2024
A mitochondrial checkpoint to NF-κB signaling
Guilbaud E, Galluzzi L. A mitochondrial checkpoint to NF-κB signaling. Cell Death & Disease 2024, 15: 477. PMID: 38961079, PMCID: PMC11222492, DOI: 10.1038/s41419-024-06868-3.Peer-Reviewed Original ResearchConceptsDownstream of mitochondrial permeabilizationUbiquitination of mitochondrial proteinsApoptotic caspasesPermeabilized mitochondriaMitochondrial permeabilizationMitochondrial proteinsMitochondrial dysfunctionAutophagic disposalNF-kB activationInflammatory programCaspaseUbiquitinMitochondriaPermeabilizationInflammatory pathwaysProteinPathwayNovel peptide inhibitor of human tumor necrosis factor-α has antiarthritic activity
Sahu D, Gupta C, Yennamalli R, Sharma S, Roy S, Hasan S, Gupta P, Sharma V, Kashyap S, Kumar S, Dwivedi V, Zhao X, Panda A, Das H, Liu C. Novel peptide inhibitor of human tumor necrosis factor-α has antiarthritic activity. Scientific Reports 2024, 14: 12935. PMID: 38839973, PMCID: PMC11153517, DOI: 10.1038/s41598-024-63790-6.Peer-Reviewed Original ResearchConceptsProtein-protein interactionsGel mobility-shift assaysCollagen-induced arthritisMobility-shift assaysCell surface receptorsFluorescence-activated cell sortingSequence strandsBinding of TNFIn silico methodsCell deathMouse modelSurface receptorsNuclear translocationTrimer formationCell culture assaysRheumatoid arthritisVicious cycle of inflammationModel of collagen-induced arthritisTumor necrosis factor-aCell sortingMouse model of collagen-induced arthritisA549 cellsCycle of inflammationInflammatory bone destructionCulture assayTemporal coordination of the transcription factor response to H2O2 stress
Jose E, March-Steinman W, Wilson B, Shanks L, Parkinson C, Alvarado-Cruz I, Sweasy J, Paek A. Temporal coordination of the transcription factor response to H2O2 stress. Nature Communications 2024, 15: 3440. PMID: 38653977, PMCID: PMC11039679, DOI: 10.1038/s41467-024-47837-w.Peer-Reviewed Original ResearchConceptsGroup of transcription factorsTranscription factorsResponse to H2O2 stressTranscription factor activityCell cycle arrestDose-dependent outcomeRepair oxidative damageOxidative stressDose-dependent activationTime-lapse imagingH2O2 stressCell deathRestoring redox balanceDose-dependentlyTranscriptionRedox balanceGlucose oxidase enzymeNF-kBFactor activityThe crosstalk between macrophages and cancer cells potentiates pancreatic cancer cachexia
Liu M, Ren Y, Zhou Z, Yang J, Shi X, Cai Y, Arreola A, Luo W, Fung K, Xu C, Nipp R, Bronze M, Zheng L, Li Y, Houchen C, Zhang Y, Li M. The crosstalk between macrophages and cancer cells potentiates pancreatic cancer cachexia. Cancer Cell 2024, 42: 885-903.e4. PMID: 38608702, PMCID: PMC11162958, DOI: 10.1016/j.ccell.2024.03.009.Peer-Reviewed Original ResearchConceptsPancreatic cancer cachexiaTumor cellsCancer cachexiaTherapeutic targetLimited treatment optionsPancreatic cancer cellsImmune microenvironmentCCL2/CCR2 axisPotential therapeutic targetTreatment optionsMuscle wastingReprogram macrophagesTumorMuscle atrophyCachexiaCancer cellsMacrophagesNon-autonomous activationMuscle remodelingCancerMuscle degradationSecretionCellsMuscleTWEAKPositive selection CRISPR screens reveal a druggable pocket in an oligosaccharyltransferase required for inflammatory signaling to NF-κB
