEnzymatic functionMechanistic functionBRCA2 proteinCentral playerHuman cells
2024
Dormant origin firing promotes head-on transcription-replication conflicts at transcription termination sites in response to BRCA2 deficiency
Goehring L, Keegan S, Lahiri S, Xia W, Kong M, Jimenez-Sainz J, Gupta D, Drapkin R, Jensen R, Smith D, Rothenberg E, Fenyö D, Huang T. Dormant origin firing promotes head-on transcription-replication conflicts at transcription termination sites in response to BRCA2 deficiency. Nature Communications 2024, 15: 4716. PMID: 38830843, PMCID: PMC11148086, DOI: 10.1038/s41467-024-48286-1.Peer-Reviewed Original ResearchConceptsTranscription termination sitesTranscription-replication conflictsDormant originsReplication stressElongating RNA polymerase IITermination sitesResponse to replication stressRNA polymerase IIR-loop formationTumor suppressor proteinPolymerase IIR-loopsLong genesRNase H2Transcription initiationOK-seqGenomic sitesSuppressor proteinCellular genomeBRCA2 deficiencyOrigin firingSuper-resolution microscopyGenomic instabilityDormant origin firingTranscription