Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.30.1 (S1 nuclease)
 3,660 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies have identified an estrogen receptor (ER) promoter upstream of the transcriptional start site originally mapped for the ER gene. We have examined promoter use in a number of breast carcinoma cell lines. MCF7, T47D, BT474, and MDA-MB-361 cell lines all use the P0 promoter, whereas BT20 and ZR75-1 do not demonstrate transcription from this upstream start site. S1 nuclease analysis was used to quantitate the amount of ER mRNA originating from the two different promoters. In MCF7, one-third of the ER mRNA results from transcription originating upstream of the major ER promoter and in T47D, 12% of the message originates from upstream transcription. Promoter use was analyzed in human mammary epithelial cells and human late proliferation endometrium. Upstream promoter use was found to be characteristic of human late proliferation endometrium but not human mammary epithelial cells. These results indicated that certain breast carcinomas demonstrate ER transcription from a promoter not normally active in normal breast epithelium. This activation may involve a factor active in normal human endometrium.
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PMID:Quantitative analysis of the transcriptional start sites of estrogen receptor in breast carcinoma. 766 25

In endometrial cancers, some overexpression of estrogen receptor (ER) mRNA occurred in comparison with the ER mRNA level in normal endometria. DNA binding domains (DBDs) of ER mRNA were detected in 100% (13/13) of the endometrial cancers, and a mutated ER-DBD mRNA was found in 3 of the 13 by S1 nuclease protection analysis. It is suggested that estrogen might lead to disorder in the promotion of estrogen-inducible proteins in these 3 endometrial cancers, which seem to have a point-mutated DBD of the ER and a functional steroid-binding domain, resulting in the dedifferentiation of the original cells, and that the development and growth of cancer cells might, in part, be driven by estrogen.
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PMID:Expression of aberrant estrogen receptor mRNA in endometrial cancers in comparison with normal endometria. 799 15