[AP-2: a nuclear effector of malignant transformation by ras oncogene].
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.
Buettner
R
R
Institut für Pathologie der Universität Regensburg.
Bauer
R
R
Imhof
A
A
Tainsky
M A
MA
Hofstaedter
F
F
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
D004268:DNA-Binding Proteins; D050656:Transcription Factor AP-2; D014157:Transcription Factors