2021
Protein Phosphatase 2A as a Therapeutic Target in Small Cell Lung Cancer
Mirzapoiazova T, Xiao G, Mambetsariev B, Nasser MW, Miaou E, Singhal SS, Srivastava S, Mambetsariev I, Nelson MS, Nam A, Behal A, Arvanitis LD, Atri P, Muschen M, Tissot FLH, Miser J, Kovach JS, Sattler M, Batra SK, Kulkarni P, Salgia R. Protein Phosphatase 2A as a Therapeutic Target in Small Cell Lung Cancer. Molecular Cancer Therapeutics 2021, 20: 1820-1835. PMID: 34253596, PMCID: PMC8722383, DOI: 10.1158/1535-7163.mct-21-0013.Peer-Reviewed Original ResearchConceptsProtein phosphatase 2APhosphatase 2ASerine/threonine phosphataseDNA damage responseRegulation of apoptosisSmall molecule inhibitorsGlycolytic ATP productionThreonine phosphataseTwo-dimensional cultureLB100ATP productionMolecule inhibitorsPP2AThree-dimensional spheroid modelEndothelial cell monolayersGlucose uptakeCell viabilitySCLC cellsTherapeutic targetApoptosisCell monolayersMass spectrometrySpheroid modelTumor spheroidsCells
2012
Increased ratio of anti-apoptotic to pro-apoptotic Bcl2 gene-family members in lithium-responders one month after treatment initiation
Lowthert L, Leffert J, Lin A, Umlauf S, Maloney K, Muralidharan A, Lorberg B, Mane S, Zhao H, Sinha R, Bhagwagar Z, Beech R. Increased ratio of anti-apoptotic to pro-apoptotic Bcl2 gene-family members in lithium-responders one month after treatment initiation. Biology Of Mood & Anxiety Disorders 2012, 2: 15. PMID: 22967286, PMCID: PMC3448519, DOI: 10.1186/2045-5380-2-15.Peer-Reviewed Original ResearchBCL2-antagonist/killer 1Insulin receptor substrate 2Pathway analysisBCL2 gene family membersGene family membersRegulation of apoptosisGene expression profilesPro-apoptotic genesAnti-apoptotic genesClinical responseBipolar disorderBlood gene expression profilesLevel of expressionMolecular basisTranscript probesExpression profilesGeneGo MetaCore softwareMetaCore softwarePeripheral blood gene expression profilesCell deathSubstrate 2GenesOpen-label treatmentGold standard medicationDifferential responseGlobal Methylation Patterns in Idiopathic Pulmonary Fibrosis
Rabinovich EI, Kapetanaki MG, Steinfeld I, Gibson KF, Pandit KV, Yu G, Yakhini Z, Kaminski N. Global Methylation Patterns in Idiopathic Pulmonary Fibrosis. PLOS ONE 2012, 7: e33770. PMID: 22506007, PMCID: PMC3323629, DOI: 10.1371/journal.pone.0033770.Peer-Reviewed Original ResearchConceptsCpG islandsMethylation patternsEpigenetic changesMethylation profilesHuman CpG island microarrayNuclear element-1 (LINE-1 or L1) retrotransposonsCellular biosynthetic processesCpG island microarrayGlobal methylation profilesRegulation of apoptosisGlobal methylation patternsLung phenotypeBRB-Array ToolsElement-1 (LINE-1 or L1) retrotransposonsCancer-specific changesBiosynthetic processesGlobal hypomethylationSpecific changesExtensive remodelingFalse discovery rateExtracellular matrix depositionArray resultsGenesHypomethylationLung cancer samples
2007
Pharmacologic Replacement of BIM BH3 Reactivates Apoptosis in Hematologic Cancer and Lymphoproliferative Disease.
LaBelle J, Fisher J, Katz S, Bird G, Lawrence C, Silverstein A, Walensky L. Pharmacologic Replacement of BIM BH3 Reactivates Apoptosis in Hematologic Cancer and Lymphoproliferative Disease. Blood 2007, 110: 524. DOI: 10.1182/blood.v110.11.524.524.Peer-Reviewed Original ResearchAnti-apoptotic proteinsBim-/- miceBcl-2 family protein interactionsBCL-2 domainsBH3-only proteinsRegulation of apoptosisApoptotic signaling pathwaysPro-apoptotic proteinsPromising pharmacologic strategyAnti-apoptotic targetsCellular homeostasisBH3 domainProtein interactionsDeath pathwaysProtein networkCellular survivalSignaling pathwaysApoptotic blockadesCell deathSAHBLymphoma cell linesBH3Apoptosis inductionProteinMitochondrial damage
2006
Macrophages and Pregnancy
Mor G, Romero R, Abrahams V. Macrophages and Pregnancy. Medical Intelligence Unit 2006, 63-72. DOI: 10.1007/0-387-34944-8_6.Peer-Reviewed Original ResearchApoptotic cell clearanceCell clearanceMaternal immune systemAnti-inflammatory cytokinesCases of pregnancyPaternal alloantigensDecidual macrophagesSuccessful pregnancyInflammatory conditionsMaternal deciduaPregnancyMacrophage productionImmune systemTissue macrophagesSurvival factorMacrophagesApoptotic cellsLethal consequencesClearanceAppropriate tissueRegulation of apoptosis
2000
Death Effector Domain Protein PEA-15 Potentiates Ras Activation of Extracellular Signal Receptor-activated Kinase by an Adhesion-independent Mechanism
Ramos J, Hughes P, Renshaw M, Schwartz M, Formstecher E, Chneiweiss H, Ginsberg M. Death Effector Domain Protein PEA-15 Potentiates Ras Activation of Extracellular Signal Receptor-activated Kinase by an Adhesion-independent Mechanism. Molecular Biology Of The Cell 2000, 11: 2863-2872. PMID: 10982386, PMCID: PMC14961, DOI: 10.1091/mbc.11.9.2863.Peer-Reviewed Original ResearchMeSH Keywords3T3 CellsAnimalsApoptosis Regulatory ProteinsCell AdhesionCell LineCHO CellsCricetinaeEnzyme ActivationGuanosine TriphosphateHumansIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase Kinase 1MiceMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesPhosphoproteinsProtein Serine-Threonine Kinasesras ProteinsRecombinant Fusion ProteinsSignal TransductionConceptsPEA-15 expressionPEA-15ERK activationMitogen-activated protein kinase kinaseMitogen-activated protein kinase pathwayAdhesion-independent mechanismsRas-dependent mannerProtein kinase kinaseRegulation of apoptosisProtein kinase pathwayChinese hamster ovary cellsRas guanosineKinase kinaseRas activationSignal receptorHamster ovary cellsH-RasKinase pathwayERK activityIntegrin activationERK signalingAnchorage dependenceOncogenic processesOvary cellsApoptosis
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