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)

The presence of gonadotropin-releasing hormone (GnRH)-binding sites in human breast carcinomas and breast tumor cell lines as well as the demonstration of the inhibitory effects of GnRH analogues on the growth of these cells raised the possibility that GnRH is produced locally by breast tumor cells themselves. Immunoreactive GnRH was shown to be present in acetic acid extracts of cultured MDA-MB-231 and ZR-75-1 breast carcinoma cells. These extracts were separated by high-performance liquid chromatography and were analyzed by means of region-specific antisera with differing GnRH sequence specificities. A peak of GnRH which coeluted with synthetic mammalian GnRH in 2 different high-performance liquid chromatography systems was similarly detected by antisera directed at the NH2 terminus, at the middle portion and at the N and COOH termini together. The GnRH gene is expressed in these breast tumor lines, as determined by S1 nuclease protection assay, oligonucleotide primer extension studies, and polymerase chain reaction amplification of complementary DNA using oligonucleotides. The primer extension studies indicate that several forms of mRNA are present. The predominant form corresponds to the excision of intron I and the use of a start site about 60 bases upstream of intron I as in the human hypothalamus. Less usage is made of other start sites further upstream. Much larger species of mRNA were also present and correspond to the retention of intron I as in human placenta. The demonstration of GnRH gene expression and the presence of immunoreactive GnRH in mammary carcinoma cells known to have GnRH-binding sites and to be affected by GnRH analogues suggests that GnRH may serve an autocrine regulatory role.
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PMID:Gonadotropin-releasing hormone gene expression in MDA-MB-231 and ZR-75-1 breast carcinoma cell lines. 202 39

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

We demonstrate for the first time, to our knowledge, a unique gene expression assay by surface-enhanced Raman scattering (SERS) using nonfluorescent Raman labels to quantify gene expression at the resolution of alternative splicing using RNA extracted from cancer cells without any amplification steps. Our approach capitalizes on the inherent plasmon-phonon mode of SERS substrates as a self-referencing standard for the detection and quantification of genetic materials. A strategy integrating S1 nuclease digestion with SERS detection was developed to quantify the expression levels of splice junction Delta(9,10), a segment of the breast cancer susceptibility gene 1 (BRCA1) from MCF-7 and MDA-MB-231 cells. Quantification results were cross-validated using two Raman tags and qualitatively confirmed by RT-PCR. Our methodology based on SERS technology provides reliable gene expression data with high sensitivity, bypassing the intricacies involved in fabricating a consistent SERS substrate.
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PMID:Quantitative surface-enhanced Raman for gene expression estimation. 1948 93

We demonstrate a surface-enhanced Raman spectroscopy (SERS) based array platform to monitor gene expression in cancer cells in a multiplex and quantitative format without amplification steps. A strategy comprising DNA/RNA hybridization, S1 nuclease digestion, and alkaline hydrolysis was adopted to obtain DNA targets specific to two splice junction variants, Delta(9,10) and Delta(5), of the breast cancer susceptibility gene 1 from MCF-7 and MDA-MB-231 breast cancer cell lines. These two targets were identified simultaneously, and their absolute quantities were estimated by a SERS strategy utilizing the inherent plasmon-phonon Raman mode of gold nanoparticle probes as a self-referencing standard to correct for the variability in surface enhancement. The results were then validated by reverse-transcription polymerase chain reaction. Our proposed methodology could be expanded to a higher level of multiplexing for quantitative gene expression analysis of any gene without any amplification steps.
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PMID:PCR-free quantification of multiple splice variants in a cancer gene by surface-enhanced Raman spectroscopy. 1978 May 15