2020
STRIPAK directs PP2A activity toward MAP4K4 to promote oncogenic transformation of human cells
Kim J, Berrios C, Kim M, Schade A, Adelmant G, Yeerna H, Damato E, Iniguez A, Florens L, Washburn M, Stegmaier K, Gray N, Tamayo P, Gjoerup O, Marto J, DeCaprio J, Hahn W. STRIPAK directs PP2A activity toward MAP4K4 to promote oncogenic transformation of human cells. ELife 2020, 9: e53003. PMID: 31913126, PMCID: PMC6984821, DOI: 10.7554/elife.53003.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsCalmodulin-Binding ProteinsCell ProliferationCell Transformation, NeoplasticFemaleGene Knockdown TechniquesHEK293 CellsHeterograftsHumansIntracellular Signaling Peptides and ProteinsMicePhosphoprotein PhosphatasesProtein Serine-Threonine KinasesSignal TransductionTranscription FactorsYAP-Signaling ProteinsConceptsStriatin-interacting phosphatase and kinaseSV40 small t antigenB subunitCell transformationPP2A subunitsHippo pathway effector YAP1Regulatory B subunitPP2A B subunitsPP2A-mediated dephosphorylationSmall t antigenInduce cell transformationPP2A functionPP2A complexPP2A activityOncogenic transformationSubunit interactionsPP2AHuman cancersT antigenMAP4K4SubunitAssociated with STCell alterationsPartial lossCells
2011
Loss of E-cadherin expression and outcome among patients with resectable pancreatic adenocarcinomas
Hong SM, Li A, Olino K, Wolfgang CL, Herman JM, Schulick RD, Iacobuzio-Donahue C, Hruban RH, Goggins M. Loss of E-cadherin expression and outcome among patients with resectable pancreatic adenocarcinomas. Modern Pathology 2011, 24: 1237-1247. PMID: 21552209, PMCID: PMC3155013, DOI: 10.1038/modpathol.2011.74.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaE-cadherin expressionPancreatic adenocarcinomaDuctal adenocarcinomaIndependent predictorsPoor outcomeCox proportional hazards regression modelingProportional hazards regression modelingPancreatic cancer outcomesWorse median survivalResectable pancreatic adenocarcinomaMinority of patientsKaplan-Meier analysisE-cadherin statusMedian survivalSurgical resectionWorse prognosisCancer outcomesSubgroup analysisPathological factorsPatient outcomesCell adhesion moleculeMortality riskTissue microarrayPartial loss
2007
Functional BSND Variants in Essential Hypertension*
Sile S, Gillani NB, Velez DR, Vanoye CG, Yu C, Byrne LM, Gainer JV, Brown NJ, Williams SM, George AL. Functional BSND Variants in Essential Hypertension*. American Journal Of Hypertension 2007, 20: 1176-1182. PMID: 17954364, DOI: 10.1016/j.amjhyper.2007.07.003.Peer-Reviewed Original ResearchConceptsThick ascending limbControl populationNormotensive control populationSodium chloride reabsorptionClC-Kb chloride channelsBlood pressure regulationLogistic regression analysisRenal salt reabsorptionChloride channelsNormotensive populationEssential hypertensionChloride reabsorptionHomogenous cohortStudy populationHypertensionAscending limbGhanaian subjectsSalt reabsorptionHispanic subjectsClC-KbCaucasian populationPartial lossSingle nucleotide polymorphismsRegression analysisRare variants
2001
Genetic and Molecular Characterization of Skb15, a Highly Conserved Inhibitor of the Fission Yeast PAK, Shk1
Kim H, Yang P, Qyang Y, Lai H, Du H, Henkel J, Kumar K, Bao S, Liu M, Marcus S. Genetic and Molecular Characterization of Skb15, a Highly Conserved Inhibitor of the Fission Yeast PAK, Shk1. Molecular Cell 2001, 7: 1095-1101. PMID: 11389855, DOI: 10.1016/s1097-2765(01)00248-9.Peer-Reviewed Original ResearchConceptsFission yeastP21-activated kinaseCytokinetic functionCytokinetic machineryCell polarityProtein functionSkb15Cytoskeletal remodelingMouse homologMicrotubule biogenesisShk1Mating responseNegative regulationActin polymerizationNull mutationCell cycleMolecular characterizationYeastSubstantial uncouplingProper executionPartial lossSchizosaccharomycesBiogenesisHomologKinase
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