2022
OligoTRAFTACs: A generalizable method for transcription factor degradation
Samarasinghe KTG, An E, Genuth MA, Chu L, Holley SA, Crews CM. OligoTRAFTACs: A generalizable method for transcription factor degradation. RSC Chemical Biology 2022, 3: 1144-1153. PMID: 36128504, PMCID: PMC9428672, DOI: 10.1039/d2cb00138a.Peer-Reviewed Original ResearchTranscription factorsOncogenic transcription factorGene expression circuitryTranscription factor degradationDNA binding abilityChordoma cell linesProteasomal degradationProteasomal pathwayZebrafish experimentsC-MycGeneralizable platformKey playersCell linesBrachyurySmall moleculesFactor degradationBinding abilityGeneralizable methodDegradationChimerasPathwayOligonucleotidePocketFirst generation
2021
Integrated mutational landscape analysis of uterine leiomyosarcomas
Choi J, Manzano A, Dong W, Bellone S, Bonazzoli E, Zammataro L, Yao X, Deshpande A, Zaidi S, Guglielmi A, Gnutti B, Nagarkatti N, Tymon-Rosario JR, Harold J, Mauricio D, Zeybek B, Menderes G, Altwerger G, Jeong K, Zhao S, Buza N, Hui P, Ravaggi A, Bignotti E, Romani C, Todeschini P, Zanotti L, Odicino F, Pecorelli S, Ardighieri L, Bilguvar K, Quick CM, Silasi DA, Huang GS, Andikyan V, Clark M, Ratner E, Azodi M, Imielinski M, Schwartz PE, Alexandrov LB, Lifton RP, Schlessinger J, Santin AD. Integrated mutational landscape analysis of uterine leiomyosarcomas. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2025182118. PMID: 33876771, PMCID: PMC8053980, DOI: 10.1073/pnas.2025182118.Peer-Reviewed Original ResearchConceptsHomologous recombination DNA repair deficiencySequencing dataWhole-genome sequencing dataRNA sequencing dataTCGA samplesCopy number variation analysisATRX/DAXXCopy number lossNumber variation analysisDNA repair deficiencyWhole-exome sequencing dataRecurrent somatic mutationsCopy number gainsCancer Genome AtlasPatient-derived xenograftsTumor suppressorAkt geneGenetic landscapeHRD signaturesPTEN geneGenesMost fusionsC-MycMutational signaturesC-myc/
2020
Derangements in HUWE1/c-MYC pathway confer sensitivity to the BET bromodomain inhibitor GS-626510 in uterine cervical carcinoma
Bonazzoli E, Bellone S, Zammataro L, Gnutti B, Guglielmi A, Pelligra S, Nagarkatti N, Manara P, Tymon-Rosario J, Zeybek B, Altwerger G, Menderes G, Han C, Ratner E, Silasi DA, Huang GS, Andikyan V, Azodi M, Schwartz PE, Santin AD. Derangements in HUWE1/c-MYC pathway confer sensitivity to the BET bromodomain inhibitor GS-626510 in uterine cervical carcinoma. Gynecologic Oncology 2020, 158: 769-775. PMID: 32600791, PMCID: PMC8253557, DOI: 10.1016/j.ygyno.2020.06.484.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnimalsCell Line, TumorFemaleHumansImidazolesIn Situ Hybridization, FluorescenceIsoxazolesMiceMiddle AgedProteinsProto-Oncogene Proteins c-mycSignal TransductionTumor Suppressor ProteinsUbiquitin-Protein LigasesUterine Cervical NeoplasmsXenograft Model Antitumor AssaysYoung AdultConceptsC-myc expressionC-Myc pathwayTwice-daily oral dosesC-MycWestern blotChemotherapy-resistant diseaseUterine cervical carcinomaPotential therapeutic targetEffective therapeutic agentDose-response decreaseCC xenograftsCell line growthOral dosesCervical carcinomaPrimary tumorDeletion/mutationClinical studiesTherapeutic targetTherapeutic agentsNormal tissuesBET inhibitorsVivo activityQRT-PCRCell proliferationGene deletion/mutationPotent BRD4 inhibitor suppresses cancer cell-macrophage interaction
