2025
Natural killer cells’ functional impairment drives the immune escape of pre-malignant clones in early-stage myelodysplastic syndromes
Rodriguez-Sevilla J, Ganan-Gomez I, Kumar B, Thongon N, Ma F, Chien K, Kim Y, Yang H, Loghavi S, Tan R, Adema V, Li Z, Tanaka T, Uryu H, Kanagal-Shamanna R, Al-Atrash G, Bejar R, Banerjee P, Lynn Cha S, Montalban-Bravo G, Dougherty M, Fernandez Laurita M, Wheeler N, Jia B, Papapetrou E, Izzo F, Dueñas D, McAllen S, Gu Y, Todisco G, Ficara F, Della Porta M, Jain A, Takahashi K, Clise-Dwyer K, Halene S, Bertilaccio M, Garcia-Manero G, Daher M, Colla S. Natural killer cells’ functional impairment drives the immune escape of pre-malignant clones in early-stage myelodysplastic syndromes. Nature Communications 2025, 16: 3450. PMID: 40216768, DOI: 10.1038/s41467-025-58662-0.Peer-Reviewed Original ResearchConceptsHematopoietic stem cellsMyelodysplastic syndromeImmune escapeMyelodysplastic syndrome hematopoietic stem cellsNatural killer (NK) cellsAberrant hematopoietic stem cellsEarly-stage myelodysplastic syndromeDevelopment of myelodysplastic syndromeStage of myelodysplastic syndromeAdoptive cell therapyFunctional in vitro studiesNatural killer cellsTime of diagnosisPreclinical in vivo studiesPre-malignant clonesDisease-related comorbiditiesPre-malignant stageSlow down disease progressionRegenerate hematopoiesisClonal cytopeniaNK cellsImmune surveillanceKiller cellsHealthy donorsPharmacological therapyOxytocin improves maternal licking behavior deficits in autism-associated Shank3 mutant dogs
Lyu W, Li Y, Yao A, Tan Q, Zhang R, Zhao J, Guo K, Jiang Y, Tian R, Zhang Y. Oxytocin improves maternal licking behavior deficits in autism-associated Shank3 mutant dogs. Translational Psychiatry 2025, 15: 76. PMID: 40050270, DOI: 10.1038/s41398-025-03296-5.Peer-Reviewed Original ResearchConceptsAutism spectrum disorderMutant damsWild-typeMaternal behaviorASD risk genesLicking behaviorAbundant scaffolding proteinImpaired social interactionEffects of oxytocinCRISPR/Cas9 methodologyRisk genesMutant dogsNursing frequencyOXT treatmentBehavioral deficitsRepetitive behaviorsPotential therapeutic strategySpectrum disorderIntegrating epidemiology and genomics data to estimate the prevalence of acquired cysteine drug targets in the U.S. cancer patient population
Arun A, Liarakos D, Mendiratta G, Kim J, Goshua G, Olson P, Stites E. Integrating epidemiology and genomics data to estimate the prevalence of acquired cysteine drug targets in the U.S. cancer patient population. The Pharmacogenomics Journal 2025, 25: 5. PMID: 40044654, DOI: 10.1038/s41397-025-00364-3.Peer-Reviewed Original ResearchConceptsGenomic dataEstimates of mutation ratesSomatic missense mutationsGenomic informationPopulation-level estimatesCancer patient populationMissense mutationsNon-epidemiologicallyCancer patientsMutation ratePathogenic mutationsCysteine residuesCancer epidemiologyMutation-specificMutation abundanceDrug targetsMutationsIntegrates epidemiologyAbundancePatient populationEpidemiologyGenomePopulationTargeted therapyResiduesDeterminants of response and molecular dynamics in HER2+ER+ breast cancers from the NA-PHER2 trial receiving HER2-targeted and endocrine therapies
Callari M, Dugo M, Barreca M, Győrffy B, Galbardi B, Vigano L, Locatelli A, Dall’Ara C, Ferrarini M, Bisagni G, Colleoni M, Mansutti M, Zamagni C, Del Mastro L, Zambelli S, Frassoldati A, Biasi O, Pusztai L, Valagussa P, Viale G, Gianni L, Bianchini G. Determinants of response and molecular dynamics in HER2+ER+ breast cancers from the NA-PHER2 trial receiving HER2-targeted and endocrine therapies. Nature Communications 2025, 16: 2195. PMID: 40038334, PMCID: PMC11880565, DOI: 10.1038/s41467-025-57293-9.Peer-Reviewed Original ResearchConceptsTumor-infiltrating lymphocytesBreast cancerEndocrine therapyImmune infiltrationPrediction of pCRAnti-HER2 therapyLuminal A phenotypeHigher immune infiltrationFemale breast cancerHER2 blockadeDeterminants of responseTumor responseInfiltrating lymphocytesCDK4/6 inhibitionAnti-HER2HER2 targetingClinical endpointsER signalingKi67Response groupCancerTherapyTherapeutic targetMolecular changesTumorModeling SMAD2 Mutations in Induced Pluripotent Stem Cells Provides Insights Into Cardiovascular Disease Pathogenesis.
