Fengshan Liang, PhD
Research Scientist In Laboratory MedicineDownloadHi-Res Photo
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Laboratory Medicine
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About
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Research Scientist In Laboratory Medicine
Appointments
Laboratory Medicine
Research ScientistPrimary
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Education & Training
- PhD
- Chinese Academy of Sciences (2004)
Research
Overview
Medical Subject Headings (MeSH)
Chemicals and Drugs; Diseases; Health Care
Research at a Glance
Yale Co-Authors
Frequent collaborators of Fengshan Liang's published research.
Publications Timeline
A big-picture view of Fengshan Liang's research output by year.
Manoj M Pillai, MBBS
Sandy Chang, MD, PhD, BS
Peili Gu, PhD
Prajwal Boddu, MD
Rekha Rai, PhD
Ryan B. Jensen, PhD
24Publications
755Citations
Publications
2024
TRF2–RAP1 represses RAD51-dependent homology-directed telomere repair by promoting BLM-mediated D-loop unwinding and inhibiting BLM–DNA2-dependent 5′-end resection
Liang F, Rai R, Sodeinde T, Chang S. TRF2–RAP1 represses RAD51-dependent homology-directed telomere repair by promoting BLM-mediated D-loop unwinding and inhibiting BLM–DNA2-dependent 5′-end resection. Nucleic Acids Research 2024, 52: 9695-9709. PMID: 39082275, PMCID: PMC11381343, DOI: 10.1093/nar/gkae642.Peer-Reviewed Original ResearchAltmetricConceptsHomology-directed repairTelomeric D-loopsD-loopChromosome fusionsD-loop formationSingle-stranded telomeric overhangsHomology searchTelomere clusteringTRFH domainPurified proteinBasic domainBlm mutantsProtect telomeresGenomic instabilityTelomeric overhangEnd resectionTRF2Molecular mechanismsTelomereTelomere lossMolecular pathwaysTelomere repairGenomeMutantsRap1The FANCI/FANCD2 complex links DNA damage response to R-loop regulation through SRSF1-mediated mRNA export
Olazabal-Herrero A, He B, Kwon Y, Gupta A, Dutta A, Huang Y, Boddu P, Liang Z, Liang F, Teng Y, Lan L, Chen X, Pei H, Pillai M, Sung P, Kupfer G. The FANCI/FANCD2 complex links DNA damage response to R-loop regulation through SRSF1-mediated mRNA export. Cell Reports 2024, 43: 113610. PMID: 38165804, PMCID: PMC10865995, DOI: 10.1016/j.celrep.2023.113610.Peer-Reviewed Original ResearchCitationsAltmetric
2023
Pot1b −/− tumors activate G-quadruplex-induced DNA damage to promote telomere hyper-elongation
Takasugi T, Gu P, Liang F, Staco I, Chang S. Pot1b −/− tumors activate G-quadruplex-induced DNA damage to promote telomere hyper-elongation. Nucleic Acids Research 2023, 51: 9227-9247. PMID: 37560909, PMCID: PMC10516629, DOI: 10.1093/nar/gkad648.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsDNA damage responseDamage responseReplication protein A (RPA) complexDependent DNA damage responseTelomere length homeostasisTelomere maintenance mechanismLength homeostasisTelomerase recruitmentPOT1 proteinsHuman POT1Mouse genomeLength maintenanceFunction disruptsReplicative immortalityTelomeresPOT1 mutationsDNA damageHuman cancersLonger telomeresPOT1bMaintenance mechanismsSerial transplantationA complexesSimilar mechanismMutations
2022
Complex Formation between FANCD2 and the Splicing Factor SRSF1 Helps Prevent R-Loop Accumulation through mRNA Export Regulation
Herrero A, Liang F, Dutta A, Huang Y, Liang Z, Gupta A, Lan L, Pillai M, Sung P, Kupfer G. Complex Formation between FANCD2 and the Splicing Factor SRSF1 Helps Prevent R-Loop Accumulation through mRNA Export Regulation. Blood 2022, 140: 5828-5829. DOI: 10.1182/blood-2022-166798.Peer-Reviewed Original Research
2021
Fanci-FANCD2 Promotes Genome Stability and DNA Repair By Down-Regulating BLM Helicase Activity
Liang F, Nagarajan A, Pillai M, Sung P, Kupfer G. Fanci-FANCD2 Promotes Genome Stability and DNA Repair By Down-Regulating BLM Helicase Activity. Blood 2021, 138: 1113. DOI: 10.1182/blood-2021-152218.Peer-Reviewed Original ResearchConceptsDNA end resectionReplication forksGenome stabilityDNA repairResection activityRAD51 recruitmentEnd resectionAmino acid deletionBloom syndromeFanconi anemiaMutant cellsFA DNA repair pathwayAcid deletionDNA damageDNA damage hypersensitivityReplication fork collapseBLM helicase activityEfficient DNA repairHolliday junction dissolutionDNA damage repairDNA repair pathwaysRAD51 foci formationDouble Holliday junction dissolutionIsolation of proteinsHU sensitivity
2020
The DNA-binding activity of USP1-associated factor 1 is required for efficient RAD51-mediated homologous DNA pairing and homology-directed DNA repair
Liang F, Miller AS, Tang C, Maranon D, Williamson EA, Hromas R, Wiese C, Zhao W, Sung P, Kupfer GM. The DNA-binding activity of USP1-associated factor 1 is required for efficient RAD51-mediated homologous DNA pairing and homology-directed DNA repair. Journal Of Biological Chemistry 2020, 295: 8186-8194. PMID: 32350107, PMCID: PMC7294083, DOI: 10.1074/jbc.ra120.013714.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsHomologous DNA pairingDNA-binding activityDNA pairingDNA repairDNA bindingFanconi anemia complementation group D2 proteinDamage repairHomology-directed DNA repairRAD51 recombinase activityFanconi anemia pathwayDNA damage sensitivityChromosome damage repairHR-mediated DNA repairDNA damage responseDNA damage repairHomologous recombination pathwayFactor 1FANCD2 deubiquitinationRole of DNAEfficient RAD51Deubiquitinase complexRecombinase RAD51Damage responseUAF1D2 protein
2019
UAF1 DNA Binding Activity Is Critical for RAD51-Mediated Homologous DNA Pairing
Liang F, Miller A, Tang C, Sung P, Kupfer G. UAF1 DNA Binding Activity Is Critical for RAD51-Mediated Homologous DNA Pairing. Blood 2019, 134: 2497. DOI: 10.1182/blood-2019-130435.Peer-Reviewed Original ResearchConceptsHomologous DNA pairingHomologous recombinationDNA binding activityDNA repairDNA bindingDNA pairingHomologous DNAFanconi anemia DNA repair pathwayHR efficiencyFA core complexDNA damageDNA damage sensitivityDNA damage resistanceDNA-binding mutantSynaptic complex assemblyBinding activityE3 ligase activityDNA damage repairDNA repair pathwaysPresynaptic complex formationFANCD2 deubiquitinationGenome maintenanceComplex formationDeubiquitinase complexMutant proteinsChromatin‐bound cGAS is an inhibitor of DNA repair and hence accelerates genome destabilization and cell death
Jiang H, Xue X, Panda S, Kawale A, Hooy RM, Liang F, Sohn J, Sung P, Gekara NO. Chromatin‐bound cGAS is an inhibitor of DNA repair and hence accelerates genome destabilization and cell death. The EMBO Journal 2019, 38: embj2019102718. PMID: 31544964, PMCID: PMC6826206, DOI: 10.15252/embj.2019102718.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsCyclic GMP-AMP synthaseHomologous recombinationDNA repairGenome destabilizationCell deathChromatin-binding proteinsGMP-AMP synthaseSsDNA filamentsGenome integrityGenomic stressInnate immune sensorsHR repairChromosomal rearrangementsStrand invasionRegulatory mechanismsUnknown roleCytosolic innate immune sensorsCell survivalTemplate dsDNAImmune sensorsBone marrow cellsMicronuclei generationOutcome of infectionMarrow cellsInnate immune activationDNA requirement in FANCD2 deubiquitination by USP1-UAF1-RAD51AP1 in the Fanconi anemia DNA damage response