Lampson B, Ramίrez A, Baro M, He L, Hegde M, Koduri V, Pfaff J, Hanna R, Kowal J, Shirole N, He Y, Doench J, Contessa J, Locher K, Kaelin W. Positive selection CRISPR screens reveal a druggable pocket in an oligosaccharyltransferase required for inflammatory signaling to NF-κB. Cell 2024, 187: 2209-2223.e16. PMID: 38670073, PMCID: PMC11149550, DOI: 10.1016/j.cell.2024.03.022.Peer-Reviewed Original ResearchConceptsWhole-genome CRISPR-Cas9 screenCRISPR-Cas9 screensCryoelectron microscopy studiesCell surface localizationLipopolysaccharide receptor Toll-like receptor 4OST complexToll-like receptor 4CRISPR screensNF-kBCatalytic subunitN-glycosylationActivate NF-kBBase editorsUncompetitive inhibition mechanismNGI-1Molecular mechanismsCatalytic siteLPS-treated cellsOligosaccharyltransferaseDruggable pocketSTT3AReceptor Toll-like receptor 4Drug mechanism of actionStructural studiesInflammatory signalingMutant p53 gains oncogenic functions through a chromosomal instability-induced cytosolic DNA response
Zhao M, Wang T, Gleber-Netto F, Chen Z, McGrail D, Gomez J, Ju W, Gadhikar M, Ma W, Shen L, Wang Q, Tang X, Pathak S, Raso M, Burks J, Lin S, Wang J, Multani A, Pickering C, Chen J, Myers J, Zhou G. Mutant p53 gains oncogenic functions through a chromosomal instability-induced cytosolic DNA response. Nature Communications 2024, 15: 180. PMID: 38167338, PMCID: PMC10761733, DOI: 10.1038/s41467-023-44239-2.Peer-Reviewed Original Research[Methods to Increase the Efficiency of Knock-in of a Construct Encoding the HIV-1 Fusion Inhibitor, MT-C34 Peptide, into the CXCR4 Locus in the CEM/R5 T Cell Line].
Golubev D, Komkov D, Shepelev M, Mazurov D, Kruglova N. [Methods to Increase the Efficiency of Knock-in of a Construct Encoding the HIV-1 Fusion Inhibitor, MT-C34 Peptide, into the CXCR4 Locus in the CEM/R5 T Cell Line]. Молекулярная Биология 2024, 58: 575-589. PMID: 39709562, DOI: 10.31857/s0026898424040044, edn: incwav.Peer-Reviewed Original ResearchConceptsNuclear localization signalNonhomologous end joiningDNA nuclear targeting sequencesKnock-inDNA repairNonhomologous end-joining pathwayNuclear targeting sequenceCXCR4 locusDNA-dependent protein kinase inhibitorBlock DNA repairKnock-in efficiencyEffective gene therapy approachGenome editing technologyTranscription factor NF-kBLocalization signalTreat HIV infectionGene therapy approachesTarget sequenceDonor plasmidCas9 nucleaseCas9 proteinEnd joiningDNA modificationsPrimary human cellsProtein kinase inhibitors
2023
Leptin-Mediated Induction of IL-6 Expression in Hofbauer Cells Contributes to Preeclampsia Pathogenesis
Ozmen A, Nwabuobi C, Tang Z, Guo X, Larsen K, Guller S, Blas J, Moore M, Kayisli U, Lockwood C, Guzeloglu-Kayisli O. Leptin-Mediated Induction of IL-6 Expression in Hofbauer Cells Contributes to Preeclampsia Pathogenesis. International Journal Of Molecular Sciences 2023, 25: 135. PMID: 38203306, PMCID: PMC10778808, DOI: 10.3390/ijms25010135.Peer-Reviewed Original ResearchMeSH KeywordsFemaleHumansInterleukin-6LeptinNF-kappa BPlacentaPre-EclampsiaPregnancySTAT5 Transcription FactorConceptsIL-6 expressionHofbauer cellsP65 NF-κBIL-6NF-κBLeptin levelsPreeclampsia pathogenesisElevated serum interleukin-6 levelsSerum interleukin-6 levelsERK1/2 MAPKInterleukin-6 levelsPro-inflammatory phenotypeAnti-inflammatory phenotypeLeptin receptor expressionIL-6 productionPathogenesis of PEPlacental leptin productionPhosphorylation levelsERK1/2 MAPK inhibitorIL-6 regulationConcentration-dependent mannerPE patientsHuman pregnancySecond trimesterLeptin concentrationsHepatocyte CYR61 polarizes profibrotic macrophages to orchestrate NASH fibrosis
