2005
AP2α alters the transcriptional activity and stability of p53
Stabach P, Thiyagarajan M, Woodfield G, Weigel R. AP2α alters the transcriptional activity and stability of p53. Oncogene 2005, 25: 2148-2159. PMID: 16288208, DOI: 10.1038/sj.onc.1209250.Peer-Reviewed Original ResearchMeSH KeywordsBreast NeoplasmsChromatin ImmunoprecipitationColonic NeoplasmsCyclin-Dependent Kinase Inhibitor p21Gene Expression Regulation, NeoplasticGenes, ReporterHumansImmunoprecipitationLiver NeoplasmsPoint MutationPromoter Regions, GeneticProtein BindingTranscription Factor AP-2Transcription, GeneticTranscriptional ActivationTumor Cells, CulturedTumor Suppressor Protein p53ConceptsTranscriptional activityEndogenous p53 target genesEndogenous p21 geneNormal transcriptional activityP53 target genesP53-mediated inductionAmino acids 305Stability of p53Expression of aP2Transcriptional coactivationP21WAF1/CIP1P21 promoterTarget genesCertain genesRegion of p53AP2αReporter assaysP21 geneFunctional partnershipP53 stabilityP53 activityCell growthPoint mutationsAP2Genes
1996
The lethal hemolytic mutation in beta I sigma 2 spectrin Providence yields a null phenotype in neonatal skeletal muscle.
Weed SA, Stabach PR, Oyer CE, Gallagher PG, Morrow JS. The lethal hemolytic mutation in beta I sigma 2 spectrin Providence yields a null phenotype in neonatal skeletal muscle. Laboratory Investigation 1996, 74: 1117-29. PMID: 8667615.Peer-Reviewed Original ResearchConceptsBeta ISpectrin skeletonSkeletal muscleMost such mutationsGene transferAdult mouse skeletal muscleDominant-negative fashionErythroid lineage cellsNeonatal skeletal muscleCultured muscle cellsAlpha beta heterodimersErythrocyte shape abnormalitiesMuscle cellsMouse skeletal muscleDefective proteinSpectrin geneAlternative transcriptsHemolytic phenotypeCDNA constructsNull phenotypeC2C12 myoblastsBeta heterodimerSpectrin mutationsSedimentation velocity analysisIntracellular distribution