2024
Short-term cultured tumor fragments to study immunotherapy combinations based on CD137 (4-1BB) agonism
Eguren-Santamaría I, Rodríguez I, Herrero-Martin C, de Piérola E, Azpilikueta A, Sánchez-Gregorio S, Bolaños E, Gomis G, Molero-Glez P, Chacón E, Mínguez J, Chiva S, Diez-Caballero F, de Andrea C, Teijeira Á, Sanmamed M, Melero I. Short-term cultured tumor fragments to study immunotherapy combinations based on CD137 (4-1BB) agonism. OncoImmunology 2024, 13: 2373519. PMID: 38988823, PMCID: PMC11236292, DOI: 10.1080/2162402x.2024.2373519.Peer-Reviewed Original ResearchConceptsTumor fragmentsImmunotherapy combinationsIFNg productionActivation markersClinical response to PD-1 blockadeResponse to PD-1 blockadeAgonistic anti-CD137 mAbAnti-PD-1 treatmentAnti-CD137 mAbAnti-PD-1PD-1 blockadeSyngeneic immunocompetent miceInfiltrating T cellsShort-term cultureUnmet medical needAnti-CD137Contralateral tumorsBilateral tumorsCancer immunotherapyTissue culture supernatantsImmunocompetent miceSolid malignanciesT cellsMAb combinationsMouse tumors
2022
Landscape of helper and regulatory antitumour CD4+ T cells in melanoma
Oliveira G, Stromhaug K, Cieri N, Iorgulescu J, Klaeger S, Wolff J, Rachimi S, Chea V, Krause K, Freeman S, Zhang W, Li S, Braun D, Neuberg D, Carr S, Livak K, Frederick D, Fritsch E, Wind-Rotolo M, Hacohen N, Sade-Feldman M, Yoon C, Keskin D, Ott P, Rodig S, Boland G, Wu C. Landscape of helper and regulatory antitumour CD4+ T cells in melanoma. Nature 2022, 605: 532-538. PMID: 35508657, PMCID: PMC9815755, DOI: 10.1038/s41586-022-04682-5.Peer-Reviewed Original ResearchConceptsHLA class IIT cellsClass IIHLA classImmune evasionHuman leukocyte antigen class IIMelanoma specimensClass II positivityTumor-reactive CD4T regulatory (Treg) cellsAntigen-presenting cellsTumor-associated antigensHLA class IHuman melanoma specimensRecognition of antigenAntitumour responseImmunosuppressive CD4Treg clonesTreg cellsRegulatory cellsCytotoxic CD4Neoantigen loadTumor antigensCD4Tumor microenvironment
2021
Identification of RAS mutant biomarkers for EGFR inhibitor sensitivity using a systems biochemical approach
McFall T, Stites E. Identification of RAS mutant biomarkers for EGFR inhibitor sensitivity using a systems biochemical approach. Cell Reports 2021, 37: 110096. PMID: 34910921, PMCID: PMC8867612, DOI: 10.1016/j.celrep.2021.110096.Peer-Reviewed Original ResearchConceptsSensitivity to EGFR inhibitionSubsets of mutationsRAS mutationsKRAS G13DCancer cell biologyEGFR inhibitionEpidermal growth factor receptor (EGFR)-targeted therapyTumor suppressor neurofibrominGene-basedBiophysical biomarkersInhibitor sensitivityCell biologyMutationsPersonalized medicineBiomarker strategiesKRAS mutantRasCancer treatmentKRASNF1BiomarkersBiophysical characteristicsG13DMutantsInhibitionMAL2 mediates the formation of stable HER2 signaling complexes within lipid raft-rich membrane protrusions in breast cancer cells
Jeong J, Shin JH, Li W, Hong JY, Lim J, Hwang JY, Chung JJ, Yan Q, Liu Y, Choi J, Wysolmerski J. MAL2 mediates the formation of stable HER2 signaling complexes within lipid raft-rich membrane protrusions in breast cancer cells. Cell Reports 2021, 37: 110160. PMID: 34965434, PMCID: PMC8762588, DOI: 10.1016/j.celrep.2021.110160.