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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of incubating purified Leydig cells in Eagle's medium and the subsequent effect of the RNA synthesis inhibitors, actinomycin D and cordycepin, on lutropin-stimulated testosterone synthesis have been investigated. The inhibiting effect was found to be inversely related to the time of preincubation; with cells preincubated for 0, 1, 2 and 3 h with Eagle's medium only, followed by 2-h incubation with lutropin with and without actinomycin D, testosterone synthesis was inhibited by 37 +/- 4, 31 +/- 3, 18 +/- 4 and 14 +/- 3% respectively (means +/- s.e.m., n = 5). In cells that had been preincubated for 3 h there was no significant effect of actinomycin D on testosterone synthesis during the first hour of incubation with lutropin. Thereafter the inhibition increased with time reaching a maximum of 30% after 5 h. The effects of preincubation were not due to endogenous lutropin in the Leydig cells because cells isolated from hypophysectomized rats gave similar results. The inhibition of [3H]uridine incorporation into the Leydig cell RNA was 80 +/- 1% with 8 microgram/ml actinomycin D. Increasing the concentration of this inhibitor to 80 microgram/ml did not significantly increase the inhibition of [3H]uridine incorporation or lutropin-stimulated steroidogenesis in preincubated and non-preincubated cells. With cordycepin the inhibition of both RNA synthesis and lutropin-stimulated testosterone synthesis in non-preincubated cells were the same; with 25.1--251 microgram/ml approx. 30--70% resp. With preincubated cells (3 h), 0--50% inhibition of testosterone synthesis was obtained respectively. The inhibitory effect of actinomycin D oimilar to that obtained with lutropin. These observations suggest that during preincubation and independently of lutropin, synthesis of intermediates, including RNAs required for stimulation of steroidogenesis, takes place and that subsequent stimulation of steroidogenesis by lutropin occurs without further de novo RNA synthesis. These results provide evidence for a permissive role of specific RNA and protein synthesis in the action of lutropin on testosterone synthesis in the Leydig cell.
Mol Cell Endocrinol 1979 Jun
PMID:Evidence for the involvement of lutropin-independent RNA synthesis in Leydig cell steroidogenesis. 22 1

Uridine blocks the in vivo conversion of thymine to thymidine in Escherichia coli, thus, one can change DNA labels by labelling first with a thymine label (e.g. 14C) and then, at the time of the change, adding 50 microgram uridine per ml and thymidine (e.g. 3H). The cells immediately start using the thymidine, ignore the thymine for several generations, and are not affected by the uridine.
Mol Gen Genet 1977 Dec 14
PMID:Inhibition of thymidine phosphorylase in vivo provides a rapid method for switching DNA labeling. 34 5

To determine the role of the cI repressor in induction provoked by thymine deprivation, we have analyzed lambda messenger RNA made during and the effect of cI repressor levels on thymineless induction. During thymineless induction, the l- and r-strand transcription of lambda is restricted to the "early" and "delayed early" RNA. This transcriptional pattern is similar to that reported for lambda mutants defective in DNA synthesis. "Late" r-strand transcription requires the addition of thymine. A decrease (to less than 10% of 0 time) in the amount of exogenous label (3H-uridine) incorporated into total RNA by the time of maximum thymineless induction was observed. Since subsequent burst sizes are not diminished by the thymine deprivation and competition experiments show that the amount of lambda message RNA present is at least as great as that in heat induced lambda cI857 lysogens, this decrease must involve either enlarged uridine pool sizes or decreased entry of label. The introduction into the lambda lysogen of a plasmid (pKB252) carrying the lambda cI gene prevents (1) the thymineless induction of lambda (curing the plasmid restores thymineless induction) and, (2) the appearance of both spontaneously induced cells and free phage. Thus, thymineless induction is dependent on the level of cI repressor and spontaneous induction also appears to be the consequence of lowered repressor levels in lambda lysogens.
Mol Gen Genet 1978 Jul 11
PMID:Effect of cI repressor level on thymineless and spontaneous induction; specificity of lambda RNA transcription. 35 50

We have determined the RNA and DNA sequences in the region specifying termination of transcription at the end of the tryptophan (trp) operon of Escherichia coli. A 3'-terminal mRNA fragment of about 150 nucleotides yielded oligonucleotide products that could be assigned to the end of trpA (the last structural gene in the operon) by correlation with the amino acid sequence of the protein product. Analysis of the DNA corresponding to this region served to align the few noncoding RNA oligonucleotide sequences and demonstrated that termination of trp transcription occurs in vivo at a site 36 nucleotides after trpA, with greater than 95% efficiency. In two different strains partially defective in the transcription termination factor rho, the purified transcript is much longer and more complex, suggesting that a significant amount of read-through occurs in these strains. This is consistent with evidence [Guarente, L. P., Mitchell, D. H. & Beckwith, J. (1977) J. Mol. Biol. 112, 423-436] that efficient termination in vivo at the end of the trp operon is a rho-dependent event. The trp terminator (trp t) shares several features with other known sites of transcription termination, including (i) a 3'-terminal RNA sequence of several uridine residues, C-A-U-U-U-U(OH), (ii) a G.C-rich region in the DNA immediately preceding the site of termination, followed by an A.T-rich region, and (iii) a region of dyad symmetry in the DNA which, in the transcript, is capable of forming a stable hairpin containing seven G.C base pairs and one A.U base pair in its stem.
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PMID:Transcription termination: nucleotide sequence at 3' end of tryptophan operon in Escherichia coli. 36 81

