2024
Sphingosine‐1‐Phosphate Signalling Inhibition Suppresses Th1‐Like Treg Generation by Reversing Mitochondrial Uncoupling
Coulombeau R, Selck C, Giang N, Al‐Mohammad A, Ng N, Maher A, Argüello R, Scalfari A, Varley J, Nicholas R, Dominguez‐Villar M. Sphingosine‐1‐Phosphate Signalling Inhibition Suppresses Th1‐Like Treg Generation by Reversing Mitochondrial Uncoupling. Immunology 2024, 174: 153-166. PMID: 39444366, PMCID: PMC11652410, DOI: 10.1111/imm.13870.Peer-Reviewed Original ResearchTh1-like TregsSphingosine-1-PhosphateSuppressive functionMitochondrial uncouplingSignaling inhibitionIncreased suppressive functionMultiple sclerosisTreg plasticityTreg reprogrammingTreg frequencyTreg generationTregsAutoimmune conditionsExpression of genesInflammatory environmentMS patientsS1P inhibitionFTY720Defective functionS1PMTORC1 signalingInhibitionReprogrammingmTORC1 Signaling in Brain Endothelial Progenitors Contributes to CCM Pathogenesis
Min W, Qin L, Zhang H, López-Giráldez F, Jiang N, Kim Y, Mohan V, Su M, Murray K, Grutzendler J, Zhou J. mTORC1 Signaling in Brain Endothelial Progenitors Contributes to CCM Pathogenesis. Circulation Research 2024, 135: e94-e113. PMID: 38957991, PMCID: PMC11293987, DOI: 10.1161/circresaha.123.324015.Peer-Reviewed Original ResearchCerebral vascular malformationsEndothelial progenitor cellsBlood-brain barrier integritySingle-cell RNA sequencing analysisDisruption of blood-brain barrier integrityBarrier integrityResident endothelial progenitor cellsRNA sequencing analysisTissue immunofluorescence analysisEndothelial cellsEPC clustersStem cell markersFocal neurological deficitsBrain's neurovascular unitMTOR signalingHuman CCM lesionsMTORC1 signalingBlood-brain barrierCapillary endothelial cellsCCM pathogenesisVascular malformationsLesion signaturesNeurological deficitsCell markersClonal expansionDEPDC5 protects CD8+ T cells from ferroptosis by limiting mTORC1-mediated purine catabolism
Li S, Ouyang X, Sun H, Jin J, Chen Y, Li L, Wang Q, He Y, Wang J, Chen T, Zhong Q, Liang Y, Pierre P, Zou Q, Ye Y, Su B. DEPDC5 protects CD8+ T cells from ferroptosis by limiting mTORC1-mediated purine catabolism. Cell Discovery 2024, 10: 53. PMID: 38763950, PMCID: PMC11102918, DOI: 10.1038/s41421-024-00682-z.Peer-Reviewed Original ResearchCD8+ T cellsPeripheral CD8+ T cellsAnti-tumor immunityT cellsTumor-infiltrating CD8+ T cellsCD8+ T cell homeostasisCD8+ T cell numbersImpaired anti-tumor immunityT cell numbersT-cell protectionT cell homeostasisCancer patient survivalLevels of xanthine oxidasePatient survivalCD8Epilepsy patientsDEPDC5Suppression of ferroptosisMTORC1 signalingFerroptosisMolecular mechanismsImmunityXanthine oxidasePurine catabolismExpressionThe mTOR pathway genes MTOR, Rheb, Depdc5, Pten, and Tsc1 have convergent and divergent impacts on cortical neuron development and function
Nguyen L, Xu Y, Nair M, Bordey A. The mTOR pathway genes MTOR, Rheb, Depdc5, Pten, and Tsc1 have convergent and divergent impacts on cortical neuron development and function. ELife 2024, 12: rp91010. PMID: 38411613, PMCID: PMC10942629, DOI: 10.7554/elife.91010.Peer-Reviewed Original ResearchConceptsMouse medial prefrontal cortexMedial prefrontal cortexFocal malformations of cortical developmentMalformations of cortical developmentExcitatory synaptic activityExcitatory synaptic transmissionCortical neuron developmentPyramidal neuron morphologyMechanisms of hyperexcitabilityResponse to therapeutic interventionsMTORC1 signalingGene-specific mechanismsPrefrontal cortexFocal malformationsBrain somatic mutationsMTOR complex 1Membrane excitabilityBiallelic inactivationClinical manifestationsGene mutationsNetwork hyperexcitabilitySynaptic transmissionSynaptic activityIntractable epilepsyRepressor geneThe mTOR pathway genes MTOR, Rheb, Depdc5, Pten, and Tsc1 have convergent and divergent impacts on cortical neuron development and function