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic Agents, ImmunologicalBreast NeoplasmsCell ProliferationCytoskeletal ProteinsDrug Resistance, NeoplasmEndocytosisFemaleHumansMembrane MicrodomainsMyelin and Lymphocyte-Associated Proteolipid ProteinsPhosphoproteinsPlasma Membrane Calcium-Transporting ATPasesReceptor, ErbB-2Sodium-Hydrogen ExchangersTrastuzumabTumor Cells, CulturedConceptsLipid raft formationBreast cancer cellsLipid raftsLipid raft resident proteinsCancer cellsRaft formationRaft-resident proteinsProximity ligation assayProtein complexesMembrane protrusionsProtein interactionsPlasma membraneLigation assayMAL2Membrane stabilityStructural organizationPotential therapeutic targetPhysical interactionMembrane retentionProteinRaftsTherapeutic targetCellsIntracellular calcium concentrationLow intracellular calcium concentrationLocalization of KRAS downstream target ARL4C to invasive pseudopods accelerates pancreatic cancer cell invasion
Harada A, Matsumoto S, Yasumizu Y, Shojima K, Akama T, Eguchi H, Kikuchi A. Localization of KRAS downstream target ARL4C to invasive pseudopods accelerates pancreatic cancer cell invasion. ELife 2021, 10: e66721. PMID: 34590580, PMCID: PMC8598236, DOI: 10.7554/elife.66721.Peer-Reviewed Original ResearchConceptsDownstream effectorsEGF-Ras pathwayCancer cell invasionPancreatic cancer patientsPancreatic cancer cellsIQGAP1ARL4CCell invasionPancreatic cancerSite of invasionCancer cellsCancer patientsExtracellular matrixPseudopodsAntisense oligonucleotidesInvasive pancreatic cancerMetastasis of pancreatic cancerActive siteInduced degradationEffectorMMP14InvasionMortality rateLocalizationOligonucleotidesProtein Phosphatase 2A as a Therapeutic Target in Small Cell Lung Cancer
Mirzapoiazova T, Xiao G, Mambetsariev B, Nasser MW, Miaou E, Singhal SS, Srivastava S, Mambetsariev I, Nelson MS, Nam A, Behal A, Arvanitis LD, Atri P, Muschen M, Tissot FLH, Miser J, Kovach JS, Sattler M, Batra SK, Kulkarni P, Salgia R. Protein Phosphatase 2A as a Therapeutic Target in Small Cell Lung Cancer. Molecular Cancer Therapeutics 2021, 20: 1820-1835. PMID: 34253596, PMCID: PMC8722383, DOI: 10.1158/1535-7163.mct-21-0013.Peer-Reviewed Original ResearchConceptsProtein phosphatase 2APhosphatase 2ASerine/threonine phosphataseDNA damage responseRegulation of apoptosisSmall molecule inhibitorsGlycolytic ATP productionThreonine phosphataseTwo-dimensional cultureLB100ATP productionMolecule inhibitorsPP2AThree-dimensional spheroid modelEndothelial cell monolayersGlucose uptakeCell viabilitySCLC cellsTherapeutic targetApoptosisCell monolayersMass spectrometrySpheroid modelTumor spheroidsCellsTargeting the T-Cell Lymphoma Epigenome Induces Cell Death, Cancer Testes Antigens, Immune-Modulatory Signaling PathwaysTargeting Peripheral T-Cell Lymphoma Epigenome
Scotto L, Kinahan C, Douglass E, Deng C, Safari M, Casadei B, Marchi E, Lue JK, Montanari F, Falchi L, Qiao C, Renu N, Bates SE, Califano A, O'Connor OA. Targeting the T-Cell Lymphoma Epigenome Induces Cell Death, Cancer Testes Antigens, Immune-Modulatory Signaling PathwaysTargeting Peripheral T-Cell Lymphoma Epigenome. Molecular Cancer Therapeutics 2021, 20: 1422-1430. PMID: 34108263, PMCID: PMC8941846, DOI: 10.1158/1535-7163.mct-20-0377.Peer-Reviewed Original ResearchMeSH KeywordsAntigens, NeoplasmAntimetabolites, AntineoplasticApoptosisAzacitidineBiomarkers, TumorCell ProliferationDNA (Cytosine-5-)-Methyltransferase 1DNA MethylationEpigenesis, GeneticEpigenomeGene Expression ProfilingGene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHumansImmunityLymphoma, T-CellMaleTestisTumor Cells, CulturedConceptsEpigenetic geneHistone