2021
Whole-genome doubling confers unique genetic vulnerabilities on tumour cells
Quinton R, DiDomizio A, Vittoria M, Kotýnková K, Ticas C, Patel S, Koga Y, Vakhshoorzadeh J, Hermance N, Kuroda T, Parulekar N, Taylor A, Manning A, Campbell J, Ganem N. Whole-genome doubling confers unique genetic vulnerabilities on tumour cells. Nature 2021, 590: 492-497. PMID: 33505027, PMCID: PMC7889737, DOI: 10.1038/s41586-020-03133-3.Peer-Reviewed Original ResearchConceptsWhole-genome doublingUnstable tetraploid cellsAccurate chromosome segregationDNA replication factorsSpindle assembly checkpointPrimary human cancer samplesHuman cancer samplesEssentiality dataChromosome segregationUnique genetic vulnerabilitiesTetraploid stateKinesin proteinsProteasome functionMitotic errorsGenetic traitsTetraploid cellsHuman cancersCancer cell linesCancer cellsCell linesKIF18ACell viabilityCancer samplesHuman tissuesCells
2019
Alterations in connexin 26 protein structure from lethal keratitis-ichthyosis-deafness syndrome mutations A88V and G45E
Lilly E, Strickler M, Milstone LM, Bunick CG. Alterations in connexin 26 protein structure from lethal keratitis-ichthyosis-deafness syndrome mutations A88V and G45E. Journal Of Dermatological Science 2019, 95: 119-122. PMID: 31331740, PMCID: PMC7263394, DOI: 10.1016/j.jdermsci.2019.07.002.Peer-Reviewed Original Research
2018
Quantitative evaluation of incomplete preweaning lethality in mice by using the CRISPR/Cas9 system
Nakamura T, Nakajima K, Ohnishi T, Yoshikawa T, Nakanishi M, Takumi T, Tsuboi T, Kato T. Quantitative evaluation of incomplete preweaning lethality in mice by using the CRISPR/Cas9 system. Scientific Reports 2018, 8: 16025. PMID: 30375401, PMCID: PMC6207718, DOI: 10.1038/s41598-018-34270-5.Peer-Reviewed Original ResearchConceptsInternational Mouse Phenotyping ConsortiumLoss-of-functionGenome-edited micePreweaning lethalityDisease-related genesFrameshift alleleHomozygous KO miceIMPC dataMolecular biology techniquesGenome editingMouse mutantsIncomplete penetranceCRISPR/Cas9 systemGenesAssociated with lethalityEhd1 geneMouse phenotypeHomozygous knockout miceMice mutantsCRISPR/Cas9Cell linesMutantsBiology techniquesAllelesKO miceCommon schizophrenia alleles are enriched in mutation-intolerant genes and in regions under strong background selection
Pardiñas A, Holmans P, Pocklington A, Escott-Price V, Ripke S, Carrera N, Legge S, Bishop S, Cameron D, Hamshere M, Han J, Hubbard L, Lynham A, Mantripragada K, Rees E, MacCabe J, McCarroll S, Baune B, Breen G, Byrne E, Dannlowski U, Eley T, Hayward C, Martin N, McIntosh A, Plomin R, Porteous D, Wray N, Caballero A, Geschwind D, Huckins L, Ruderfer D, Santiago E, Sklar P, Stahl E, Won H, Agerbo E, Als T, Andreassen O, Bækvad-Hansen M, Mortensen P, Pedersen C, Børglum A, Bybjerg-Grauholm J, Djurovic S, Durmishi N, Pedersen M, Golimbet V, Grove J, Hougaard D, Mattheisen M, Molden E, Mors O, Nordentoft M, Pejovic-Milovancevic M, Sigurdsson E, Silagadze T, Hansen C, Stefansson K, Stefansson H, Steinberg S, Tosato S, Werge T, GERAD1 Consortium, CRESTAR Consortium, Collier D, Rujescu D, Kirov G, Owen M, O’Donovan M, Walters J. Common schizophrenia alleles are enriched in mutation-intolerant genes and in regions under strong background selection. Nature Genetics 2018, 50: 381-389. PMID: 29483656, PMCID: PMC5918692, DOI: 10.1038/s41588-018-0059-2.Peer-Reviewed Original ResearchConceptsMutation-intolerant genesGenetic architecture of schizophreniaGenome-wide association studiesChromosome conformation dataGenome fine mappingVariant association signalsAssociation signalsFine-mappingGenetic architectureCausal genesGenomic studiesAssociation studiesRisk variantsSelection pressureGenesLociBrain expressionAssociated with poor qualityBiologyConformational dataDecreased life expectancyChromosomeDebilitating psychiatric conditionAllelesLife expectancy