Nguyen L, Xu Y, Nair M, Bordey A. The mTOR pathway genes MTOR, Rheb, Depdc5, Pten, and Tsc1 have convergent and divergent impacts on cortical neuron development and function. ELife 2024, 12 DOI: 10.7554/elife.91010.3.Peer-Reviewed Original ResearchMouse medial prefrontal cortexMedial prefrontal cortexFocal malformations of cortical developmentMalformations of cortical developmentExcitatory synaptic activityExcitatory synaptic transmissionCortical neuron developmentPyramidal neuron morphologyMechanisms of hyperexcitabilityResponse to therapeutic interventionsMTORC1 signalingGene-specific mechanismsPrefrontal cortexFocal malformationsBrain somatic mutationsMTOR complex 1Membrane excitabilityBiallelic inactivationClinical manifestationsGene mutationsNetwork hyperexcitabilitySynaptic transmissionSynaptic activityIntractable epilepsyRepressor gene
2023
ClpP/ClpX deficiency impairs mitochondrial functions and mTORC1 signaling during spermatogenesis
Guo C, Xiao Y, Gu J, Zhao P, Hu Z, Zheng J, Hua R, Hai Z, Su J, Zhang J, Yeung W, Wang T. ClpP/ClpX deficiency impairs mitochondrial functions and mTORC1 signaling during spermatogenesis. Communications Biology 2023, 6: 1012. PMID: 37798322, PMCID: PMC10556007, DOI: 10.1038/s42003-023-05372-2.Peer-Reviewed Original ResearchConceptsMitochondrial unfolded protein responseMitochondrial functionActivate mitochondrial unfolded protein responseMTORC1 signalingMale germ cellsAffecting energy supplyUnfolded protein responseRapamycin treatment in vivoConditional knockoutMatrix peptidasesProteolytic subunitProtein homeostasisDecreased testicular sizeRegulating meiosisSeminiferous tubulesProtein responseGerm cellsSpermatogenesisClpXClpPMTORC1 pathwaySpermatocytesVacuolar structuresMeiosisTesticular size
2021
mTORC1 Signaling Regulates Proinflammatory Macrophage Function and Metabolism.
Collins S, Oh M, Sun I, Chan-Li Y, Zhao L, Powell J, Horton M. mTORC1 Signaling Regulates Proinflammatory Macrophage Function and Metabolism. The Journal Of Immunology 2021, 207: 913-922. PMID: 34290107, DOI: 10.4049/jimmunol.2100230.Peer-Reviewed Original ResearchConceptsKey regulatorImmune cell functionEnhanced histone acetylationCell functionRapid energy sourceClass III histoneDifferentiation of macrophagesHistone acetylationMacrophage functionMTORC1 signalingCellular metabolismOxidative phosphorylationCell metabolismMTOR signalingGlycolytic metabolismAntimicrobial compoundsGenetic deletionM2 macrophagesMouse macrophagesProper wound healingMetabolic programmingSignificant defectsM1 functionImmune cell metabolismSignaling
2013
NO triggers RGS4 degradation to coordinate angiogenesis and cardiomyocyte growth
Jaba IM, Zhuang ZW, Li N, Jiang Y, Martin KA, Sinusas AJ, Papademetris X, Simons M, Sessa WC, Young LH, Tirziu D. NO triggers RGS4 degradation to coordinate angiogenesis and cardiomyocyte growth. Journal Of Clinical Investigation 2013, 123: 1718-1731. PMID: 23454748, PMCID: PMC3613910, DOI: 10.1172/jci65112.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, BiologicalAnimalsCell EnlargementCells, CulturedCoronary VesselsEndothelium, VascularHeart VentriclesMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLMice, TransgenicMultiprotein ComplexesMyocytes, CardiacNeovascularization, PhysiologicNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthasePlacenta Growth FactorPregnancy ProteinsProteinsProteolysisProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyRGS ProteinsSignal TransductionTOR Serine-Threonine KinasesConceptsCardiomyocyte growthAkt/mTORC1 signalingNovel NO-dependent mechanismProteasomal degradationCoordination of angiogenesisMTORC1 signalingConditional overexpressionMurine cardiac tissueG proteinsTransgenic expressionAkt/Physiological mechanismsMyocyte growthVessel growthGrowth factorTransgenic miceHypertrophic responseAngiogenesisKnockout miceMyocardial hypertrophyExpressionGrowthCardiac hypertrophyNOS inhibitor L-NAMEInduction
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