2024
Mechanical power is maximized during contractile ring-like formation in a biomimetic dividing cell model
Sakamoto R, Murrell M. Mechanical power is maximized during contractile ring-like formation in a biomimetic dividing cell model. Nature Communications 2024, 15: 9731. PMID: 39523366, PMCID: PMC11551154, DOI: 10.1038/s41467-024-53228-y.Peer-Reviewed Original ResearchConceptsMyosin-induced stressContractile ring assemblyCell division mechanismActin filamentsActin cortexCleavage furrowDivision planeActomyosin flowsGiant unilamellar vesiclesRing assemblyCell divisionMyosin activityContractile ring-like structureShape changesRing-like structureDivision mechanismEnergetic costSymmetric divisionActinRing-like formationCell modelUnilamellar vesiclesIn vitro modelFurrowCells
2023
Cellular allostatic load is linked to increased energy expenditure and accelerated biological aging
Bobba-Alves N, Sturm G, Lin J, Ware S, Karan K, Monzel A, Bris C, Procaccio V, Lenaers G, Higgins-Chen A, Levine M, Horvath S, Santhanam B, Kaufman B, Hirano M, Epel E, Picard M. Cellular allostatic load is linked to increased energy expenditure and accelerated biological aging. Psychoneuroendocrinology 2023, 155: 106322. PMID: 37423094, PMCID: PMC10528419, DOI: 10.1016/j.psyneuen.2023.106322.Peer-Reviewed Original ResearchConceptsCellular agingCellular energy expenditureDNA methylation clockMitochondrial oxidative phosphorylationStress adaptationMtDNA instabilityOXPHOS activityMethylation clockOxidative phosphorylationMetabolic shiftEnergetic costHuman fibroblast lineCellular basisPhysiological responsesFibroblast linesStress triggersPotential driversBiological agingEnergy expenditureChronic activationLifespanDamaging effectsPrimary human fibroblast linesCytokine secretionPhosphorylationOxPhos defects cause hypermetabolism and reduce lifespan in cells and in patients with mitochondrial diseases
Sturm G, Karan K, Monzel A, Santhanam B, Taivassalo T, Bris C, Ware S, Cross M, Towheed A, Higgins-Chen A, McManus M, Cardenas A, Lin J, Epel E, Rahman S, Vissing J, Grassi B, Levine M, Horvath S, Haller R, Lenaers G, Wallace D, St-Onge M, Tavazoie S, Procaccio V, Kaufman B, Seifert E, Hirano M, Picard M. OxPhos defects cause hypermetabolism and reduce lifespan in cells and in patients with mitochondrial diseases. Communications Biology 2023, 6: 22. PMID: 36635485, PMCID: PMC9837150, DOI: 10.1038/s42003-022-04303-x.Peer-Reviewed Original ResearchConceptsIntegrated stress responseOXPHOS defectsMitochondrial diseaseCellular energy expenditureMitochondrial DNA instabilityPatient-derived fibroblastsMitochondrial oxidative phosphorylationCell divisionExtracellular secretionOxidative phosphorylationStress responseDNA instabilityMechanistic basisEnergetic costEpigenetic agingGeneral mechanismOXPHOSBiological agingExcess energy expenditurePotential mechanismsEnergy expenditureCellsMulti-system disorderMetabokinesRNAseq
2020
Contribution of increasing plasma membrane to the energetic cost of early zebrafish embryogenesis
Rodenfels J, Sartori P, Golfier S, Nagendra K, Neugebauer K, Howard J. Contribution of increasing plasma membrane to the energetic cost of early zebrafish embryogenesis. Molecular Biology Of The Cell 2020, 31: 520-526. PMID: 32049586, PMCID: PMC7202076, DOI: 10.1091/mbc.e19-09-0529.Peer-Reviewed Original ResearchConceptsPlasma membraneEarly zebrafish embryogenesisEnergetic costSpecific developmental eventsTotal plasma membraneCell proliferationTwo-cell stageZebra fish embryosZebrafish embryogenesisTotal cell surface areaDNA replicationCell divisionEarly embryosDevelopmental eventsCleavage divisionsCell surface areaTotal cell numberCleavage stagesEmbryo volumeEmbryosCell numberMembraneTotal energy budgetProliferationEmbryogenesis
2008
Quality control despite mistranslation caused by an ambiguous genetic code
Ruan B, Palioura S, Sabina J, Marvin-Guy L, Kochhar S, LaRossa RA, Söll D. Quality control despite mistranslation caused by an ambiguous genetic code. Proceedings Of The National Academy Of Sciences Of The United States Of America 2008, 105: 16502-16507. PMID: 18946032, PMCID: PMC2575449, DOI: 10.1073/pnas.0809179105.Peer-Reviewed Original ResearchConceptsGenetic codeAa-tRNAWild-type proteinAminoacyl-tRNA synthetasesInactive mutant proteinsHeat shock responseE. coliMutant proteinsReporter proteinMissense suppressionFunctional proteinsCognate tRNASelective pressureAminoacyl-tRNAActive enzymeShock responseProtein synthesisNative conformationEnergetic costAmino acidsMissense mutationsProteinBiochemical evidenceCorrect pairingProtein quality
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