2015
Expression of the CTCFL Gene during Mouse Embryogenesis Causes Growth Retardation, Postnatal Lethality, and Dysregulation of the Transforming Growth Factor β Pathway
Sati L, Zeiss C, Yekkala K, Demir R, McGrath J. Expression of the CTCFL Gene during Mouse Embryogenesis Causes Growth Retardation, Postnatal Lethality, and Dysregulation of the Transforming Growth Factor β Pathway. Molecular And Cellular Biology 2015, 35: 3436-3445. PMID: 26169830, PMCID: PMC4561735, DOI: 10.1128/mcb.00381-15.Peer-Reviewed Original ResearchConceptsGrowth factor β pathwayHuman vascular malformationsTestis-expressed genesΒ pathwayParalog of CTCFEmbryonic stem cellsTransforming Growth Factor-β PathwayPrior mouse modelsMouse embryogenesisBioinformatics analysisCancer-testis antigensDownstream targetsES cellsPostnatal lethalityCTCFLEmbryogenesis resultsTGFB pathwayGenesStem cellsVascular defectsPathwayExpressionTransgenic miceEye malformationsPhenotypeAn allelic series of miR-17∼92–mutant mice uncovers functional specialization and cooperation among members of a microRNA polycistron
Han Y, Vidigal J, Mu P, Yao E, Singh I, González A, Concepcion C, Bonetti C, Ogrodowski P, Carver B, Selleri L, Betel D, Leslie C, Ventura A. An allelic series of miR-17∼92–mutant mice uncovers functional specialization and cooperation among members of a microRNA polycistron. Nature Genetics 2015, 47: 766-775. PMID: 26029871, PMCID: PMC4485521, DOI: 10.1038/ng.3321.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisB-LymphocytesCarcinogenesisCells, CulturedEyelidsGene FrequencyGenes, LethalGenome-Wide Association StudyIntellectual DisabilityLimb Deformities, CongenitalMaleMice, 129 StrainMice, Inbred C57BLMice, TransgenicMicrocephalyMicroRNAsMultigene FamilyMutationTracheoesophageal FistulaInactivating mutations in MFSD2A, required for omega-3 fatty acid transport in brain, cause a lethal microcephaly syndrome
Guemez-Gamboa A, Nguyen LN, Yang H, Zaki MS, Kara M, Ben-Omran T, Akizu N, Rosti RO, Rosti B, Scott E, Schroth J, Copeland B, Vaux KK, Cazenave-Gassiot A, Quek DQ, Wong BH, Tan BC, Wenk MR, Gunel M, Gabriel S, Chi NC, Silver DL, Gleeson JG. Inactivating mutations in MFSD2A, required for omega-3 fatty acid transport in brain, cause a lethal microcephaly syndrome. Nature Genetics 2015, 47: 809-813. PMID: 26005868, PMCID: PMC4547531, DOI: 10.1038/ng.3311.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAnimalsBiological TransportBlood-Brain BarrierBrainCase-Control StudiesChildChild, PreschoolConsanguinityFatty Acids, Omega-3FemaleGenes, LethalGenetic Association StudiesHEK293 CellsHumansInfantMaleMice, KnockoutMicrocephalyMutation, MissenseSymportersSyndromeTumor Suppressor ProteinsZebrafish
2014
A new paradigm for transcription factor TFIIB functionality