Mooring M, Yeung G, Luukkonen P, Liu S, Akbar M, Zhang G, Balogun O, Yu X, Mo R, Nejak-Bowen K, Poyurovsky M, Booth C, Konnikova L, Shulman G, Yimlamai D. Hepatocyte CYR61 polarizes profibrotic macrophages to orchestrate NASH fibrosis. Science Translational Medicine 2023, 15: eade3157. PMID: 37756381, PMCID: PMC10874639, DOI: 10.1126/scitranslmed.ade3157.Peer-Reviewed Original ResearchConceptsNonalcoholic steatohepatitisLiver inflammationNonalcoholic fatty liver diseaseProgression of NASHCysteine-rich angiogenic inducer 61Fatty liver diseaseLiver-specific knockout miceImproved glucose toleranceType 2 diabetesGlucose toleranceLiver diseaseNASH progressionProfibrotic macrophagesProinflammatory propertiesReduced fibrosisCardiovascular diseaseProfibrotic phenotypeFibrotic developmentKnockout miceNF-κBMetabolic diseasesNASH dietPDGFB expressionFibrosisProfibrotic programNoncanonical HPV carcinogenesis drives radiosensitization of head and neck tumors
Schrank T, Kothari A, Weir W, Stepp W, Rehmani H, Liu X, Wang X, Sewell A, Li X, Tasoulas J, Kim S, Yarbrough G, Xie Y, Flamand Y, Marur S, Hayward M, Wu D, Burtness B, Anderson K, Baldwin A, Yarbrough W, Issaeva N. Noncanonical HPV carcinogenesis drives radiosensitization of head and neck tumors. Proceedings Of The National Academy Of Sciences Of The United States Of America 2023, 120: e2216532120. PMID: 37523561, PMCID: PMC10410762, DOI: 10.1073/pnas.2216532120.Peer-Reviewed Original ResearchConceptsNF-κB-related genesEstrogen receptor alpha expressionDeintensification of therapyTreatment-related morbidityTumor-infiltrating CD4Receptor alpha expressionHPV carcinogenesisRadiosensitization of headOncogenic subtypesPIK3CA alterationsHNSCC tumorsPatient outcomesNeck tumorsT cellsTreatment responseHNSCC cellsTherapeutic intensityAtypical featuresIndependent cohortAlpha expressionNF-κBActive tumorTNF receptorTumorsPatient dataCroquemort elicits activation of the immune deficiency pathway in ticks
O’Neal A, Singh N, Rolandelli A, Laukaitis H, Wang X, Shaw D, Young B, Narasimhan S, Dutta S, Snyder G, Samaddar S, Marnin L, Butler L, Mendes M, Paz F, Valencia L, Sundberg E, Fikrig E, Pal U, Weber D, Pedra J. Croquemort elicits activation of the immune deficiency pathway in ticks. Proceedings Of The National Academy Of Sciences Of The United States Of America 2023, 120: e2208673120. PMID: 37155900, PMCID: PMC10193931, DOI: 10.1073/pnas.2208673120.Peer-Reviewed Original ResearchConceptsImmune deficiency (IMD) pathwayIMD pathwayNon-insect arthropodsPeptidoglycan recognition proteinsJun N-terminal kinaseN-terminal kinaseArthropod immunityMembrane localizationRecognition proteinsLyme disease spirocheteEcdysteroid synthesisMicrobial moietiesDistinct mechanismsProteinArthropodsPathwayHost defenseElicit activationCroquemortPancrustaceaHomologInsectsActivationCrustaceansKinaseLoss of CEACAM1 in endothelial cells causes hepatic fibrosis
Muturi H, Ghadieh H, Abdolahipour R, Stankus H, Belew G, Liu J, Jahromi M, Lee A, Singer B, Angeli-Pahim I, Sehrawat T, Malhi H, Verhulst S, van Grunsven L, Zarrinpar A, Duarte S, Najjar S. Loss of CEACAM1 in endothelial cells causes hepatic fibrosis. Metabolism 2023, 144: 155562. PMID: 37088122, PMCID: PMC10330196, DOI: 10.1016/j.metabol.2023.155562.Peer-Reviewed Original ResearchConceptsFl/Hepatic fibrosisEndothelial lossVisceral obesityImmunohistochemical analysisWild-type HSCsEndothelial cellsHepatic fibrosis stageLiver tissue biopsiesHepatic stellate cellsNF-κB signalingLiver endothelial cellsNF-κB targetsLiver transplantAdult patientsBariatric surgerySystemic inflammationInflammatory infiltrationLiver biopsyNASH pathogenesisInsulin resistanceFibrosis stageInsulin sensitivityHepatic fibrogenesisMale miceFN (Fibronectin)-Integrin α5 Signaling Promotes Thoracic Aortic Aneurysm in a Mouse Model of Marfan Syndrome
