title: [AP-2: a nuclear effector of malignant transformation by ras oncogene].
abstract: We have applied a series of cell clones established from the human teratocarcinoma cell line PA-1 to study the effect of malignant transformation by ras-oncogenes on the regulation of cell growth and differentiation. A particular aim of this study was to identify nuclear gene-regulatory factors that are affected by ras-transformation. We show that a key nuclear target of ras is the transcription factor AP-2. AP-2 function is inhibited through the ras-controlled signal transduction cascade by at least two different mechanisms, i.e. inhibition of an AP-2 coregulatory factor and by expression of an alternatively spliced inhibitory AP-2 protein.
authors.affiliation: Institut für Pathologie der Universität Regensburg.
authors.forename: R
authors.initials: R
authors.lastname: Buettner
authors.forename: R
authors.initials: R
authors.lastname: Bauer
authors.forename: A
authors.initials: A
authors.lastname: Imhof
authors.forename: M A
authors.initials: MA
authors.lastname: Tainsky
authors.forename: F
authors.initials: F
authors.lastname: Hofstaedter
mesh_terms: D017398:Alternative Splicing; D002460:Cell Line; D002471:Cell Transformation, Neoplastic; D002999:Clone Cells; D004268:DNA-Binding Proteins / Q000096:biosynthesis / Q000378:metabolism*; D005260:Female; D011905:Genes, ras; D006801:Humans; D010051:Ovarian Neoplasms; D018243:Teratocarcinoma; D050656:Transcription Factor AP-2; D014157:Transcription Factors / Q000096:biosynthesis / Q000378:metabolism*; D014407:Tumor Cells, Cultured
chemical_list: D004268:DNA-Binding Proteins; D050656:Transcription Factor AP-2; D014157:Transcription Factors