Gelev V, Zabolotny JM, Lange M, Hiromura M, Yoo SW, Orlando JS, Kushnir A, Horikoshi N, Paquet E, Bachvarov D, Schaffer PA, Usheva A. A new paradigm for transcription factor TFIIB functionality. Scientific Reports 2014, 4: 3664. PMID: 24441171, PMCID: PMC3895905, DOI: 10.1038/srep03664.Peer-Reviewed Original ResearchMeSH KeywordsAcetylationAnimalsBinding SitesCell CycleCell LineDatasets as TopicGene ExpressionGene Expression ProfilingGene Expression RegulationGene Expression Regulation, ViralGene Knockdown TechniquesGene SilencingGenes, LethalGenome, HumanHerpesvirus 1, HumanHumansOrgan SpecificityProtein BindingRNA Polymerase IITranscription Factor TFIIBTranscription Initiation SiteTranscription, GeneticTranscriptomeConceptsTranscription initiationGene expressionGeneral transcription factor TFIIBTranscription factor TFIIBRNA polymerase IIGlobal gene expressionHuman gene expressionPolymerase IIGene transcriptionBioinformatics analysisBioinformatics studiesGene promoterHuman promotersCellular functionalityMitotic chromatidsTFIIBCell linesTranscriptionPromoterExpression
2013
Depletion of a Putatively Druggable Class of Phosphatidylinositol Kinases Inhibits Growth of p53-Null Tumors
Emerling B, Hurov J, Poulogiannis G, Tsukazawa K, Choo-Wing R, Wulf G, Bell E, Shim H, Lamia K, Rameh L, Bellinger G, Sasaki A, Asara J, Yuan X, Bullock A, DeNicola G, Song J, Brown V, Signoretti S, Cantley L. Depletion of a Putatively Druggable Class of Phosphatidylinositol Kinases Inhibits Growth of p53-Null Tumors. Cell 2013, 155: 844-857. PMID: 24209622, PMCID: PMC4070383, DOI: 10.1016/j.cell.2013.09.057.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBreast NeoplasmsCell Line, TumorCell ProliferationCell RespirationCellular SenescenceEmbryo, MammalianGene Knockdown TechniquesGenes, LethalHeterograftsHumansMiceNeoplasm TransplantationPhosphotransferases (Alcohol Group Acceptor)Reactive Oxygen SpeciesSignal TransductionTumor Suppressor Protein p53ConceptsReactive oxygen speciesP53-null tumorsBreast cancer cell linesCancer cell linesBreast cancerType 2Druggable classesAbsence of p53Tumor formationInhibits growthCell linesCancerHomozygous deletionMiceTP53Oxygen speciesP53Enhanced levelsHigh levelsDramatic reductionXenograftsLittermatesTumorsSynthetic lethalityApelin-APJ Signaling Is a Critical Regulator of Endothelial MEF2 Activation in Cardiovascular Development
Kang Y, Kim J, Anderson JP, Wu J, Gleim SR, Kundu RK, McLean DL, Kim JD, Park H, Jin SW, Hwa J, Quertermous T, Chun HJ. Apelin-APJ Signaling Is a Critical Regulator of Endothelial MEF2 Activation in Cardiovascular Development. Circulation Research 2013, 113: 22-31. PMID: 23603510, PMCID: PMC3739451, DOI: 10.1161/circresaha.113.301324.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusAdipokinesAnimalsApelinApelin ReceptorsCardiovascular AbnormalitiesCardiovascular SystemEndocardiumEndothelium, VascularFemaleFetal HeartGene Expression Regulation, DevelopmentalGenes, LethalGTP-Binding Protein alpha Subunits, G12-G13Histone DeacetylasesIntercellular Signaling Peptides and ProteinsKruppel-Like Transcription FactorsMaleMEF2 Transcription FactorsMiceMice, Inbred C57BLMice, KnockoutMyogenic Regulatory FactorsPhosphorylationProtein Processing, Post-TranslationalReceptors, G-Protein-CoupledSignal TransductionTranscription, GeneticConceptsCardiovascular developmentVentricular wall developmentMyocyte enhancer factor 2Embryonic lethal phenotypeCardiovascular developmental defectsFactor 2Apelin-APJHistone deacetylase 4MEF2 functionModel organismsLethal phenotypeEmbryonic lethalityTranscriptional targetsMEF2 activationKrüppel-like factor 2Wall developmentHDAC5 phosphorylationCushion formationNuclear localizationVascular smooth muscle cellsEndothelial cellsDevelopmental defectsMolecular mechanismsCritical regulatorLigand apelin