Liang F, Miller AS, Longerich S, Tang C, Maranon D, Williamson EA, Hromas R, Wiese C, Kupfer GM, Sung P. DNA requirement in FANCD2 deubiquitination by USP1-UAF1-RAD51AP1 in the Fanconi anemia DNA damage response. Nature Communications 2019, 10: 2849. PMID: 31253762, PMCID: PMC6599204, DOI: 10.1038/s41467-019-10408-5.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsFANCD2 deubiquitinationDNA damage response pathwayFanconi anemiaUSP1-UAF1 complexDNA damage toleranceDNA damage responseDamage response pathwayImportance of DNAGenome repairDamage responseResponse pathwaysUAF1DNA requirementsCellular settingsFA pathwayDNA bindingDownstream eventsDeubiquitinationRAD51AP1DNA crosslinksBiochemical systemsBone marrow failureChromosomal lesionsMultigenic diseasesMultifaceted roleBinding of FANCI-FANCD2 Complex to RNA and R-Loops Stimulates Robust FANCD2 Monoubiquitination
Liang Z, Liang F, Teng Y, Chen X, Liu J, Longerich S, Rao T, Green AM, Collins NB, Xiong Y, Lan L, Sung P, Kupfer GM. Binding of FANCI-FANCD2 Complex to RNA and R-Loops Stimulates Robust FANCD2 Monoubiquitination. Cell Reports 2019, 26: 564-572.e5. PMID: 30650351, PMCID: PMC6350941, DOI: 10.1016/j.celrep.2018.12.084.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsR-loopsCo-transcriptional R-loopsFANCI-FANCD2 complexFanconi anemiaR-loop structuresSeries of RNADNA replicative stressGuanine-rich sequencesFANCD2 monoubiquitinationGenomic lociID2 complexReplicative stressFA cellsRNA transcriptionFA pathwayComplex bindsDNA hybridsCancer predispositionBone marrow failureDNA damageRNAMonoubiquitinationDevelopmental abnormalitiesMarrow failureSsRNA
Academic Achievements & Community Involvement
activity UAF1 DNA Binding Activity is Critical for RAD51-Mediated Homologous DNA Pairing.
Oral PresentationUAF1 DNA Binding Activity is Critical for RAD51-Mediated Homologous DNA Pairing.Details01/01/2019 - PresentChicago, IL, United StatesSponsored by The 31st Annual FA Scientific Symposium.activity The Role of UAF1 in the Fanconi Anemia Pathway Regulation of Homologous Recombination-Mediated Genome Maintenance.
Poster PresentationThe Role of UAF1 in the Fanconi Anemia Pathway Regulation of Homologous Recombination-Mediated Genome Maintenance.Details01/01/2016 - PresentWashington, DC, United StatesSponsored by The 2016 American Society of Hematology (ASH) meeting.activity Promotion of RAD51-mediated Homologous DNA Pairing by the RAD51AP1-UAF1 Complex.
Poster PresentationPromotion of RAD51-mediated Homologous DNA Pairing by the RAD51AP1-UAF1 Complex.Details01/01/2016 - PresentBellevue, WA, United StatesSponsored by The 28th Annual FA Scientific Symposium.activity RAD51AP1-UAF1 Promotes RAD51-mediated Homologous DNA Pairing.
Poster PresentationRAD51AP1-UAF1 Promotes RAD51-mediated Homologous DNA Pairing.Details01/01/2015 - PresentFalmouth, MA, United StatesSponsored by Yale Molecular Biophysics and Biochemistry Research Meetingactivity Coordination of chromatid separation and spindle elongation by antagonistic activities of mitotic and S-phase CDKs
Poster PresentationCoordination of chromatid separation and spindle elongation by antagonistic activities of mitotic and S-phase CDKsDetails01/01/2012 - PresentAtlanta, GA, United StatesSponsored by SERYM