Yin M, Guo Y, Hu R, Cai WL, Li Y, Pei S, Sun H, Peng C, Li J, Ye R, Yang Q, Wang N, Tao Y, Chen X, Yan Q. Potent BRD4 inhibitor suppresses cancer cell-macrophage interaction. Nature Communications 2020, 11: 1833. PMID: 32286255, PMCID: PMC7156724, DOI: 10.1038/s41467-020-15290-0.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, OralAnimalsCell CommunicationCell Cycle ProteinsCell Line, TumorCell ProliferationDisease Models, AnimalDown-RegulationDrug DesignFemaleHumansHypoxia-Inducible Factor 1, alpha SubunitMacrophage Colony-Stimulating FactorMacrophagesMice, Inbred BALB CMice, NudeNeoplasmsPhosphorylationProto-Oncogene Proteins c-mycReceptors, Granulocyte-Macrophage Colony-Stimulating FactorSignal TransductionTranscription FactorsTreatment OutcomeConceptsTumor growthMajor clinical stagesBET inhibitorsProliferation of tumorsExtraterminal domain (BET) family proteinsTumor cell proliferationClinical stageTumor shrinkageSyngeneic modelPotent BRD4 inhibitorsSmall molecule inhibitorsSolid tumorsBRD4 inhibitionTumor cellsOral bioavailabilityCancer treatmentCell proliferationBRD4 inhibitorsMolecule inhibitorsMultiple mechanismsC-MycTumorsInhibitors
2019
Characterization of Long Noncoding RNA and mRNA Profiles in Sepsis-Induced Myocardial Depression
Zhang TN, Goodwin JE, Liu B, Li D, Wen R, Yang N, Xia J, Zhou H, Zhang T, Song WL, Liu CF. Characterization of Long Noncoding RNA and mRNA Profiles in Sepsis-Induced Myocardial Depression. Molecular Therapy - Nucleic Acids 2019, 17: 852-866. PMID: 31472370, PMCID: PMC6722300, DOI: 10.1016/j.omtn.2019.07.020.Peer-Reviewed Original ResearchGene Ontology term enrichmentMRNA profilesCell apoptosisMyocardial depressionBasic molecular mechanismsLong noncoding RNAPVT1 geneTerm enrichmentNoncoding RNAsRNA sequencingSeptic shockNovel lncRNAMolecular mechanismsRat modelLncRNAsFunctional roleRelated pathwaysC-MycHypodynamic septic shockCaspase-3Intensive care unitExpression of MyD88Bcl-2ApoptosisLeft ventricular tissue
2018
Role of eIF3a in 4-amino-2-trifluoromethyl-phenyl retinate-induced cell differentiation in human chronic myeloid leukemia K562 cells
Li G, Wang K, Li Y, Ruan J, Wang C, Qian Y, Zu S, Dai B, Meng Y, Zhou R, Ge J, Chen F. Role of eIF3a in 4-amino-2-trifluoromethyl-phenyl retinate-induced cell differentiation in human chronic myeloid leukemia K562 cells. Gene 2018, 683: 195-209. PMID: 30340049, DOI: 10.1016/j.gene.2018.10.035.Peer-Reviewed Original ResearchConceptsMyeloid differentiation marker CD11bCyclin D1Trans retinoic acid (ATRA) derivativeK562 cellsAnti-tumor effectsChronic myeloid leukemia K562 cellsMyeloid leukemia cell differentiationRetinoic acid derivativesCell differentiationG0/G1 phaseExpression of eIF3aC-MycHuman chronic myeloid leukemia K562 cellsDifferentiation marker CD11bTumor cell proliferationRole of eIF3aActivation of ERK1/2Marker CD11bCML cellsLeukemia cell differentiationP-ERKLeukemia K562 cellsPhenyl retinateP-RafEIF3a expressionInhibition of BET Bromodomain Proteins with GS-5829 and GS-626510 in Uterine Serous Carcinoma, a Biologically Aggressive Variant of Endometrial Cancer
Bonazzoli E, Predolini F, Cocco E, Bellone S, Altwerger G, Menderes G, Zammataro L, Bianchi A, Pettinella F, Riccio F, Han C, Yadav G, Lopez S, Manzano A, Manara P, Buza N, Hui P, Wong S, Litkouhi B, Ratner E, Silasi DA, Huang GS, Azodi M, Schwartz PE, Schlessinger J, Santin AD. Inhibition of BET Bromodomain Proteins with GS-5829 and GS-626510 in Uterine Serous Carcinoma, a Biologically Aggressive Variant of Endometrial Cancer. Clinical Cancer Research 2018, 24: 4845-4853. PMID: 29941483, PMCID: PMC6168417, DOI: 10.1158/1078-0432.ccr-18-0864.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAnimalsAntineoplastic AgentsApoptosisAurora Kinase AAurora Kinase BAzepinesCell Line, TumorCell ProliferationCystadenocarcinoma, SerousDose-Response Relationship, DrugEndometrial NeoplasmsExome SequencingFemaleGene Expression Regulation, NeoplasticHumansMiceMiddle AgedPhosphorylationPrimary Cell CultureProteinsProto-Oncogene Proteins c-mycTriazolesUterine NeoplasmsXenograft Model Antitumor AssaysConceptsUterine serous carcinomaPrimary USC cell linesUSC cell linesC-myc expressionCell linesC-MycChemotherapy-resistant diseaseQRT-PCRHigh c-myc expressionDose-dependent decreaseDose-dependent increasePotential therapeutic targetEffective therapeutic agentMouse xenograft modelClin Cancer ResFresh frozen tumor tissueC-myc gene amplificationUSC xenograftsEndometrial cancerAggressive variantSerous carcinomaWhole-exome sequencing studiesClinical studiesConcentrations/dosesXenograft model4-Amino-2-Trifluoromethyl-Phenyl Retinate induced leukemia cell differentiation by decreasing eIF6
Wang K, Wang C, Zhu C, Li G, Li Y, Feng Y, Ruan J, Zhu F, Meng Y, Zhou R, Chen F. 4-Amino-2-Trifluoromethyl-Phenyl Retinate induced leukemia cell differentiation by decreasing eIF6. Biochemical And Biophysical Research Communications 2018, 503: 2033-2039. PMID: 30078681, DOI: 10.1016/j.bbrc.2018.07.153.Peer-Reviewed Original ResearchConceptsLeukemia cell differentiationTrans retinoic acid (ATRA) derivativeEukaryotic translation initiation factor 6Cell proliferationEffects of ATPRRetinoic acid derivativesCell differentiationSurface antigen CD11bDifferentiation of K562Potential molecular mechanismsProliferation of K562Leukemia cell linesPhenyl retinateATPRInnovative treatmentsLeukemia cellsCell surface antigen CD11bC-MycCell linesFactor 6Induced differentiationK562ProliferationMolecular mechanismsCBF
2017
BET protein proteolysis targeting chimera (PROTAC) exerts potent lethal activity against mantle cell lymphoma cells
Sun B, Fiskus W, Qian Y, Rajapakshe K, Raina K, Coleman KG, Crew AP, Shen A, Saenz DT, Mill CP, Nowak AJ, Jain N, Zhang L, Wang M, Khoury JD, Coarfa C, Crews CM, Bhalla KN. BET protein proteolysis targeting chimera (PROTAC) exerts potent lethal activity against mantle cell lymphoma cells. Leukemia 2017, 32: 343-352. PMID: 28663582, DOI: 10.1038/leu.2017.207.Peer-Reviewed Original ResearchConceptsMantle cell lymphoma cellsMCL cellsCell lymphoma cellsARV-825ARV-771Lymphoma cellsGreater survival improvementSuperior preclinical activityCDK4/6 inhibitor palbociclibNuclear factor-κB (NF-κB) target genesExtraterminal protein inhibitorSurvival improvementInhibitor palbociclibPreclinical activityCDKN1A/p21Inhibitor treatmentSuperior pharmacological propertiesVivo growthCyclin D1Pharmacological propertiesProtein expressionMore apoptosisVivo evaluationIncomplete inhibitionC-MycNovel BET protein proteolysis-targeting chimera exerts superior lethal activity than bromodomain inhibitor (BETi) against post-myeloproliferative neoplasm secondary (s) AML cells
Saenz DT, Fiskus W, Qian Y, Manshouri T, Rajapakshe K, Raina K, Coleman KG, Crew AP, Shen A, Mill CP, Sun B, Qiu P, Kadia TM, Pemmaraju N, DiNardo C, Kim MS, Nowak AJ, Coarfa C, Crews CM, Verstovsek S, Bhalla KN. Novel BET protein proteolysis-targeting chimera exerts superior lethal activity than bromodomain inhibitor (BETi) against post-myeloproliferative neoplasm secondary (s) AML cells. Leukemia 2017, 31: 1951-1961. PMID: 28042144, PMCID: PMC5537055, DOI: 10.1038/leu.2016.393.Peer-Reviewed Original ResearchConceptsBET protein inhibitorARV-825Messenger RNAReverse phase protein arrayPhase protein arrayRNA-seqHematopoietic progenitor cellsNormal hematopoietic progenitor cellsBET proteinsE3 ubiquitin ligase cereblonLevels of p21Extraterminal (BET) proteinsBcl-xLBromodomain inhibitorsC-MycJAK inhibitor ruxolitinibBRD4Protein arraysProgenitor cellsProtein expressionHEL92.1.7 cellsImproved survivalLeukemia burdenNSG miceProfound depletion