Chen M, Cavinato C, Hansen J, Tanaka K, Ren P, Hassab A, Li D, Youshao E, Tellides G, Iyengar R, Humphrey J, Schwartz M. FN (Fibronectin)-Integrin α5 Signaling Promotes Thoracic Aortic Aneurysm in a Mouse Model of Marfan Syndrome. Arteriosclerosis Thrombosis And Vascular Biology 2023, 43: e132-e150. PMID: 36994727, PMCID: PMC10133209, DOI: 10.1161/atvbaha.123.319120.Peer-Reviewed Original ResearchConceptsContractile gene expressionSmooth muscle cellsGene expressionMgR miceWild-type smooth muscle cellsMarfan miceAortic aneurysmMouse modelMarfan syndromeMouse aortic smooth muscle cellsPathogenesis of TAACytoplasmic domainVascular smooth muscle cellsThoracic aortic aneurysmAortic smooth muscle cellsCultured smooth muscle cellsNF-kB activationNF-kB inhibitionMolecular mechanismsIntegrin α2ECM remodelingElastic fiber integrityPhenotypic modulationMarfan's aneurysmsMgR/
2022
A transcriptional cycling model recapitulates chromatin-dependent features of noisy inducible transcription
Bullock ME, Moreno-Martinez N, Miller-Jensen K. A transcriptional cycling model recapitulates chromatin-dependent features of noisy inducible transcription. PLOS Computational Biology 2022, 18: e1010152. PMID: 36084132, PMCID: PMC9491597, DOI: 10.1371/journal.pcbi.1010152.Peer-Reviewed Original ResearchConceptsGene expression noiseExpression noiseTranscriptional burstingPromoter statesDifferent chromatin environmentsChromatin environmentChromatin statePause releaseTranscription factor NFChromatin accessibilityChromatin remodelingTranscriptional noiseChromatin locationsInducible transcriptionSubstantial phenotypic heterogeneityTranscriptional activationTranscription factorsTranscript distributionPolymerase complexTarget genesPolymerase bindingGene expressionPromoter activityViral activationBiological processesActivation of targetable inflammatory immune signaling is seen in myelodysplastic syndromes with SF3B1 mutations
Choudhary GS, Pellagatti A, Agianian B, Smith MA, Bhagat TD, Gordon-Mitchell S, Sahu S, Pandey S, Shah N, Aluri S, Aggarwal R, Aminov S, Schwartz L, Steeples V, Booher RN, Ramachandra M, Samson M, Carbajal M, Pradhan K, Bowman TV, Pillai MM, Will B, Wickrema A, Shastri A, Bradley RK, Martell RE, Steidl UG, Gavathiotis E, Boultwood J, Starczynowski DT, Verma A. Activation of targetable inflammatory immune signaling is seen in myelodysplastic syndromes with SF3B1 mutations. ELife 2022, 11: e78136. PMID: 36040792, PMCID: PMC9427103, DOI: 10.7554/elife.78136.Peer-Reviewed Original ResearchConceptsAcute myeloid leukemiaMyelodysplastic syndromeNF-kB activationLymphoma SocietyMDS/acute myeloid leukemiaNational InstitutePathogenesis of MDSInterleukin-1 receptor-associated kinase 4Expression of IRAK4Inflammatory-immune pathwaysInflammatory cytokine productionSpecific oncogenic pathwaysCareer development grantsHealth research trainingCritical downstream mediatorCytokine productionMyeloid leukemiaPreclinical modelsNew York State DepartmentXenograft modelImmune pathwaysNF-kB.MDS samplesTRAF6 activationLeukemic growthInflammatory stress signaling via NF-kB alters accessible cholesterol to upregulate SREBP2 transcriptional activity in endothelial cells