2010
Coilin-dependent snRNP assembly is essential for zebrafish embryogenesis
Strzelecka M, Trowitzsch S, Weber G, Lührmann R, Oates AC, Neugebauer KM. Coilin-dependent snRNP assembly is essential for zebrafish embryogenesis. Nature Structural & Molecular Biology 2010, 17: 403-409. PMID: 20357773, DOI: 10.1038/nsmb.1783.Peer-Reviewed Original Research
2008
The let-7 microRNA target gene, Mlin41/Trim71 is required for mouse embryonic survival and neural tube closure
Maller Schulman BR, Liang X, Stahlhut C, DelConte C, Stefani G, Slack FJ. The let-7 microRNA target gene, Mlin41/Trim71 is required for mouse embryonic survival and neural tube closure. Cell Cycle 2008, 7: 3935-3942. PMID: 19098426, PMCID: PMC2895810, DOI: 10.4161/cc.7.24.7397.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsGenes, LethalHeLa CellsHumansMiceMice, KnockoutMicroRNAsMutationNeural TubeTranscription FactorsConceptsLin-41Neural tube closureTube closureTerminal differentiationPrecocious cell cycle exitNematode Caenorhabditis elegansMore complex organismsCell cycle exitKey developmental eventsMicroRNA target genesNeural tube closure defectsLet-7 microRNACaenorhabditis elegansEpidermal skin cellsEmbryonic lethalityCycle exitComplex organismsTarget genesLet-7Developmental eventsDisease genesMouse mutantsClosure defectsMutantsFunctional role
2005
Orphan Nuclear Receptor LRH-1 Is Required To Maintain Oct4 Expression at the Epiblast Stage of Embryonic Development
Gu P, Goodwin B, Chung A, Xu X, Wheeler DA, Price RR, Galardi C, Peng L, Latour AM, Koller BH, Gossen J, Kliewer SA, Cooney AJ. Orphan Nuclear Receptor LRH-1 Is Required To Maintain Oct4 Expression at the Epiblast Stage of Embryonic Development. Molecular And Cellular Biology 2005, 25: 3492-3505. PMID: 15831456, PMCID: PMC1084298, DOI: 10.1128/mcb.25.9.3492-3505.2005.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlastocystCell DifferentiationDNA-Binding ProteinsDown-RegulationEmbryo, MammalianEmbryonic DevelopmentGene Expression Regulation, DevelopmentalGene SilencingGenes, LethalMiceOctamer Transcription Factor-3Receptors, Cytoplasmic and NuclearResponse ElementsStem CellsTranscription FactorsUp-RegulationConceptsInner cell massEpiblast stageES cellsOct4 expressionOrphan nuclear receptor LRH-1Embryonic developmentLRH-1Proximal enhancerCell lineagesNuclear receptor LRH-1Developmental stagesGerm cell lineagePluripotent cell lineageDifferentiation time pointsEmbryonic stem cellsReporter gene expressionEssential roleUndifferentiated ES cellsCell massSF-1 response elementExpression of Oct4Early developmental stagesOct4 geneDistal enhancerProximal promoter
2003
Screens for piwi Suppressors in Drosophila Identify Dosage-Dependent Regulators of Germline Stem Cell Division
Smulders-Srinivasan TK, Lin H. Screens for piwi Suppressors in Drosophila Identify Dosage-Dependent Regulators of Germline Stem Cell Division. Genetics 2003, 165: 1971-1991. PMID: 14704180, PMCID: PMC1462913, DOI: 10.1093/genetics/165.4.1971.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, Genetically ModifiedArgonaute ProteinsCell DivisionChromosomesDrosophilaDrosophila ProteinsFemaleGene DosageGene Expression Regulation, DevelopmentalGenes, LethalGerm CellsInfertility, MaleMaleProteinsRNA-Induced Silencing ComplexStem CellsSuppression, GeneticTranscription, GeneticZygoteConceptsStem cell divisionGermline stem cell divisionGenes/sequencesCell divisionFemale-specific lethalityDosage-dependent regulatorGermline stem cellsStem cell maintenanceDrosophila third chromosomeFamily of genesDosage-sensitive mannerPiwi mutantsZygotic functionMutant backgroundPiwi genesThird chromosomeMale germlineMale sterilitySuppressor mutationsSuch genesCell maintenanceGenetic regulationPlant kingdomTranscription factorsTranscriptional level