deacetylaseSuppression of genesHDAC inhibitorsDNA methyltransferase inhibitorTranscriptional inductionDNA methylationMaster regulatorDNMT inhibitorsEpigenetic diseasePeripheral T-cell lymphomaGene expressionMethyltransferase inhibitorMechanistic basisCell deathGenesCancer-testis antigensTestis antigensEpigenomeMutationsCholesterol metabolismInhibitorsInductionMatrisomeTh1-like phenotypeHDAC Inhibition Induces Cell Cycle Arrest and Mesenchymal-Epithelial Transition in a Novel Pleural-Effusion Derived Uterine Carcinosarcoma Cell Line
Stockhammer P, Okumus Ö, Hegedus L, Rittler D, Ploenes T, Herold T, Kalbourtzis S, Bankfalvi A, Sucker A, Kimmig R, Aigner C, Hegedus B. HDAC Inhibition Induces Cell Cycle Arrest and Mesenchymal-Epithelial Transition in a Novel Pleural-Effusion Derived Uterine Carcinosarcoma Cell Line. Pathology & Oncology Research 2021, 27: 636088. PMID: 34257602, PMCID: PMC8262245, DOI: 10.3389/pore.2021.636088.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic Combined Chemotherapy ProtocolsBiomarkers, TumorCarcinosarcomaCell Cycle CheckpointsCisplatinEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHistone DeacetylasesHumansMiddle AgedMutationPaclitaxelPhthalazinesPiperazinesPleural Effusion, MalignantPrognosisPyrazolesQuinolinesTumor Cells, CulturedUterine NeoplasmsVorinostatConceptsEpithelial-mesenchymal transitionUterine carcinosarcomaPleural effusionMesenchymal-epithelial transitionCell linesPatient-derived preclinical modelsMalignant pleural effusionMetastatic tumor lesionsVimentin-positive tumorsE-cadherinCarcinosarcoma cell lineInduces cell cycle arrestHistone deacetylase inhibitionFirst-line chemotherapeuticsΒ-catenin expressionE-cadherin expressionPSmad2 expressionCell cycle analysisPositive tumorsAggressive malignancyMetastatic tumorsDisease progressionCell cycle arrestNovel therapiesPreclinical modelsBET proteolysis targeted chimera-based therapy of novel models of Richter Transformation-diffuse large B-cell lymphoma
Fiskus W, Mill CP, Perera D, Birdwell C, Deng Q, Yang H, Lara BH, Jain N, Burger J, Ferrajoli A, Davis JA, Saenz DT, Jin W, Coarfa C, Crews CM, Green MR, Khoury JD, Bhalla KN. BET proteolysis targeted chimera-based therapy of novel models of Richter Transformation-diffuse large B-cell lymphoma. Leukemia 2021, 35: 2621-2634. PMID: 33654205, PMCID: PMC8410602, DOI: 10.1038/s41375-021-01181-w.Peer-Reviewed Original ResearchMeSH KeywordsAdenineAnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBiomarkers, TumorBridged Bicyclo Compounds, HeterocyclicCell ProliferationCell Transformation, NeoplasticGene Expression Regulation, NeoplasticHumansLymphoma, Large B-Cell, DiffuseMicePiperidinesProteinsProteolysisSulfonamidesTumor Cells, CulturedXenograft Model Antitumor AssaysConceptsLarge B-cell lymphomaB-cell lymphomaRichter transformationBET protein inhibitorLymphoma burdenImproved survivalCombination therapyC-Myc levelsEffective therapyNovel therapiesCell lymphomaXenograft modelProtein inhibitorTherapyBET inhibitorsProtein expressionCLLGenetic alterationsLymphomaInhibitorsIRF4Single-cell RNA-seqHuman modelCRISPR knockoutCellsRole of MBD3-SOX2 axis in residual myeloma following pomalidomide
Verma R, Branagan AR, Xu ML, Flavell RA, Dhodapkar KM, Dhodapkar MV. Role of MBD3-SOX2 axis in residual myeloma following pomalidomide. Leukemia 2021, 35: 3319-3323. PMID: 33603141, PMCID: PMC8371090, DOI: 10.1038/s41375-021-01145-0.Peer-Reviewed Original Research
2020
Flow Cytometric Analyses of p53-Mediated Cell Cycle Arrest and Apoptosis in Cancer Cells
Al Zouabi NN, Roberts CM, Lin ZP, Ratner ES. Flow Cytometric Analyses of p53-Mediated Cell Cycle Arrest and Apoptosis in Cancer Cells. Methods In Molecular Biology 2020, 2255: 43-53. PMID: 34033093, DOI: 10.1007/978-1-0716-1162-3_5.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisCell Cycle CheckpointsFemaleFlow CytometryHumansOvarian NeoplasmsTumor Cells, CulturedTumor Suppressor Protein p53ConceptsGene of interestCell cycle arrestCycle arrestCell typesDNA damaging agentsP53-mediated cell cycle arrestCell cycle progressionTumor suppressor p53Cellular contextEctopic expressionExogenous stressCell cycle distributionDamaging agentsCycle progressionTumor suppressorSuppressor p53Stable expressionPhenotypic analysisCell survivalCell deathGenomic damageP53 functionGenesEnvironmental insultsCycle distributionLRRC31 inhibits DNA repair and sensitizes breast cancer brain metastasis to radiation therapy
Chen Y, Jiang T, Zhang H, Gou X, Han C, Wang J, Chen AT, Ma J, Liu J, Chen Z, Jing X, Lei H, Wang Z, Bao Y, Baqri M, Zhu Y, Bindra RS, Hansen JE, Dou J, Huang C, Zhou J. LRRC31 inhibits DNA repair and sensitizes breast cancer brain metastasis to radiation therapy. Nature Cell Biology 2020, 22: 1276-1285. PMID: 33005030, PMCID: PMC7962994, DOI: 10.1038/s41556-020-00586-6.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsBrain NeoplasmsBreast NeoplasmsCell ProliferationDNA DamageDNA RepairFemaleGamma RaysHumansMiceMice, Inbred BALB CMice, NudeMutS Homolog 2 ProteinNuclear ProteinsPhosphorylationRadiation-Sensitizing AgentsSignal TransductionTumor Cells, CulturedXenograft Model Antitumor AssaysInducible de novo expression of neoantigens in tumor cells and mice
Damo M, Fitzgerald B, Lu Y, Nader M, William I, Cheung JF, Connolly KA, Foster GG, Akama-Garren E, Lee DY, Chang GP, Gocheva V, Schmidt LM, Boileve A, Wilson JH, Cui C, Monroy I, Gokare P, Cabeceiras P, Jacks T, Joshi NS. Inducible de novo expression of neoantigens in tumor cells and mice. Nature Biotechnology 2020, 39: 64-73. PMID: 32719479, PMCID: PMC7854852, DOI: 10.1038/s41587-020-0613-1.Peer-Reviewed Original ResearchConceptsT cell responsesLevel of regulationRNA splicingDNA recombinationGenetic regulationTolerance mechanismsInducible expressionNeoantigen expressionCell responsesNaïve T-cell responsesCD4 T cell responsesTumor cell linesPeripheral tolerance mechanismsT cell toleranceCentral T cell toleranceCell linesExpressionNovo expressionTight controlEndogenous CD8Antitumor immunityPeripheral toleranceAutoimmune diseasesT cellsThymus resultsKu80-Targeted pH-Sensitive Peptide–PNA Conjugates Are Tumor Selective and Sensitize Cancer Cells to Ionizing Radiation
Kaplan AR, Pham H, Liu Y, Oyaghire S, Bahal R, Engelman DM, Glazer PM. Ku80-Targeted pH-Sensitive Peptide–PNA Conjugates Are Tumor Selective and Sensitize Cancer Cells to Ionizing Radiation. Molecular Cancer Research 2020, 18: 873-882. PMID: 32098827, PMCID: PMC7272299, DOI: 10.1158/1541-7786.mcr-19-0661.Peer-Reviewed Original ResearchConceptsCancer cellsTumor cellsLocal tumor irradiationTumor-selective radiosensitizationMouse tumor modelsKu80 expressionNovel agentsTumor irradiationTumor growthTumor microenvironmentTumor modelRadiation treatmentTherapeutic agentsSubcutaneous mouse tumor modelTumorsMiceCancer therapyHealthy tissueAcute toxicitySpecific targetingSelective effectPNA antisenseTumor-SelectiveAcidic culture conditionsSensitize cancer cellsCannabinoids Promote Progression of HPV-Positive Head and Neck Squamous Cell Carcinoma via p38 MAPK Activation