Ward T, Morton S, Venturini G, Tai W, Jang M, Gorham J, Delaughter D, Wasson L, Khazal Z, Homsy J, Gelb B, Chung W, Bruneau B, Brueckner M, Tristani-Firouzi M, DePalma S, Seidman C, Seidman J. Modeling SMAD2 Mutations in Induced Pluripotent Stem Cells Provides Insights Into Cardiovascular Disease Pathogenesis. Journal Of The American Heart Association 2025, 14: e036860. PMID: 40028843, DOI: 10.1161/jaha.124.036860.Peer-Reviewed Original ResearchConceptsLoss-of-functionCongenital heart diseaseChromatin accessibilityMissense variantsCHD probandsPluripotent stem cellsHomozygous loss-of-functionCHD-associated genesHeterozygous loss-of-functionTranscription factor bindingMutant induced pluripotent stem cellsChromatin immunoprecipitation dataChromatin peaksStem cellsChromatin interactionsInduced pluripotent stem cellsFactor bindingTranscription factor NanogExome sequencingImmunoprecipitation dataTranscription factorsRNA sequencingChromatinMissenseMolecular consequencesTANGO2 is an acyl-CoA binding protein
Lujan A, Foresti O, Wojnacki J, Bigliani G, Brouwers N, Pena M, Androulaki S, Hashidate-Yoshida T, Kalyukina M, Novoselov S, Shindou H, Malhotra V. TANGO2 is an acyl-CoA binding protein. Journal Of Cell Biology 2025, 224: e202410001. PMID: 40015245, PMCID: PMC11867700, DOI: 10.1083/jcb.202410001.Peer-Reviewed Original ResearchConceptsAcyl-CoA binding proteinPeriphery of lipid dropletsAcyl-coenzyme A binding proteinA-binding proteinsAcyl-coenzyme AMitochondrial lumenHeme transportBinding proteinTANGO2Cellular localizationLipid dropletsStructural regionsLipid metabolismHeightened energy demandsMutationsProteinResiduesNrdEMetabolic crisisBindingMetabolismHemeSevere cardiomyopathyLipidFAK inhibition combined with the RAF-MEK clamp avutometinib overcomes resistance to targeted and immune therapies in BRAF V600E melanoma
Lubrano S, Cervantes-Villagrana R, Faraji F, Ramirez S, Sato K, Adame-Garcia S, Officer A, Arang N, Rigiracciolo D, Anguiano Quiroz P, Martini C, Wang Y, Ferguson F, Bacchiocchi A, Halaban R, Coma S, Holmen S, Pachter J, Aplin A, Gutkind J. FAK inhibition combined with the RAF-MEK clamp avutometinib overcomes resistance to targeted and immune therapies in BRAF V600E melanoma. Cancer Cell 2025, 43: 428-445.e6. PMID: 40020669, PMCID: PMC11903146, DOI: 10.1016/j.ccell.2025.02.001.Peer-Reviewed Original ResearchConceptsBRAF V600E melanomaFocal adhesion kinaseV600E melanomaFAK inhibitorActivated focal adhesion kinaseFocal adhesion kinase inhibitionRaf-MEKActivation of focal adhesion signalingFocal adhesion kinase inhibitorResistance to BRAFiSyngeneic mouse modelMAPK pathway inhibitionFocal adhesion signalingPro-apoptotic activityMelanoma patientsAdhesion signalingImmune therapyBRAF mutationsBRAFiTranscriptome analysisMelanomaMouse modelPathway inhibitionBRAFMelanoma cellsPTEN mutations impair CSF dynamics and cortical networks by dysregulating periventricular neural progenitors
DeSpenza T, Kiziltug E, Allington G, Barson D, McGee S, O’Connor D, Robert S, Mekbib K, Nanda P, Greenberg A, Singh A, Duy P, Mandino F, Zhao S, Lynn A, Reeves B, Marlier A, Getz S, Nelson-Williams C, Shimelis H, Walsh L, Zhang J, Wang W, Prina M, OuYang A, Abdulkareem A, Smith H, Shohfi J, Mehta N, Dennis E, Reduron L, Hong J, Butler W, Carter B, Deniz E, Lake E, Constable R, Sahin M, Srivastava S, Winden K, Hoffman E, Carlson M, Gunel M, Lifton R, Alper S, Jin S, Crair M, Moreno-De-Luca A, Luikart B, Kahle K. PTEN mutations