2016
ERK and p38 MAPK Activities Determine Sensitivity to PI3K/mTOR Inhibition via Regulation of MYC and YAP
Muranen T, Selfors L, Hwang J, Gallegos L, Coloff J, Thoreen C, Kang S, Sabatini D, Mills G, Brugge J. ERK and p38 MAPK Activities Determine Sensitivity to PI3K/mTOR Inhibition via Regulation of MYC and YAP. Cancer Research 2016, 76: 7168-7180. PMID: 27913436, PMCID: PMC5161652, DOI: 10.1158/0008-5472.can-16-0155.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsBlotting, WesternCell Line, TumorCell ProliferationDrug Resistance, NeoplasmExtracellular Signal-Regulated MAP KinasesFemaleFluorescent Antibody TechniqueHeterograftsHumansMAP Kinase Signaling SystemMiceMice, Inbred NODMicroscopy, ConfocalNeoplasms, Experimentalp38 Mitogen-Activated Protein KinasesPhosphoinositide-3 Kinase InhibitorsPhosphoproteinsProtein Kinase InhibitorsProto-Oncogene MasProto-Oncogene Proteins c-mycSignal TransductionTOR Serine-Threonine KinasesTranscription FactorsYAP-Signaling ProteinsConceptsPI3K/mTOR inhibitorMTOR inhibitorsTumor cellsPI3K/mTOR pathwayCell-targeted therapiesTranscriptional regulator c-MycPI3K/mTORAnimal tumor modelsUpregulation of MYCChronic inhibitionInhibition of p38Cellular signaling mechanismsTumor growthMTOR pathwayTumor modelAberrant activationTherapyStress kinase p38C-MycKinase p38InhibitionConstitutive ERK activityAttractive targetContext-dependent mechanismsProliferation arrestSynergistic Anti-Tumor Efficacy of BET Inhibitors JQ1 and Otx-015 in Combination with Dasatinib in Preclinical Models of T-Cell Lymphomas
Rizzitano S, Cavanè A, Piazzoni M, Vendramin A, Gimondi S, Biancon G, Malan S, Dodero A, Corradini P, Carniti C. Synergistic Anti-Tumor Efficacy of BET Inhibitors JQ1 and Otx-015 in Combination with Dasatinib in Preclinical Models of T-Cell Lymphomas. Blood 2016, 128: 3967. DOI: 10.1182/blood.v128.22.3967.3967.Peer-Reviewed Original ResearchPeripheral T-cell lymphomaT-cell lymphomaT cell receptorChou-Talalay combination indexDose-dependent mannerCell cycle distributionFlow cytometryCell cycle arrestC-myc expressionPreclinical modelsTK inhibitorsCell linesLeukemia cell linesInhibitor dasatinibC-MycWestern blottingG1 populationGene expression profilingSynergistic anti-tumor effectBET inhibitorsLong-term remissionG0/G1 phase arrestStem cell transplantationSynergistic anti-tumor efficacyMitochondrial depolarizationSuperior Lethal Activity of Novel BET Protein Proteolysis Targeting Chimera (BETP-PROTACs) Versus Betp Bromodomain Inhibitor (BETi) Against Post-Myeloproliferative Neoplasm (MPN) Secondary (s) AML Cells
Saenz D, Fiskus W, Raina K, Manshouri T, Coleman K, Winkler J, Qian Y, Crew A, Shen A, Mill C, Sun B, Verstovsek S, Crews C, Bhalla K. Superior Lethal Activity of Novel BET Protein Proteolysis Targeting Chimera (BETP-PROTACs) Versus Betp Bromodomain Inhibitor (BETi) Against Post-Myeloproliferative Neoplasm (MPN) Secondary (s) AML Cells. Blood 2016, 128: 747. DOI: 10.1182/blood.v128.22.747.747.Peer-Reviewed Original ResearchTyk2 tyrosine kinaseMPN-MFARV-825Stem/progenitor cellsHEL92.1.7 cellsHematopoietic stem/progenitor cellsProgenitor cellsC-MycP-STAT5ARV-771BETi treatmentMass cytometry approachProtein expressionLoss of responseNormal hematopoietic progenitor cellsNotable clinical benefitJAK-STATProtein array analysisNegative myeloproliferative neoplasmsBcl-xLMedian survivalClinical outcomesClinical benefitHematopoietic progenitor cellsWestern analysisNovel BET Protein Proteolysis Targeting Chimeras (BETP-PROTACs) Exert Potent Single Agent and Synergistic Activity with Ibrutinib and Venetoclax Against Human Mantle Cell Lymphoma Cells