2002
The Divergent U12-Type Spliceosome Is Required for Pre-mRNA Splicing and Is Essential for Development in Drosophila
Otake LR, Scamborova P, Hashimoto C, Steitz JA. The Divergent U12-Type Spliceosome Is Required for Pre-mRNA Splicing and Is Essential for Development in Drosophila. Molecular Cell 2002, 9: 439-446. PMID: 11864616, DOI: 10.1016/s1097-2765(02)00441-0.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingAnimalsAnimals, Genetically ModifiedBase SequenceDrosophila melanogasterDrosophila ProteinsGenes, LethalIntronsLarvaMolecular Sequence DataMutagenesis, InsertionalNerve Tissue ProteinsNuclear ProteinsNucleic Acid ConformationProtein IsoformsRibonucleoprotein, U4-U6 Small NuclearRibonucleoproteins, Small NuclearRNA PrecursorsRNA SplicingRNA, Small NuclearSequence AlignmentSequence Homology, Nucleic AcidSpliceosomesTranscription FactorsTransgenesConceptsU12-type spliceosomeThird instar larvalU12-type intronsPre-mRNA splicingU4atac/U6atacMetazoan organismsHomeodomain proteinsU5 snRNPsDrosophila melanogasterU12 spliceosomeMRNA intronsU12 snRNASingle locusU6atacInstar larvalSpliceosomeEmbryonic stagesCNS developmentIntronsMinor classU12DrosophilaMelanogasterVertebratesSnRNPs
2001
Targeted Attenuation of Electrical Activity in Drosophila Using a Genetically Modified K+ Channel
White B, Osterwalder T, Yoon K, Joiner W, Whim M, Kaczmarek L, Keshishian H. Targeted Attenuation of Electrical Activity in Drosophila Using a Genetically Modified K+ Channel. Neuron 2001, 31: 699-711. PMID: 11567611, DOI: 10.1016/s0896-6273(01)00415-9.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAnimalsBehavior, AnimalCells, CulturedDrosophila melanogasterDrosophila ProteinsFemaleGene DosageGene Expression Regulation, DevelopmentalGene TargetingGenes, LethalLarvaMembrane PotentialsMusclesMutationNervous SystemNeural InhibitionNeuronsNeurons, AfferentPhenotypePhotoreceptor Cells, InvertebratePotassium ChannelsShaker Superfamily of Potassium ChannelsSynaptic TransmissionTransgenesBcl-XL–Caspase-9 Interactions in the Developing Nervous System: Evidence for Multiple Death Pathways
Zaidi A, D'Sa-Eipper C, Brenner J, Kuida K, Zheng T, Flavell R, Rakic P, Roth K. Bcl-XL–Caspase-9 Interactions in the Developing Nervous System: Evidence for Multiple Death Pathways. Journal Of Neuroscience 2001, 21: 169-175. PMID: 11150333, PMCID: PMC6762421, DOI: 10.1523/jneurosci.21-01-00169.2001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisbcl-2-Associated X Proteinbcl-X ProteinCaspase 3Caspase 9CaspasesCells, CulturedCytarabineGanglia, SpinalGenes, LethalHeterozygoteHomozygoteImmunohistochemistryIn Situ Nick-End LabelingLiverMiceMice, KnockoutNervous SystemNeuronsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2TelencephalonTumor Suppressor Protein p53ConceptsGene family membersCaspase-9 deficiencyCaspase-9Telencephalic neural precursor cellsCell deathDouble homozygous mutantsCaspase family membersMultiple death pathwaysNormal nervous system developmentBcl-2Nervous system developmentBax-deficient neuronsNeuronal apoptosisTelencephalic neuronsDeficient embryosNeural precursor cellsDeath pathwaysFamily membersHomozygous mutantsApoptotic pathwayObligate pathwayBcl-xLApoptosis inducersDeficient neuronsTargeted disruption