impair CSF dynamics and cortical networks by dysregulating periventricular neural progenitors. Nature Neuroscience 2025, 28: 536-557. PMID: 39994410, DOI: 10.1038/s41593-024-01865-3.Peer-Reviewed Original ResearchConceptsNeural progenitor cellsCongenital hydrocephalusCSF dynamicsIncreased CSF productionDe novo mutationsFrequent monogenic causeEverolimus treatmentCSF shuntingNonsurgical treatmentPTEN mutationsAqueductal stenosisInhibitory interneuronsVentriculomegalyProgenitor cellsChoroid plexusMonogenic causeCortical networksIncreased survivalBrain ventriclesCortical deficitsNeural progenitorsGene PTENCSF productionNkx2.1PTENSomatic variations in the meiosis‐specific gene CrMER3 confer seedlessness in a citrus bud sport
Fan Y, Du Z, He X, Liu Z, Zhuang J, Xiao G, Duan Y, Tan F, Xie K, Jiao W, Zhang F, Yang C, Guo W, Wu X. Somatic variations in the meiosis‐specific gene CrMER3 confer seedlessness in a citrus bud sport. Journal Of Integrative Plant Biology 2025, 67: 1649-1664. PMID: 39981730, DOI: 10.1111/jipb.13872.Peer-Reviewed Original ResearchConceptsKompetitive allele-specific PCRFruit cropsSeedless cultivarsSeedless hybridsSeedless varietiesFresh consumptionBud sportsCitrus germplasmSeed abortionSeedlessCultivarsWild mandarinAllele-specific PCRCitrusCropFruitBreedingNatural variationNatural mutationsSterilizationCultivated mandarinsMandarinMeiosis defectsGermplasmMeiotic prophase IOlaparib in treatment‐refractory isocitrate dehydrogenase 1 (IDH1)– and IDH2‐mutant cholangiocarcinoma: Safety and antitumor activity from the phase 2 National Cancer Institute 10129 trial
Cecchini M, Pilat M, Uboha N, Azad N, Cho M, Davis E, Ahnert J, Tinoco G, Shapiro G, Khagi S, Powers B, Spencer K, Groisberg R, Drappatz J, Chen L, Das B, Bao X, Li J, Narayan A, Vu D, Patel A, Niger M, Doroshow D, Durecki D, Boerner S, Bindra R, Ivy P, Shyr D, Shyr Y, LoRusso P. Olaparib in treatment‐refractory isocitrate dehydrogenase 1 (IDH1)– and IDH2‐mutant cholangiocarcinoma: Safety and antitumor activity from the phase 2 National Cancer Institute 10129 trial. Cancer 2025, 131: e35755. PMID: 39917990, DOI: 10.1002/cncr.35755.Peer-Reviewed Original ResearchConceptsProgression-free survivalHomologous recombination deficiencyClinical benefitNational Cancer InstituteIDH inhibitorsMedian progression-free survivalAccumulation of 2-hydroxyglutaratePhase 2 clinical trialIsocitrate dehydrogenase inhibitorsMedian overall survivalSingle-agent activityNovel combination therapiesEnhance patient selectionSubgroup of patientsOverall survivalOpen-labelCombination therapyIDH mutationsPatient selectionRecombination deficiencySolid tumorsTumor progressionClinical trialsOlaparibCholangiocarcinomaProtein codes promote selective subcellular compartmentalization
Kilgore H, Chinn I, Mikhael P, Mitnikov I, Van Dongen C, Zylberberg G, Afeyan L, Banani S, Wilson-Hawken S, Lee T, Barzilay R, Young R. Protein codes promote selective subcellular compartmentalization. Science 2025, 387: 1095-1101. PMID: 39913643, DOI: 10.1126/science.adq2634.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceCell CompartmentationCell NucleolusHumansMutationProtein FoldingProteinsConceptsProtein sequencesSubcellular compartmentsDiverse subcellular compartmentsProtein language modelsAmino acid sequenceProtein codingAcid sequenceSubcellular localizationDiverse proteinsHuman proteinsSubcellular compartmentalizationFolding codePathological mutationsCompartment localizationProteinSequenceCompartmentMutationsAminoNucleolusCompartmentalizationCellsA neoantigen vaccine generates antitumour immunity in renal cell carcinoma