Liu C, Sadat S, Ebisumoto K, Sakai A, Panuganti B, Ren S, Goto Y, Haft S, Fukusumi T, Ando M, Saito Y, Guo T, Tamayo P, Yeerna H, Kim W, Hubbard J, Sharabi A, Gutkind J, Califano J. Cannabinoids Promote Progression of HPV-Positive Head and Neck Squamous Cell Carcinoma via p38 MAPK Activation. Clinical Cancer Research 2020, 26: 2693-2703. PMID: 31932491, PMCID: PMC7538010, DOI: 10.1158/1078-0432.ccr-18-3301.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCannabinoidsCell MovementCell ProliferationFemaleHead and Neck NeoplasmsHumansMiceMice, Nudep38 Mitogen-Activated Protein KinasesPapillomaviridaePapillomavirus InfectionsPrognosisReceptors, CannabinoidSquamous Cell Carcinoma of Head and NeckTumor Cells, CulturedXenograft Model Antitumor AssaysConceptsHead and neck squamous cell carcinomaHPV-positive head and neck squamous cell carcinomaHPV-positive HNSCC cell linesNeck squamous cell carcinomaHNSCC cell linesSingle-sample gene set enrichment analysisSquamous cell carcinomaP38 MAPK pathway activationHNSCC cohortCell carcinomaMAPK pathway activationHPV-negative head and neck squamous cell carcinomaHuman papillomavirus (HPV)-related headCell linesAnimal modelsCannabinoid receptor activationHPV- HNSCC patientsHead and neck squamous cell carcinomas dataMarijuana usePathway activationDaily marijuana useWhole-genome expression analysisCannabinoid exposureHNSCC patientsP38 MAPK activationGene X environment: the cellular environment governs the transcriptional response to environmental chemicals
Burman A, Garcia-Milian R, Whirledge S. Gene X environment: the cellular environment governs the transcriptional response to environmental chemicals. Human Genomics 2020, 14: 19. PMID: 32448403, PMCID: PMC7247264, DOI: 10.1186/s40246-020-00269-1.Peer-Reviewed Original ResearchConceptsTranscriptional responseCellular environmentCellular contextGenetic sexUnique gene networksGene regulatory networksEnvironment interactionEnvironmental chemicalsGene expression studiesUnique transcriptional profileGene expression array dataExpression array dataPhenotype of cellsGene networksRegulatory networksTranscriptional profilesBiological functionsCellular organizationExpression studiesFemale cellsCellular responsesPhysiological cuesHuman gene expression studiesMolecular pathwaysGenetic resultsKMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer
Alam H, Tang M, Maitituoheti M, Dhar S, Kumar M, Han C, Ambati C, Amin S, Gu B, Chen T, Lin Y, Chen J, Muller F, Putluri N, Flores E, DeMayo F, Baseler L, Rai K, Lee M. KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer. Cancer Cell 2020, 37: 599-617.e7. PMID: 32243837, PMCID: PMC7178078, DOI: 10.1016/j.ccell.2020.03.005.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinoma of LungAnimalsAntimetabolitesApoptosisBiomarkers, TumorCell ProliferationDeoxyglucoseDNA-Binding ProteinsEnhancer Elements, GeneticGene Expression Regulation, NeoplasticGlycolysisHistone-Lysine N-MethyltransferaseHistonesHumansLung NeoplasmsMiceMice, KnockoutMice, NudeMutationMyeloid-Lymphoid Leukemia ProteinNeoplasm ProteinsPeriod Circadian ProteinsPrognosisTumor Cells, CulturedXenograft Model Antitumor AssaysConceptsLung cancerLung-specific lossHuman lung cancer cellsExpression of Per2Lung cancer cellsHistone methyltransferase KMT2DLung tumor suppressorTumor suppressive roleMultiple glycolytic genesLung tumorigenesisEpigenetic modifiersPharmacological inhibitionTherapeutic vulnerabilitiesGlycolytic inhibitorCancerCancer cellsKMT2DFunction mutationsTumor suppressorPer2GlycolysisGlycolytic genesMutationsMiceLoss of CHD1 Promotes Heterogeneous Mechanisms of Resistance to AR-Targeted Therapy via Chromatin Dysregulation