Sun B, Fiskus W, Zhang L, Raina K, Coleman K, Winkler J, Qian Y, Crew A, Shen A, Saenz D, Mill C, Wang M, Crews C, Bhalla K. Novel BET Protein Proteolysis Targeting Chimeras (BETP-PROTACs) Exert Potent Single Agent and Synergistic Activity with Ibrutinib and Venetoclax Against Human Mantle Cell Lymphoma Cells. Blood 2016, 128: 1058. DOI: 10.1182/blood.v128.22.1058.1058.Peer-Reviewed Original ResearchTarget gene expressionBruton's tyrosine kinaseC-MycARV-825Transcription factorsPrimary MCL cellsTranscriptional activityGene expressionTyrosine kinaseBcl-xLE3 ubiquitin ligase activityMCL cellsUbiquitin ligase activityHuman mantle cell lymphoma cellsB-cell receptor signalingCell receptor signalingBinding of BRD4Regulation of mRNAInk4a/ArfAcetylated chromatinCopy number gainsLigase activityHematopoietic progenitor cellsBET proteinsBETi treatment
2014
Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation
Yan L, Zhou J, Gao Y, Ghazal S, Lu L, Bellone S, Yang Y, Liu N, Zhao X, Santin AD, Taylor H, Huang Y. Regulation of tumor cell migration and invasion by the H19/let-7 axis is antagonized by metformin-induced DNA methylation. Oncogene 2014, 34: 3076-3084. PMID: 25088204, DOI: 10.1038/onc.2014.236.Peer-Reviewed Original ResearchConceptsTumor cell migrationDNA methylationCell migrationTumor suppressorH19/letPotent tumor suppressorExpression of oncogenesDiverse human cancersMetastasis-promoting genesAnti-diabetic drug metforminLet-7C-MycHuman cancersH19Cell growthNovel mechanismEndometrial cancerPoor prognosisRegulationDrug metforminMethylationTherapeutic opportunitiesSuppressorTumor cellsOncogene
2013
MiR-145 functions as a tumor-suppressive RNA by targeting Sox9 and adducin 3 in human glioma cells
Rani S, Rathod S, Karthik S, Kaur N, Muzumdar D, Shiras A. MiR-145 functions as a tumor-suppressive RNA by targeting Sox9 and adducin 3 in human glioma cells. Neuro-Oncology 2013, 15: 1302-1316. PMID: 23814265, PMCID: PMC3779040, DOI: 10.1093/neuonc/not090.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBlotting, WesternBrain NeoplasmsCalmodulin-Binding ProteinsCell AdhesionCell CycleCell MovementCell ProliferationGliomaHumansMiceMice, Inbred NODMice, SCIDMicroRNAsNeoplastic Stem CellsReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSOX9 Transcription FactorConceptsAdducin 3MiR-145Overexpression of moleculesCell proliferationGlioma cellsHNGC-2 cellsModel cell systemMiR-145 promoterTumor suppressive functionMiR-145 functionsGuanine (CpG) islandsMiR-145 overexpressionEctopic expressionGrowth-suppressive effectsMiR-145 lossHuman glioma cellsCell adhesionC-MycFunctional studiesN-cadherinGlioma cell linesGlioblastoma cellsN-mycSOX9E-cadherinInhibition of Signal Transducer and Activator of Transcription 3 and Cyclooxygenase-2 Is Involved in Radiosensitization of Cepharanthine in HeLa Cells
