作者: D.P. Hollywood , H.C. Hurst
DOI: 10.1002/J.1460-2075.1993.TB05891.X
关键词: Biology 、 Transcription (biology) 、 Messenger RNA 、 DNA-binding protein 、 Cell culture 、 Cancer research 、 Transcription factor 、 Gene 、 Gene expression 、 Receptor tyrosine kinase 、 Molecular biology
摘要: The c-erbB-2 receptor tyrosine kinase proto-oncogene product is overexpressed in 20-30% of breast carcinomas and this has been shown to correlate with poor prognosis. Previous analysis tumour-derived lines demonstrated that although the gene often amplified, overexpression can occur from a single-copy gene. Moreover, whether or not overexpressing cells produce 6- 8-fold more mRNA per copy than low-expressing cells. In paper, we examine possible mechanisms causing deregulation accumulation. Nuclear run-on studies indicated extra accumulation was due increased transcription Promoter analyses using 5' flanking sequences linked CAT showed promoter active Coupling deletion functional footprinting experiments, nuclear extracts derived both low cells, allowed identification DNA-binding protein, OB2-1, which considerably abundant range lines. We discuss role OB2-1 tumour