Zhang Z, Zhou C, Li X, Barnes S, Deng S, Hoover E, Chen C, Lee Y, Zhang Y, Wang C, Metang L, Wu C, Tirado C, Johnson N, Wongvipat J, Navrazhina K, Cao Z, Choi D, Huang C, Linton E, Chen X, Liang Y, Mason C, de Stanchina E, Abida W, Lujambio A, Li S, Lowe S, Mendell J, Malladi V, Sawyers C, Mu P. Loss of CHD1 Promotes Heterogeneous Mechanisms of Resistance to AR-Targeted Therapy via Chromatin Dysregulation. Cancer Cell 2020, 37: 584-598.e11. PMID: 32220301, PMCID: PMC7292228, DOI: 10.1016/j.ccell.2020.03.001.Peer-Reviewed Original ResearchMeSH KeywordsAndrogen AntagonistsAnimalsApoptosisBiomarkers, TumorCell ProliferationChromatinDNA HelicasesDNA-Binding ProteinsDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHigh-Throughput Screening AssaysHumansMaleMiceProstatic Neoplasms, Castration-ResistantReceptors, AndrogenRNA, Small InterferingTranscription FactorsTumor Cells, CulturedXenograft Model Antitumor AssaysConceptsAntiandrogen resistanceChromatin dysregulationCHD1 lossProstate cancerGenomic copy number alterationsRNA-seq analysisResistance to hormonal therapyCopy number alterationsAR-targeted therapiesMetastatic prostate cancerATAC-seqClosed chromatinRNA-seqTranscriptional plasticityTranscription factorsFunctional screeningTranscriptomic changesMechanisms of resistanceHormone therapyLineage programsChromatinCHD1Global changeIntegrated analysisTherapyLoss of Estrogen Receptors is Associated with Increased Tumor Aggression in Laryngeal Squamous Cell Carcinoma
Verma A, Schwartz N, Cohen DJ, Patel V, Nageris B, Bachar G, Boyan BD, Schwartz Z. Loss of Estrogen Receptors is Associated with Increased Tumor Aggression in Laryngeal Squamous Cell Carcinoma. Scientific Reports 2020, 10: 4227. PMID: 32144339, PMCID: PMC7060328, DOI: 10.1038/s41598-020-60675-2.Peer-Reviewed Original ResearchConceptsSquamous cell carcinomaERβ expressionCell carcinomaLaryngeal squamous cell carcinomaEstrogen receptor-dependent mechanismHigh ESR1 expressionClinical cancer stageCancer Genome AtlasImproved survivalTumor burdenPathological stageResponsive cancersCancer stageERα36 expressionHistopathological markersEstrogen receptorXenograft tumorsESR1 expressionTumor aggressionEpithelial samplesLSCCDependent mechanismGenome AtlasERα66CarcinomaAn in vitro mimic of in‐cell solvation for protein folding studies
Davis CM, Deutsch J, Gruebele M. An in vitro mimic of in‐cell solvation for protein folding studies. Protein Science 2020, 29: 1046-1054. PMID: 31994240, PMCID: PMC7096716, DOI: 10.1002/pro.3833.Peer-Reviewed Original ResearchConceptsPhosphoglycerate kinaseLysis bufferCytoplasmic protein interactionsSignificant nonadditive effectsVariety of proteinsProtein folding studiesEukaryotic cellsProtein foldingProtein interactionsCellular crowdingProtein-like sequencesEffect of FicollFolding studiesHydrophobic patchVariable major protein-like sequenceNonadditive effectsCellular effectsProteinCell environmentInert macromoleculesBiomolecular interactionsCellsTest tubeSmall crowdersMimics
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