Braun D, Moranzoni G, Chea V, McGregor B, Blass E, Tu C, Vanasse A, Forman C, Forman J, Afeyan A, Schindler N, Liu Y, Li S, Southard J, Chang S, Hirsch M, LeBoeuf N, Olive O, Mehndiratta A, Greenslade H, Shetty K, Klaeger S, Sarkizova S, Pedersen C, Mossanen M, Carulli I, Tarren A, Duke-Cohan J, Howard A, Iorgulescu J, Shim B, Simon J, Signoretti S, Aster J, Elagina L, Carr S, Leshchiner I, Getz G, Gabriel S, Hacohen N, Olsen L, Oliveira G, Neuberg D, Livak K, Shukla S, Fritsch E, Wu C, Keskin D, Ott P, Choueiri T. A neoantigen vaccine generates antitumour immunity in renal cell carcinoma. Nature 2025, 639: 474-482. PMID: 39910301, PMCID: PMC11903305, DOI: 10.1038/s41586-024-08507-5.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAntigens, NeoplasmCancer VaccinesCarcinoma, Renal CellClass I Phosphatidylinositol 3-KinasesDNA-Binding ProteinsFemaleHumansIpilimumabKidney NeoplasmsMaleMiddle AgedMutationPrecision MedicineT-LymphocytesTranscription FactorsTumor Suppressor ProteinsUbiquitin ThiolesteraseVon Hippel-Lindau Tumor Suppressor ProteinConceptsPersonalized cancer vaccinesRenal cell carcinomaDriver mutationsAntitumour immunityCell carcinomaI trialResected clear cell renal cell carcinomaImmune responseT cell immune responsesClear cell renal cell carcinomaHigh-risk RCCDose-limiting toxicityLow mutational burdenCell renal cell carcinomaEffective adjuvant therapyPhase I trialT cell reactivityAbsence of recurrenceCirculating immune responsesCell immune responseAutologous tumorNeoantigen vaccinesCancer vaccinesAdjuvant therapyMutational burdenDeep mutational scanning of the Trypanosoma brucei developmental regulator RBP6 reveals an essential disordered region influenced by positive residues
Rojas-Sánchez S, Kolev N, Tschudi C. Deep mutational scanning of the Trypanosoma brucei developmental regulator RBP6 reveals an essential disordered region influenced by positive residues. Nature Communications 2025, 16: 1168. PMID: 39885181, PMCID: PMC11782513, DOI: 10.1038/s41467-025-56553-y.Peer-Reviewed Original ResearchConceptsN-terminal intrinsically disordered regionRNA binding protein 6RNA recognition motifDeep mutational scanningMutational scanningDisordered regionsProtein-RNA interactionsIntrinsically disordered regionsComplex developmental programPositively charged residuesSingle-point variantsProtein-RNARNA recognitionDeleterious mutationsMutational constraintsProcyclic formsAnimal African trypanosomiasisTrypanosoma bruceiCharged residuesPrimary structureRegained infectivityDevelopmental programRegulatory roleProtein 6Positive residuesMonitoring molecular markers associated with antimalarial drug resistance in south-east Senegal from 2021 to 2023
Wade A, Sene S, Caspar E, Diallo F, Platon L, Thiebaut L, Pouye M, Ba A, Thiam L, Fall M, Sadio B, Desamours I, Guerra N, Hagadorn K, Amambua-Ngwa A, Bei A, Vigan-Womas I, Ménard D, Mbengue A. Monitoring molecular markers associated with antimalarial drug resistance in south-east Senegal from 2021 to 2023. Journal Of Antimicrobial Chemotherapy 2025, 80: 828-839. PMID: 39846779, PMCID: PMC11879165, DOI: 10.1093/jac/dkaf006.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAntimalarialsArtemisininsChildChild, PreschoolDrug CombinationsDrug ResistanceFemaleHumansMalaria, FalciparumMaleMembrane Transport ProteinsMiddle AgedMultidrug Resistance-Associated ProteinsMutationPlasmodium falciparumProtozoan ProteinsPyrimethamineSenegalSulfadoxineTetrahydrofolate DehydrogenaseYoung AdultConceptsArtemisinin-based combination therapyMolecular markers associated with antimalarial drug resistanceArtemisinin-based combination therapy efficacyP. falciparum infectionSulfadoxine-pyrimethamine resistanceAntimalarial drug resistanceInvestigated gene polymorphismsCQ-RResistance in vitroVenous blood samplesClinical outcome studiesI356TK76TPfcrt mutationsChloroquine resistanceAntimalarial resistancePfmdr-1CQ useMalaria eliminationCombination therapyResistance surveillanceGene polymorphismsPlasmodium falciparumDrug resistanceAmplicon deep sequencingCFTR dictates monocyte adhesion by facilitating integrin clustering but not activation
Younis D, Marosvari M, Liu W, Pulikkot S, Cao Z, Zhou B, Vella A, McArdle S, Hu L, Chen Y, Gan W, Yu J, Bruscia E, Fan Z. CFTR dictates monocyte adhesion by facilitating integrin clustering but not activation. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2412717122. PMID: 39813254, PMCID: PMC11760921, DOI: 10.1073/pnas.2412717122.Peer-Reviewed Original ResearchConceptsIntegrin clusteringCF transmembrane conductance regulatorCystic fibrosisAdhesion defectsPathogenesis of cystic fibrosisClinically relevant disease modelsMembrane recruitmentTransmembrane conductance regulatorIntegrin activationTherapeutic strategy designRelevant disease modelsIntegrinCF monocytesCell adhesionMonocyte dysfunctionPatients' monocytesTissue infectionsConductance regulatorSuperresolution microscopyCortex formationLeukocyte-dependent inflammationInflammatory pathogenesisLeukocyte adhesionMonocytesInflammationMultiomics dissection of human RAG deficiency reveals distinctive patterns of immune dysregulation but a common inflammatory signature
Bosticardo M, Dobbs K, Delmonte O, Martins A, Pala F, Kawai T, Kenney H, Magro G, Rosen L, Yamazaki Y, Yu H, Calzoni E, Lee Y, Liu C, Stoddard J, Niemela J, Fink D, Castagnoli R, Ramba M, Cheng A, Riley D, Oikonomou V, Shaw E, Belaid B, Keles S, Al-Herz W, Cancrini C, Cifaldi C, Baris S, Sharapova S, Schuetz C, Gennery A, Freeman A, Somech R, Choo S, Giliani S, Güngör T, Drozdov D, Meyts I, Moshous D, Neven B, Abraham R, El-Marsafy A, Kanariou M, King A, Licciardi F, Cruz-Muñoz M, Palma P, Poli C, Adeli M, Algeri M, Alroqi F, Bastard P, Bergerson J, Booth C, Brett A, Burns S, Butte M, Padem N, de la Morena M, Dbaibo G, de Ravin S, Dimitrova D, Djidjik R, Dorna M, Dutmer C, Elfeky R, Facchetti F, Fuleihan R, Geha R, Gonzalez-Granado L, Haljasmägi L, Ale H, Hayward A, Hifanova A, Ip W, Kaplan B, Kapoor N, Karakoc-Aydiner E, Kärner J, Keller M, Dávila Saldaña B, Kiykim A, Kuijpers T, Kuznetsova E, Latysheva E, Leiding J, Locatelli F, Alva-Lozada G, McCusker C, Celmeli F, Morsheimer M, Ozen A, Parvaneh N, Pasic S, Plebani A, Preece K, Prockop S, Sakovich I, Starkova E, Torgerson T, Verbsky J, Walter J, Ward B, Wisner E, Draper D, Myint-Hpu K, Truong P, Lionakis M, Similuk M, Walkiewicz M, Klion A, Holland S, Oguz C, Bogunovic D, Kisand K, Su H, Tsang J, Kuhns D, Villa A, Rosenzweig S, Pittaluga S, Notarangelo L, Ghosh R, Siefert B, Tokita M, Yan J, Jodarski C, Kamen M, Gore R, Reynolds-Lallement N, Lewis K, Bannon S, Borges A, Gentile N. Multiomics dissection of human RAG deficiency reveals distinctive patterns of immune dysregulation but a common inflammatory signature. Science Immunology 2025, 10: eadq1697. PMID: 39792639, DOI: 10.1126/sciimmunol.adq1697.Peer-Reviewed Original ResearchConceptsRAG deficiencyRecombination-activating geneImmune dysregulationInflammatory signaturePattern of immune dysregulationT helper 2B cell developmentType I interferonOmenn syndromeImmunological phenotypeImmune profileSelf-antigensB cellsClinical managementDefective TI interferonCellular indicesImmunopathologyPatientsMultiomics approachPhenotypeHypomorphic formDysregulationLineage-specific contributionsDeficiencyThe WAVE complex in developmental and adulthood brain disorders
Kim H, Berdasco C, Nairn A, Kim Y. The WAVE complex in developmental and adulthood brain disorders. Experimental & Molecular Medicine 2025, 57: 13-29. PMID: 39774290, PMCID: PMC11799376, DOI: 10.1038/s12276-024-01386-w.Peer-Reviewed Original ResearchConceptsWiskott-Aldrich syndrome protein family verprolin-homologous proteinActin polymerizationCellular processesArp2/3 complex-mediated actin polymerizationRegulatory proteinsOrganization of actin filamentsMaintenance of neuronal plasticityBrain disordersActin regulatory proteinsAutism spectrum disorderPathophysiology of Alzheimer's diseaseDe novo mutationsIntellectual disabilityActin filamentsExtracellular cuesSpectrum disorderMaladaptive feedingDevelopmental disordersAging brainHeteropentameric complexNeuronal plasticityIntracellular signalingIntracellular eventsBehavioral adaptationsDisordersMetabolic rewiring in skin epidermis drives tolerance to oncogenic mutations
Hemalatha A, Li Z, Gonzalez D, Matte-Martone C, Tai K, Lathrop E, Gil D, Ganesan S, Gonzalez L, Skala M, Perry R, Greco V. Metabolic rewiring in skin epidermis drives tolerance to oncogenic mutations. Nature Cell Biology 2025, 27: 218-231. PMID: 39762578, PMCID: PMC11821535, DOI: 10.1038/s41556-024-01574-w.Peer-Reviewed Original ResearchConceptsWild-type cellsOxidative tricarboxylic acid cycleOncogenic mutationsTricarboxylic acid cycleSingle-cell resolutionMutant phenotypeMutant cellsMutant epidermisCell competitionMetabolic rewiringAcid cycleCellular redoxStem cellsMutant modelsSkin epithelial stem cellsEpidermal stem cellsContribution of glucoseEpithelial stem cellsCytosolic redoxRedox ratioMetabolic stateMutationsHrasG12VSkin epidermisCellsPhenotypic variability in phosphate transport disorders highlights need for individualized treatment strategies
Zhu Z, Bergwitz C. Phenotypic variability in phosphate transport disorders highlights need for individualized treatment strategies. Kidney International 2025, 107: 12-15. PMID: 39746740, DOI: 10.1016/j.kint.2024.10.020.Peer-Reviewed Original ResearchConceptsPhosphate-wasting disordersIndividualized treatment strategiesLong-term outcomesGenetic variantsPathogenic variantsPhenotypic variabilitySLC34A3 geneClinical presentationTreatment strategiesTreatment challengesTransport disordersTreatment outcomesAffected individualsTherapeutic strategiesPotential treatment challengesBiochemical profileVariantsDisordersGenesOutcomesPhenotypeNpt2cSLC34A3Npt2aCross-modal sensory compensation increases mosquito attraction to humans
Morita T, Lyn N, von Heynitz R, Goldman O, Sorrells T, DeGennaro M, Matthews B, Houri-Zeevi L, Vosshall L. Cross-modal sensory compensation increases mosquito attraction to humans. Science Advances 2025, 11: eadn5758. PMID: 39742477, PMCID: PMC11691641, DOI: 10.1126/sciadv.adn5758.Peer-Reviewed Original Research
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