Fang Z, Li Y, Chen Z, Wang J, Zhu L. Inhibition of Signal Transducer and Activator of Transcription 3 and Cyclooxygenase-2 Is Involved in Radiosensitization of Cepharanthine in HeLa Cells. International Journal Of Gynecological Cancer 2013, 23: 608-614. PMID: 23466568, DOI: 10.1097/igc.0b013e31828a05fd.Peer-Reviewed Original ResearchConceptsHeLa cellsSignal transducerTranscription 3C-MycSTAT3 target genesCell cycle regulators c-MycBcl-2Antiapoptotic Bcl-2Target genesWestern blot analysisHeLa cell lineApoptosis inductionBlot analysisNude mouse xenograftsCell linesReduced expressionSTAT3Apoptosis analysisMouse xenograftsSignificant radiosensitizationIR treatmentClonogenic assayActivatorCellsCytotoxic effects
2012
AID-Targeting and Hypermutation of Non-Immunoglobulin Genes Does Not Correlate with Proximity to Immunoglobulin Genes in Germinal Center B Cells
Gramlich HS, Reisbig T, Schatz DG. AID-Targeting and Hypermutation of Non-Immunoglobulin Genes Does Not Correlate with Proximity to Immunoglobulin Genes in Germinal Center B Cells. PLOS ONE 2012, 7: e39601. PMID: 22768095, PMCID: PMC3387148, DOI: 10.1371/journal.pone.0039601.Peer-Reviewed Original ResearchConceptsNon-Ig genesC-MycIg genesAID targetingGerminal center B cellsDouble-strand break endsImportant regulatory elementsNon-immunoglobulin genesMYC transgeneHeavy chain geneRegulatory elementsBreak endsIg heavy chain genesIg lociHuman MYCGenesB cellsSuch translocationsImmunoglobulin lociImmunoglobulin genesTranslocation partnersChain geneHuman Burkitt lymphomaSomatic hypermutationNuclear position
2011
Transplantation of Adult Mouse iPS Cell-Derived Photoreceptor Precursors Restores Retinal Structure and Function in Degenerative Mice
Tucker BA, Park IH, Qi SD, Klassen HJ, Jiang C, Yao J, Redenti S, Daley GQ, Young MJ. Transplantation of Adult Mouse iPS Cell-Derived Photoreceptor Precursors Restores Retinal Structure and Function in Degenerative Mice. PLOS ONE 2011, 6: e18992. PMID: 21559507, PMCID: PMC3084746, DOI: 10.1371/journal.pone.0018992.Peer-Reviewed Original ResearchConceptsRetinal functionNormal retinal physiologyOuter nuclear layerRetinal precursorsC-MycRetinal degenerative diseasesRetinal outer nuclear layerDelivery of neurotransmittersRetinal degenerative (rd) miceRetinal transplantationSubretinal transplantationNuclear layerAdult miceDsRed miceTransplantationRetinal structureRetinal physiologyPhotoreceptor markersDegenerative diseasesMiceRetroviral inductionFunctional anatomyPhotoreceptor precursorsPhotoreceptor cellsFibroblast-derived iPSCs
2010
Quantitative Characterization of the Interactions among c-myc Transcriptional Regulators FUSE, FBP, and FIR
Hsiao HH, Nath A, Lin CY, Folta-Stogniew EJ, Rhoades E, Braddock DT. Quantitative Characterization of the Interactions among c-myc Transcriptional Regulators FUSE, FBP, and FIR. Biochemistry 2010, 49: 4620-4634. PMID: 20420426, DOI: 10.1021/bi9021445.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceBase SequenceCarrier ProteinsDimerizationDNA HelicasesDNA-Binding ProteinsGuanine Nucleotide Exchange FactorsHumansModels, MolecularMolecular Sequence DataNucleic Acid ConformationProtein BindingProto-Oncogene Proteins c-mycRepressor ProteinsRho Guanine Nucleotide Exchange FactorsRNA Splicing FactorsRNA-Binding ProteinsSolutionsTrans-ActivatorsConceptsDNA strand preferencesProtein-DNA interactionsC-myc transcriptionPotent oncogenic factorHuman c-mycFBP bindsTranscriptional regulationActive transcriptionNear-physiological conditionsTripartite interactionCell homeostasisInhibitory complexStrand preferenceC-MycOncogenic factorRegulatory systemUnique modeTranscriptionStrand DNABiological experimentsComplex formationLow micromolar rangeDNADifferent conformationsMicromolar range
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