Fowler JWM, Zhang R, Tao B, Boutagy NE, Sessa WC. Inflammatory stress signaling via NF-kB alters accessible cholesterol to upregulate SREBP2 transcriptional activity in endothelial cells. ELife 2022, 11: e79529. PMID: 35959888, PMCID: PMC9395194, DOI: 10.7554/elife.79529.Peer-Reviewed Original ResearchConceptsAcute inflammatory responseEndothelial cellsCholesterol homeostasisInflammatory stressInflammatory responsePro-inflammatory cytokinesSite of injuryCholesterol biosynthetic gene expressionNF-κB DNA bindingHuman endothelial cellsMultiple sclerosisInflammatory activationPrimary human endothelial cellsVascular endotheliumNF-κB-inducible genesTissue damageInducible targetAberrant activationRole of cholesterolSREBP2 activationMicrobial infectionsCholesterolKey transcription regulatorHomeostasisLeukocytesFenofibrate Downregulates NF-κB Signaling to Inhibit Pro-inflammatory Cytokine Secretion in Human THP-1 Macrophages and During Primary Biliary Cholangitis
Gallucci GM, Alsuwayt B, Auclair AM, Boyer JL, Assis DN, Ghonem NS. Fenofibrate Downregulates NF-κB Signaling to Inhibit Pro-inflammatory Cytokine Secretion in Human THP-1 Macrophages and During Primary Biliary Cholangitis. Inflammation 2022, 45: 2570-2581. PMID: 35838934, PMCID: PMC10853883, DOI: 10.1007/s10753-022-01713-1.Peer-Reviewed Original ResearchConceptsPrimary biliary cholangitisPrimary sclerosing cholangitisAnti-inflammatory mechanismsChronic liver diseaseNF-κB signalingBiliary cholangitisLiver diseaseNF-κB p50IL-1βIL-8Peroxisome proliferator-activated receptor alphaPro-inflammatory cytokine secretionProliferator-activated receptor alphaIncomplete biochemical responseAnti-inflammatory effectsAddition of fenofibratePro-inflammatory cytokinesPPARα-dependent mannerHuman THP-1 macrophagesP65 protein expressionLabel therapeutic optionTHP-1 macrophagesTHP-1 cellsSclerosing cholangitisAdult patientsIncorporating signaling dynamics into fate decision
Guo S. Incorporating signaling dynamics into fate decision. Blood 2022, 140: 79-80. PMID: 35834282, PMCID: PMC9283969, DOI: 10.1182/blood.2022016420.Peer-Reviewed Original ResearchInhibitory Effect of Biotransformed-Fucoidan on the Differentiation of Osteoclasts Induced by Receptor for Activation of Nuclear Factor-κB Ligand
Park B, Yu S, Kim S, Lee J, Choi S, Chang J, Yang E, Kim K, Ahn S. Inhibitory Effect of Biotransformed-Fucoidan on the Differentiation of Osteoclasts Induced by Receptor for Activation of Nuclear Factor-κB Ligand. Journal Of Microbiology And Biotechnology 2022, 32: 1017-1025. PMID: 35879294, PMCID: PMC9628933, DOI: 10.4014/jmb.2203.03001.Peer-Reviewed Original ResearchConceptsNuclear factor-κB ligandBone marrow macrophagesOsteoclast differentiationBone homeostasisBackground of osteoporosisLow molecular weight fucoidanExpression of NFATc1Effect of fucoidanDifferentiation of osteoclastsResistant acid phosphatase activityHarmful side effectsSide effectsPharmaceutical treatmentWeight fucoidanKey transcriptional factorOsteoporosisMarrow macrophagesDifferentiated osteoclastsInhibitory effectOsteoclastsRT-PCRC-fosSafe natural productThe Role of PARP‐1 and NF‐κB in Bile‐Induced DNA Damage and Oncogenic Profile in Hypopharyngeal Cells
Doukas PG, Vageli DP, Judson BL. The Role of PARP‐1 and NF‐κB in Bile‐Induced DNA Damage and Oncogenic Profile in Hypopharyngeal Cells. The Laryngoscope 2022, 133: 1146-1155. PMID: 35791892, DOI: 10.1002/lary.30284.Peer-Reviewed Original ResearchConceptsHypopharyngeal cellsAcidic bileNF-κBNF-κB activationGamma-H2A histone family member XHypopharyngeal squamous cell carcinomaOncogenic profileNuclear factor kappa BPARP-1Squamous cell carcinomaB-cell lymphoma 2 expressionNF-κB transcriptional activityFactor kappa BDNA damageEnzyme-linked immunosorbent assayH2A histone family member XCell survivalDNA/RNA damageHypopharyngeal carcinogenesisReflux contentsAnti-apoptotic phenotypeCell carcinomaWidespread DNA damageBAY 11PARP-1 overexpression
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply