Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.6 (RNA polymerase)
 34,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of ornithine decarboxylase in androgen-dependent mouse mammary tumor (Shionogi Carcinoma 115) was reduced to 25% by castration of tumor-bearing mice and restored to the normal level 12 h after administration of testosterone or 5 alpha-dihydrotestosterone. Administration of estradiol-17 beta to the tumor-bearing castrated mice also stimulated the enzyme activity while progesterone and cortisol had little effect. On the other hand, the enzyme activity was affected by neither castration nor androgen injection to CS 2, which is a subline of SC 115 and completely independent of androgen for growth. The inhibition of ornithine decarboxylase activity in SC 115 by injecting alpha-difluoromethylornithine did not affect the enhancement of RNA polymerase I activity by androgen, showing independent elevation of the levels of the two enzymes by androgen.
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PMID:Effect of androgen on ornithine decarboxylase activity in androgen-dependent mouse mammary tumor (Shionogi Carcinoma 115) and its androgen-independent subline (CS 2). 375 19

Molecular clones containing the 3' half of newly integrated mouse mammary tumor virus (MMTV) DNA with adjacent mouse cellular sequences were characterized. In addition, we cloned the long terminal redundancy joint from the unintegrated circular form of MMTV DNA. The entire nucleotide sequence of the integrated and part of the unintegrated terminal redundancy was determined; this allowed us to delineate the boundaries of the MMTV long terminal redundancy, which comprises 1,327 base pairs. The position of possible RNA polymerase II initiation and termination signals corresponded closely to the expected regions of viral RNA initiation and termination specified by current models. The MMTV long terminal redundancy also contained a large open reading frame with sufficient information for a protein of 198 amino acids. Initial comparison of flanking 3' cellular sequences from three independent integrated clones suggested there was no host sequence specificity in the MMTV integration event. However, specificity of integration with respect to viral sequences was precise.
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PMID:Regulatory and coding potential of the mouse mammary tumor virus long terminal redundancy. 626 Sep 76

Adenosine 5'-O-(2-thiotriphosphate) (ATP beta S) and guanosine 5'-O-(2-thiotriphosphate) (GTP beta S) were used to demonstrate initiation of mouse mammary tumor virus (MMTV) RNA in preparations of whole nuclei from control and glucocorticoid-treated MMTV-infected rat hepatoma tissue culture cells. RNA chains initiated in the cell-free reaction retain a thiol group at the 5' end and can be separated from thiol-free RNA chains by chromatography on mercury-Sepharose. The abundance of MMTV sequences was determined by nucleic acid hybridization with filter-bound DNA representing four different regions of the MMTV genome. About six times more MMTV RNA is initiated with GTP beta S than with ATP beta S. Most of the cell-free initiation of MMTV RNA occurs within or very near a 380-nucleotide section of the proviral long terminal repeat that is the presumptive site of transcription initiation in vivo. The sensitivity of MMTV RNA initiation and synthesis to alpha-amanitin and actinomycin D are characteristic of DNA-directed transcription by RNA polymerase II. Nuclei from glucocorticoid-treated cells initiate approximately 10 times more MMTV RNA than nuclei from control cells.
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PMID:Region-specific initiation of mouse mammary tumor virus RNA synthesis by endogenous RNA polymerase II in preparations of cell nuclei. 629 6

Two procedures were devised to examine initial events in the glucocorticoid-regulated transcription of integrated murine mammary tumor virus (MTV) DNA sequences. First, cells in monolayer culture were exposed for brief periods to dexamethasone and then permeabilized in situ with digitonin to allow entry of 32P-labeled ribonucleoside triphosphates and measurement of transcription rates. The results revealed that the rate of MTV RNA synthesis is stimulated selectively by dexamethasone after an apparent lag of approximately equal to 1 min and is half-maximal by 8-9 min. Second, the time course of transcription elongation was monitored by quantitating in single strand nuclease protection assays the accumulation of RNA sequences from different regions of the 7.8-kilobase MTV transcription unit. These experiments suggested that the rate of MTV RNA elongation in the presence of hormone does not differ substantially from elongation rates calculated for other genes transcribed by RNA polymerase II. Moreover, dexamethasone increased in parallel and to the same extent the levels of RNA from various segments of the transcription unit, implying that transcripts are elongated across the MTV element at a constant rate. We conclude that glucocorticoids stimulate MTV transcription solely via a rapid and selective increase in the efficiency of transcription initiation.
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PMID:Early events in the stimulation of mammary tumor virus RNA synthesis by glucocorticoids. Novel assays of transcription rates. 633 56

In mouse Ltk- cells that were transfected with recombinant bacteriophage DNA containing a complete proviral copy of an integrated endogenous mouse mammary tumor virus (MMTV) with its flanking cellular sequences, the newly acquired MMTV proviruses were transcribed in a glucocorticoid-responsive fashion. After hormone treatment of selected cell clones in culture we isolated the nuclei, elongated the nascent RNA chains in vitro, and determined the number of RNA polymerase II molecules on the transcribed MMTV DNA as well as on the flanking mouse DNA sequences. We found that the specific increase in the polymerase loading after hormone treatment is proportional to the increase in the amount of stable MMTV mRNA. When the DNA sequences which are responsible for hormone-receptor binding and for the increased MMTV mRNA levels were deleted, no increase in RNA polymerase II loading on MMTV DNA was observed. Nuclear RNA chains which were transcribed in response to hormone treatment were detected not only from the transfected MMTV DNA but also from the mouse DNA sequences adjacent to the 3' end of the provirus.
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PMID:Dexamethasone increases the number of RNA polymerase II molecules transcribing integrated mouse mammary tumor virus DNA and flanking mouse sequences. 633 May 27

To observe the effect of sex hormones on RNA synthesis of androgen-dependent tumors, mice of DD/S strain bearing androgen-dependent mouse mammary tumor (SC 115) were treated with the hormones, and RNA polymerase activities in isolated nuclei of the tumor were measured. The activity of RNA polymerase I in SC 115 was diminished to approximately 60% of the control level by castration, and it was restored to the precastrated level 12 hr after treatment with 0.2 mg of testosterone. While the activity of RNA polymerase II in the tumor was scarcely influenced by castration, it reached 150% of the castrated level 24 hr after administration of testosterone. In CS 1, a subline of SC 115 with partial loss of androgen dependency on growth, castration and testosterone treatment caused similar but less prominent effects on the activities of RNA polymerase. Administration of estradiol-17 beta to castrated animals also increased the activity of RNA polymerase I, but to a lesser degree than testosterone, in both SC 115 and CS 1. However, only SC 115 demonstrated an increase in RNA polymerase II after estrogen treatment.
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PMID:Effect of sex hormones on RNA synthesis of androgen-dependent mouse mammary tumor (Shionogi carcinoma). 688 72

The role of the basal transcription factor TFIIE was investigated in RNA polymerase II transcription reactions reconstituted with purified proteins. Using negatively supercoiled templates, which circumvent the requirement for TFIIH, we observed that transcription from the adenovirus major-late (ML) core promoter is more dependent on TFIIE than transcription from the adenovirus E4 (E4) or mouse mammary tumor virus (MMTV) promoters. For all three promoters, an increase in the ionic strength of the reaction mixtures led to an increased dependence on TFIIE. Analysis of hybrid ML/MMTV promoters showed that the region encompassing the start site, from -10 to +10, dictates this dependence. Transcription from a relaxed E4 template with a pre-melted -8 to +2 region was completely independent of both TFIIE and TFIIH. We propose that on negatively supercoiled templates TFIIE can facilitate promoter melting.
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PMID:The requirement for the basal transcription factor IIE is determined by the helical stability of promoter DNA. 788 84

The mouse mammary tumor virus long terminal repeat (MMTV-LTR) participates in the control of gene expression by providing a series of important DNA binding sites at which trans-acting factors interact. Among these factors are the steroid receptor, nuclear factor I (NFI) and the TATA box factor (TFIID). The binding of these proteins facilitates the assembly of a transcriptionally competent complex, that includes RNA polymerase II, and activates the expression of juxtaposed genes in cis. A particular DNA sequence, distinct from previously identified regulatory elements, was found in the present study to activate gene expression in trans. The sequence is located between nucleotides +3 and +43 near the 3' terminus of the LTR. This sequence binds a protein that may actively repress the expression of genes that are not located immediately in cis. This protein was purified by ion exchange chromatography and has an approximate molecular weight of 31,000 daltons, as judged by SDS-PAGE. Gel retardation experiments reveal that progressively larger protein--DNA complexes are formed when the amount of this factor is increased relative to the DNA binding site. Furthermore, this protein was found to preferentially aggregate DNA molecules containing the LTR sequence between bases +3 and +43. These results reveal the existence of a unique modulatory role for the LTR in regulating gene expression in trans.
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PMID:Positive regulation of tRNA gene expression by the mouse mammary tumor virus-long terminal repeat in vitro. 838 15

The yeast two-hybrid system was used to isolate a clone from a 17-day-old mouse embryo cDNA library that codes for a novel 812-aa long protein fragment, glucocorticoid receptor-interacting protein 1 (GRIP1), that can interact with the hormone binding domain (HBD) of the glucocorticoid receptor. In the yeast two-hybrid system and in vitro, GRIP1 interacted with the HBDs of the glucocorticoid, estrogen, and androgen receptors in a hormone-regulated manner. When fused to the DNA binding domain of a heterologous protein, the GRIP1 fragment activated a reporter gene containing a suitable enhancer site in yeast cells and in mammalian cells, indicating that GRIP1 contains a transcriptional activation domain. Overexpression of the GRIP1 fragment in mammalian cells interfered with hormone-regulated expression of mouse mammary tumor virus-chloramphenicol acetyltransferase gene and constitutive expression of cytomegalovirus-beta-galactosidase reporter gene, but not constitutive expression from a tRNA gene promoter. This selective squelching activity suggests that GRIM can interact with an essential component of the RNA polymerase II transcription machinery. Finally, while a steroid receptor HBD fused with a GAL4 DNA binding domain did not, by itself, activate transcription of a reporter gene in yeast, coexpression of this fusion protein with GRIP1 strongly activated the reporter gene. Thus, in yeast, GRIP1 can serve as a coactivator, potentiating the transactivation functions in steroid receptor HBDs, possibly by acting as a bridge between HBDs of the receptors and the basal transcription machinery.
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PMID:GRIP1, a novel mouse protein that serves as a transcriptional coactivator in yeast for the hormone binding domains of steroid receptors. 864 9

Pregnancy-dependent mammary tumors (PDMT) of GR/A mice and transplantable PDMT (TPDMT-4 line) in DDD mice, are exceptionally stable in hormone dependence, continue to grow until parturition and regress soon after delivery. In order to study the regression mechanism of PDMT and TPDMT-4, morphological and biochemical changes were examined in the tumors removed on day 18 (TPDMT-4) or day 20 (PDMT) of pregnancy, and on the expected parturient and the following postpartum days. DNA fragmentation occurred from day 18 (TPDMT-4) or day 20 (PDMT) of pregnancy to the day after parturition. Apoptotic cells were demonstrated by an in situ 3'-end labeling method, and the plateau of the number of apoptotic cells was observed on the parturient day in PDMT and on the day after parturition in TPDMT-4. Reverse transcriptase polymerase chain reaction showed that expression of Fas was slightly increased but that of bcl-2 was decreased during the process of involution of TPDMT-4 and PDMT. These results suggest that both an increase in expression of Fas and decrease in expression of bcl-2 are involved in the apoptosis of pregnancy-dependent mammary tumor cells after parturition.
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PMID:Apoptosis of pregnancy-dependent mammary tumor and transplantable pregnancy-dependent mammary tumor in mice. 901 89


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