2023
TDAG51 promotes transcription factor FoxO1 activity during LPS‐induced inflammatory responses
Park E, Jeon H, Lee N, Yu J, Park H, Satoh T, Akira S, Furuyama T, Lee C, Choi J, Rho J. TDAG51 promotes transcription factor FoxO1 activity during LPS‐induced inflammatory responses. The EMBO Journal 2023, 42: e111867. PMID: 37203866, PMCID: PMC10308371, DOI: 10.15252/embj.2022111867.Peer-Reviewed Original ResearchConceptsBone marrow-derived macrophagesInflammatory mediator productionInflammatory responseMediator productionTranscription factor FOXO1Lethal shockLPS-induced inflammatory responseSerum proinflammatory cytokine levelsToll-like receptor (TLR)-mediated inflammatory responsesFoxO1 activitySystemic inflammatory responseProinflammatory cytokine levelsMarrow-derived macrophagesTLR2/4 signaling pathwayFoxO1 nuclear accumulationT cellsCytokine levelsLipopolysaccharide (LPS)-induced inflammatory responsesTDAG51 deficiencyDouble deficiencyLPS-induced inflammatory mediator productionLPS stimulationInnate immunityCytoplasmic translocationLPS
2019
TDAG51 is a crucial regulator of maternal care and depressive-like behavior after parturition
Yun H, Park E, Choi S, Shin B, Yu J, Yu J, Amarasekara D, Kim S, Lee N, Choi J, Choi Y, Rho J. TDAG51 is a crucial regulator of maternal care and depressive-like behavior after parturition. PLOS Genetics 2019, 15: e1008214. PMID: 31251738, PMCID: PMC6599150, DOI: 10.1371/journal.pgen.1008214.Peer-Reviewed Original ResearchConceptsDepressive-like behaviorPostpartum depressionDevelopment of postpartum depressionImpaired maternal behaviorRegulation of maternal careMonoamine neurotransmitter levelsCombination of physical changesNest-building testInfluence of genetic risk factorsTDAG51 deficiencyMaternity careGenetic risk factorsPup retrievalMental disordersPsychiatric illnessNeurotransmitter levelsMaternal behaviorPostpartumRisk factorsDepressionBuilding testsT-cell death-associated geneDeath-associated genesNursesCare
2013
TDAG51 deficiency promotes oxidative stress-induced apoptosis through the generation of reactive oxygen species in mouse embryonic fibroblasts
Park E, Kim J, Ha T, Choi J, Soo Hong K, Rho J. TDAG51 deficiency promotes oxidative stress-induced apoptosis through the generation of reactive oxygen species in mouse embryonic fibroblasts. Experimental & Molecular Medicine 2013, 45: e35-e35. PMID: 23928855, PMCID: PMC3789259, DOI: 10.1038/emm.2013.67.Peer-Reviewed Original ResearchConceptsMouse embryonic fibroblastsApoptotic cell deathCell deathOxidative stress-induced apoptotic cell deathReactive oxygen speciesPleckstrin homology-like domain familyPromotes oxidative stress-induced apoptosisActivation of caspase-3Stress responseStress-induced cell deathT-cell death-associated genePro-apoptotic functionOxidative stress-induced cell deathOxidative stress-induced apoptosisTDAG51 deficiencyDeath-associated genesStress-induced apoptosisReceptor-mediated cell deathPro-apoptotic genesResponse to oxidative stressCellular stress responseEndoplasmic reticulum stressOxygen speciesProduction of intracellular reactive oxygen speciesIntracellular reactive oxygen species