2000
Of mice and men: Dissecting the genetic pathway that controls left‐right asymmetry in mice and humans
Schneider H, Brueckner M. Of mice and men: Dissecting the genetic pathway that controls left‐right asymmetry in mice and humans. American Journal Of Medical Genetics 2000, 97: 258-270. PMID: 11376437, DOI: 10.1002/1096-8628(200024)97:4<258::aid-ajmg1276>3.0.co;2-8.Peer-Reviewed Original ResearchMeSH KeywordsAbnormalities, MultipleAnimalsBody PatterningCiliaDyneinsEctodermEmbryonic and Fetal DevelopmentEndodermFetal ProteinsGastrulaGene Expression Regulation, DevelopmentalGenesGenes, HomeoboxGenes, LethalHomeodomain ProteinsHumansKinesinsMiceMice, Mutant StrainsMutationNotochordPhenotypeSpecies SpecificityTranscription FactorsConceptsLeft-right asymmetrySpontaneous mouse mutationGenetic pathwaysHuman homologueMouse mutationNode monociliaHuman mutationsHuman phenotypesFinal phenotypeOrchestrated mannerPathways resultsMouse phenotypeGenesLaterality determinationMutationsPhenotypeModel systemDifferent stepsMonociliaHomologuesCombination of analysisMicePathwayHuman developmentInitial asymmetry
1999
A large-scale insertional mutagenesis screen in zebrafish
Amsterdam A, Burgess S, Golling G, Chen W, Sun Z, Townsend K, Farrington S, Haldi M, Hopkins N. A large-scale insertional mutagenesis screen in zebrafish. Genes & Development 1999, 13: 2713-2724. PMID: 10541557, PMCID: PMC317115, DOI: 10.1101/gad.13.20.2713.Peer-Reviewed Original ResearchConceptsLarge-scale insertional mutagenesis screenInsertional mutagenesis screenEmbryonic lethal mutationsMutagenesis screenLethal mutationsRecessive embryonic lethal mutationsMutated genesProviral insertionEfficiency of mutagenesisBlastula-stage embryosFrequency of mutationsChemical mutagen ENUDominant mutantsGene cloningInsertional mutagenRecessive mutantGerm lineEmbryonic mutationsFounder fishDominant mutationsMutantsGenesDevelopmental defectsPilot screenMutations
1998
Targeted Disruption of the Mouse Caspase 8 Gene Ablates Cell Death Induction by the TNF Receptors, Fas/Apo1, and DR3 and Is Lethal Prenatally
Varfolomeev E, Schuchmann M, Luria V, Chiannilkulchai N, Beckmann J, Mett I, Rebrikov D, Brodianski V, Kemper O, Kollet O, Lapidot T, Soffer D, Sobe T, Avraham K, Goncharov T, Holtmann H, Lonai P, Wallach D. Targeted Disruption of the Mouse Caspase 8 Gene Ablates Cell Death Induction by the TNF Receptors, Fas/Apo1, and DR3 and Is Lethal Prenatally. Immunity 1998, 9: 267-276. PMID: 9729047, DOI: 10.1016/s1074-7613(00)80609-3.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCaspase 8Caspase 9CaspasesCell DeathCells, CulturedCysteine EndopeptidasesDNA, Complementaryfas ReceptorFetal DeathFibroblastsGene TargetingGenes, LethalGestational AgeMiceMice, Inbred C57BLMice, KnockoutPhenotypeReceptors, Tumor Necrosis FactorReceptors, Tumor Necrosis Factor, Member 25Transcription, GeneticConceptsFas/APO1Death inductionJun N-terminal kinaseHeart muscle developmentCaspase-8 geneCell death inductionWild-type fibroblastsN-terminal kinaseTNF receptorNull embryosMuscle developmentAlpha phosphorylationHematopoietic colony-forming cellsCaspase-8Cell deathColony-forming cellsIkappaB-alpha phosphorylationTargeted disruptionNonredundant roleEmbryonal developmentEmbryosAPO1Fibroblast strainsNGF familyReceptors
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply