2024
Bioinformatic prediction of proteins relevant to functions of the bacterial OLE ribonucleoprotein complex
Fernando C, Breaker R. Bioinformatic prediction of proteins relevant to functions of the bacterial OLE ribonucleoprotein complex. MSphere 2024, 9: e00159-24. PMID: 38771028, PMCID: PMC11332333, DOI: 10.1128/msphere.00159-24.Peer-Reviewed Original ResearchOLE RNANoncoding RNA classesRNP complexesRNA classesSequence conservationProtein partnersBiochemical functionsDiverse stress conditionsProtein binding partnersEmergence of proteinsPhylogenetic profilesRibonucleoprotein complexSpore formationBacterial speciesCellular stressExtremophilic bacteriaProtein componentsRibonucleoproteinGenetic disruptionRNATransport proteinsRelevant to functionBioinformatics predictionGram-positivePrimitive organismsGenetic disruption of the bacterial raiA motif noncoding RNA causes defects in sporulation and aggregation
Soares L, King C, Fernando C, Roth A, Breaker R. Genetic disruption of the bacterial raiA motif noncoding RNA causes defects in sporulation and aggregation. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 121: e2318008121. PMID: 38306478, PMCID: PMC10861870, DOI: 10.1073/pnas.2318008121.Peer-Reviewed Original ResearchConceptsMotif RNAsGenetic disruptionSecondary structure modelKnock-out strainTrans-acting factorsNoncoding RNAsCell differentiation processAbundant RNATransfer RNANcRNA classesRibosomal RNASpore formationMotif genesCellular processesBacterial speciesCellular functionsBioinformatics analysisExpression analysisMotifRNAGenesBiochemical mechanismsNcRNAsDifferentiation processStructural probesDisruption of the bacterial OLE RNP complex impairs growth on alternative carbon sources
Lyon S, Wencker F, Fernando C, Harris K, Breaker R. Disruption of the bacterial OLE RNP complex impairs growth on alternative carbon sources. PNAS Nexus 2024, 3: pgae075. PMID: 38415217, PMCID: PMC10898510, DOI: 10.1093/pnasnexus/pgae075.Peer-Reviewed Original ResearchRNP complexesMinimal mediumWild-type cellsAlternative carbon sourcesUnfavorable growth conditionsOLE RNASuppressor selectionDiverse stressesCarbon/energy sourceProtein secretionCarbon sourceGenetic disruptionCellular adaptationNoncoding RNAsFunctional linkRNAGrowth conditionsRibonucleoproteinImpaired growthPhosphate homeostasisFundamental processesHomeostasisShort-chain alcoholsElevated MgCarbon/energyDynamic effects of ventral hippocampal NRG3/ERBB4 signaling on nicotine withdrawal-induced responses
Fisher M, Prantzalos E, O'Donovan B, Anderson T, Sahoo P, Twiss J, Ortinski P, Turner J. Dynamic effects of ventral hippocampal NRG3/ERBB4 signaling on nicotine withdrawal-induced responses. Neuropharmacology 2024, 247: 109846. PMID: 38211698, PMCID: PMC10923109, DOI: 10.1016/j.neuropharm.2024.109846.Peer-Reviewed Original ResearchConceptsAnxiety-like behaviorNeuregulin 3Ventral hippocampusAnxiety-related behaviorDrugs of abuseSmoking cessation therapySingle nucleotide polymorphismsNicotine withdrawalAnxiety-relatedErbB-4Nicotine addictionKnock-down miceGABAergic transmissionNeuronal mechanismsCA1 areaCessation therapyNicotineSynaptic expressionWithdrawalRelapse rateFemale miceNetwork activityGenetic factorsNucleotide polymorphismsGenetic disruption
2023
Evidence that OLE RNA is a component of a major stress‐responsive ribonucleoprotein particle in extremophilic bacteria
Breaker R, Harris K, Lyon S, Wencker F, Fernando C. Evidence that OLE RNA is a component of a major stress‐responsive ribonucleoprotein particle in extremophilic bacteria. Molecular Microbiology 2023, 120: 324-340. PMID: 37469248, DOI: 10.1111/mmi.15129.Peer-Reviewed Original ResearchConceptsOLE RNAPrecise biochemical functionFundamental cellular processesCell growthTOR complexesProtein partnersRibonucleoprotein complexesCellular processesRNP complexesBiochemical functionsGram-positive bacteriaNoncoding RNAsRibonucleoprotein particleExtremophilic bacteriaBacterial speciesGenetic disruptionStress conditionsDiverse pathwaysRNAMetabolic adaptationCell membraneExtreme environmentsCarbon sourceBacteriaComplexesAP-1–independent NFAT signaling maintains follicular T cell function in infection and autoimmunity
Seth A, Yokokura Y, Choi J, Shyer J, Vidyarthi A, Craft J. AP-1–independent NFAT signaling maintains follicular T cell function in infection and autoimmunity. Journal Of Experimental Medicine 2023, 220: e20211110. PMID: 36820828, PMCID: PMC9998660, DOI: 10.1084/jem.20211110.Peer-Reviewed Original ResearchConceptsTfh cellsT cellsFollicular helper T cellsLupus-prone miceT cell subsetsTfh cell developmentHelper T cellsHumoral immune responseT cell functionGerminal center B cellsT cell statesRenal injuryAutoantibody productionCell subsetsPrimary T cellsImmune responseB cellsPharmacologic inhibitionTherapeutic insightsCell functionGenetic disruptionNFATCell developmentCellsGene expression
2022
Unfolded protein response IRE1/XBP1 signaling is required for healthy mammalian brain aging
Cabral‐Miranda F, Tamburini G, Martinez G, Ardiles A, Medinas D, Gerakis Y, Hung M, Vidal R, Fuentealba M, Miedema T, Duran‐Aniotz C, Diaz J, Ibaceta‐Gonzalez C, Sabusap C, Bermedo‐Garcia F, Mujica P, Adamson S, Vitangcol K, Huerta H, Zhang X, Nakamura T, Sardi S, Lipton S, Kennedy B, Henriquez J, Cárdenas J, Plate L, Palacios A, Hetz C. Unfolded protein response IRE1/XBP1 signaling is required for healthy mammalian brain aging. The EMBO Journal 2022, 41: embj2022111952. PMID: 36314651, PMCID: PMC9670206, DOI: 10.15252/embj.2022111952.Peer-Reviewed Original ResearchConceptsUnfolded protein responseER stress sensor IRE1Stress sensor IRE1IRE1/XBP1 signalingTranscription factor XBP1Mammalian brain agingNeurodegenerative diseasesProteostasis networkEndoplasmic reticulum stressProteomic profilingProtein responseCell senescenceGenetic disruptionBrain agingXBP1 expressionReticulum stressMammalian brainMajor risk factorActive formHealthy brain agingSynaptic functionXBP1Age-related cognitive declinePathwayHippocampal tissue
2020
Integrative Genomics Implicates Genetic Disruption of Prenatal Neurogenesis in Congenital Hydrocephalus
Panchagnula S, Jin S, Dong W, Kundishora A, Moreno-De-Luca A, Furey C, Allocco A, Walker R, Nelson-Williams C, Smith H, Dunbar A, Conine S, Lu Q, Zen X, Sierant M, Knight J, Sullivan W, Phan D, DeSpenza T, Reeves B, Karimy J, Marlier A, Castaldi C, Tikhonova I, Li B, Peña; H, Broach J, Kabachelor E, Ssenyonga P, Hehnly C, Ge L, Keren B, Timberlake A, Goto J, Mangano F, Johnston J, Butler W, Warf B, Smith E, Schiff S, Limbrick D, Heuer G, Jackson E, Iskandar B, Mane S, Haider S, Guclu B, Bayri Y, Sahin Y, Duncan C, Apuzzo M, DiLuna M, Hoffman E, Sestan N, Ment L, Alper S, Bilguvar K, Geschwind D, Günel M, Lifton R, Kahle K. Integrative Genomics Implicates Genetic Disruption of Prenatal Neurogenesis in Congenital Hydrocephalus. Neurosurgery 2020, 67 DOI: 10.1093/neuros/nyaa447_572.Peer-Reviewed Original ResearchExome sequencing implicates genetic disruption of prenatal neuro-gliogenesis in sporadic congenital hydrocephalus
Jin SC, Dong W, Kundishora AJ, Panchagnula S, Moreno-De-Luca A, Furey CG, Allocco AA, Walker RL, Nelson-Williams C, Smith H, Dunbar A, Conine S, Lu Q, Zeng X, Sierant MC, Knight JR, Sullivan W, Duy PQ, DeSpenza T, Reeves BC, Karimy JK, Marlier A, Castaldi C, Tikhonova IR, Li B, Peña HP, Broach JR, Kabachelor EM, Ssenyonga P, Hehnly C, Ge L, Keren B, Timberlake AT, Goto J, Mangano FT, Johnston JM, Butler WE, Warf BC, Smith ER, Schiff SJ, Limbrick DD, Heuer G, Jackson EM, Iskandar BJ, Mane S, Haider S, Guclu B, Bayri Y, Sahin Y, Duncan CC, Apuzzo MLJ, DiLuna ML, Hoffman EJ, Sestan N, Ment LR, Alper SL, Bilguvar K, Geschwind DH, Günel M, Lifton RP, Kahle KT. Exome sequencing implicates genetic disruption of prenatal neuro-gliogenesis in sporadic congenital hydrocephalus. Nature Medicine 2020, 26: 1754-1765. PMID: 33077954, PMCID: PMC7871900, DOI: 10.1038/s41591-020-1090-2.Peer-Reviewed Original ResearchConceptsCongenital hydrocephalusPoor neurodevelopmental outcomesPost-surgical patientsCerebrospinal fluid accumulationNeural stem cell biologyGenetic disruptionWhole-exome sequencingPrimary pathomechanismEarly brain developmentNeurodevelopmental outcomesHigh morbidityCSF diversionMutation burdenFluid accumulationBrain ventriclesCH casesBrain developmentDe novo mutationsPatientsExome sequencingCSF dynamicsDisease mechanismsHydrocephalusNovo mutationsCell types
2016
Anabolic actions of Notch on mature bone
Liu P, Ping Y, Ma M, Zhang D, Liu C, Zaidi S, Gao S, Ji Y, Lou F, Yu F, Lu P, Stachnik A, Bai M, Wei C, Zhang L, Wang K, Chen R, New M, Rowe D, Yuen T, Sun L, Zaidi M. Anabolic actions of Notch on mature bone. Proceedings Of The National Academy Of Sciences Of The United States Of America 2016, 113: e2152-e2161. PMID: 27036007, PMCID: PMC4839423, DOI: 10.1073/pnas.1603399113.Peer-Reviewed Original ResearchConceptsOvariectomy-induced bone lossEGFP reporter miceStimulation of NotchBone lossAnabolic actionAnabolic responseReporter miceMature micePresenilin 1Bone healingLigand Jagged1Bone formationTime pointsMiceAdult boneGenetic disruptionMature boneBone matrixConditional activationNotch expressionTerminal osteoblast differentiationNotch activationOsteoblast differentiationBoneOsteocytesPre-BCR signaling in precursor B-cell acute lymphoblastic leukemia regulates PI3K/AKT, FOXO1 and MYC, and can be targeted by SYK inhibition
Köhrer S, Havranek O, Seyfried F, Hurtz C, Coffey G, Kim E, ten Hacken E, Jäger U, Vanura K, O'Brien S, Thomas D, Kantarjian H, Ghosh D, Wang Z, Zhang M, Ma W, Jumaa H, Debatin K, Müschen M, Meyer L, Davis R, Burger J. Pre-BCR signaling in precursor B-cell acute lymphoblastic leukemia regulates PI3K/AKT, FOXO1 and MYC, and can be targeted by SYK inhibition. Leukemia 2016, 30: 1246-1254. PMID: 26847027, PMCID: PMC5459356, DOI: 10.1038/leu.2016.9.Peer-Reviewed Original ResearchConceptsB-cell acute lymphoblastic leukemiaSpleen tyrosine kinaseAcute lymphoblastic leukemiaPI3K/AktLymphoblastic leukemiaTherapeutic targetPrecursor B-cell acute lymphoblastic leukemiaPromising new therapeutic targetNew therapeutic targetsGene expression signaturesImmune phenotypeImportant downstream mediatorSYK inhibitionMouse modelPre-BCR signalingReceptor signalingDownstream mediatorExpression signaturesGenetic disruptionLeukemiaExquisite dependencyTyrosine kinaseAktFOXO1Signaling
2012
Normal Hematopoiesis and Neurofibromin-Deficient Myeloproliferative Disease Require Erk
Staser K, Zeng Y, Park S, Rhodes S, He Y, Shew M, Gehlhausen J, Cerabona D, Chen S, Sun Z, Nalepa G, Yang F, Clapp D. Normal Hematopoiesis and Neurofibromin-Deficient Myeloproliferative Disease Require Erk. Blood 2012, 120: 704. DOI: 10.1182/blood.v120.21.704.704.Peer-Reviewed Original ResearchMEK-ERK inhibitorsNeurofibromatosis type 1Myeloproliferative diseaseRas GTPase-activating proteinDevelopment of juvenile myelomonocytic leukemiaGTPase-activating proteinFatal myeloproliferative diseaseDiverse cell typesTumor suppressor geneGenetically engineered murine modelsResistant to traditional therapiesRaf-MEK-ERKNf1-deficient miceProgenitor cell numbersJuvenile myelomonocytic leukemiaTranscription factorsActivator proteinGenetic studiesPhosphorylated kinasesSuppressor geneGenetic disruptionMitogenic roleMyelomonocytic leukemiaHematopoietic stemHSPC proliferation
2011
Cilia in the CNS: The Quiet Organelle Claims Center Stage
Louvi A, Grove EA. Cilia in the CNS: The Quiet Organelle Claims Center Stage. Neuron 2011, 69: 1046-1060. PMID: 21435552, PMCID: PMC3070490, DOI: 10.1016/j.neuron.2011.03.002.Peer-Reviewed Original ResearchConceptsPrimary ciliaSonic hedgehog (Shh) signal transductionHedgehog signal transductionHuman disease syndromesProtein traffickingBrain tumor formationSignal transductionCellular organellesGenetic disruptionSpecialized modeNeuronal signalingCiliaTumor formationAdult CNSAdult neurogenesisEukaryotesVertebratesOrganellesTransductionTraffickingSignalingBiologyDisease syndromeMajor linesNeurogenesis
2010
The Na+-dependent chloride-bicarbonate exchanger SLC4A8 mediates an electroneutral Na+ reabsorption process in the renal cortical collecting ducts of mice
Leviel F, Hübner CA, Houillier P, Morla L, Moghrabi S, Brideau G, Hatim H, Parker MD, Kurth I, Kougioumtzes A, Sinning A, Pech V, Riemondy KA, Miller RL, Hummler E, Shull GE, Aronson PS, Doucet A, Wall SM, Chambrey R, Eladari D. The Na+-dependent chloride-bicarbonate exchanger SLC4A8 mediates an electroneutral Na+ reabsorption process in the renal cortical collecting ducts of mice. Journal Of Clinical Investigation 2010, 120: 1627-1635. PMID: 20389022, PMCID: PMC2860930, DOI: 10.1172/jci40145.Peer-Reviewed Original ResearchConceptsNa-Cl cotransporterSodium transportMaintenance of euvolemiaTransepithelial NaCl absorptionDucts of miceEpithelial sodium channelIntravascular volumeIndependent Cl-/HCO3Sodium balanceMouse CCDAmiloride-sensitive epithelial sodium channelSodium absorptionExcretion resultsFluid homeostasisGenetic ablationNaCl absorptionSodium channelsMiceCl-/HCO3NaCl transportSlc4a8Genetic disruptionNovel roleHydrochlorothiazideDuct
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