3'(2')-O-acyl derivatives of the uridine triphosphate were synthesized. Acyl residues contained fluorescent dye; fluoresceine or rodamine C. Optical properties and stability of UTP analogues were studied. Their ability to serve as the substrates for calf thymus terminal deoxyribonucleotidyl transferase and E. coli RNA polymerase was also examined. It was shown that both enzymes were able to use tested analogues as substrates. Incorporation of the analogues into nascent RNA and DNA chains inhibited the synthetic reaction because of primer inactivation. The rate of the incorporation of the analogues showed an exponential time dependence
Mol Biol (Mosk)
PMID:[Addition of the fluorescent label to the 3'-OH end of DNA and the 3'-OH end of nascent RNA]. 37 5

Alkylation of E. coli tRNAPhe, bound to the cognate synthetase was investigated. The alkylating reagent is a derivative of 2-chloroethylamine: 2',3'-O-[4(N-2-chloroethyl-N-methylamino)-benzylidene]-uridine-5'-methylphosphate. It was found that the enzyme protects from the reaction D-stem (guanosine G24) and the region of juxtaposition of acceptor stem and D-stem (S4U8 and C13) in the tRNAPhe.
Mol Biol (Mosk)
PMID:[Chemical modification of the complex of tRNA Phe with phenylalanyl-tRNA synthetase from Escherichia coli]. 38 93

Utilizing a method which quantitatively extracts high molecular weight RNA, including intact precursor as well as mature ribosomal RNAs, adenylated molecules have been isolated from nuclear- and cytoplasmic-enriched fractions of Physarum microplasmodia labeled with [3H]-uridine. Electrophoretic analysis of denatured adenylated RNA from the nuclear-enriched fraction indicated the presence of a population of large molecules not found in the cytoplasmic-enriched fraction.
Mol Biol Rep 1979 Feb 15
PMID:Polyadenylated RNA in the lower eukaryote Physarum polycephalum. 44 Mar 2

RNA synthesis, correlation of various histones and acetylation and phosphorylation of the chromatin proteins were studied in the rat heart during monthly hypothyroidism. It was shown that [3H]uridine incorporation into heart RNA decreases considerably at hypothyrosis. The alteration in relative amounts of the histone H4 subfractions, which does not depend on the method of hypothyrosis reproduction (inhibition of thyroid function by 1-methyl-2-mercaptoimidazole, thyroidectomy) was detected by the method of analytical electrophoresis in 15% polyacrylamide gels containing 3.125 M urea and 0.9 N acetic acid. Increased incorporation of [32P]phosphate into histone fraction H2b and total fraction of acidic chromatin proteins was observed in vivo. Increased incorporation of labeled acetate into the total histone fraction and reduced incorporation into acidic nuclear proteins were obtained. It was shown that the increased incorporation of acetate into the total histone fraction was due to the increased acetylation of histones H3, H2b, H4 and acid-soluble chromatin proteins characteristic of tissues with a low level of replication. It is assumed that the observed changes of nuclear proteins reflect the process of chromatin reorganization caused by a prolonged deficiency of thyroid hormones.
Mol Biol (Mosk)
PMID:[RNA synthesis and modifications of heart nuclear proteins during thyroid hormone deficiency]. 46 Jan 95

Evaporation of a solution of thymidine plus either the exo or the endo diastereomer of uridine cyclic 2',3'-O, O-phosphorothioate (U greater than p(S) in 1,2-diaminoethane hydrochloride buffer gave the 2',5' and 3',5' isomers of (P-thio) uridylylthymidine (Up(S)dT) in a ratio of 1:2 with a combined yield of about 20%. These isomers were re-converted to U greater than p(S) and dT by a reaction that is known to proceed by an in-line mechanism. Both the 2',5' and 3',5' isomers gave as product the same diasteromer of U greater than p(S) that had been used originally in their formation. These dry-state 'prebiotic' reactions (Verlander, Lohrmann, and Orgel 1973) are thus shown to be stereospecific, and both the 2',5' and 3',5' internucleotide bonds are formed by an in-line mechanism.
J Mol Evol 1979 Nov
PMID:Geometry of the dry-state oligomerization of 2',3'-cyclic phosphates. 51 40

Treatment of normal guinea pig embryo cells with 5-bromodeoxyuridine (BUdR) activates endogenous guinea pig retrovirus. In this report the effect of BUdR treatment upon the level of endogenous retroviral RNA in normal guinea pig embryo cells was determined by using hybridization of viral complementary DNA (cDNA) to cellular RNA. We found that 0.0075% (120 copies per cell) of total RNA of untreated cells was virus-specific, whereas 0.32% (5,120 copies per cell) of total cellular RNA obtained from cells 48 h after BUdR treatment was virus-specific. Thus, BUdR causes an approximately 40-fold amplification of virus-specific RNA after 48 h of treatment. Several lines of evidence favor the hypothesis that the amplification of virus-specific RNA observed after BUdR treatment involves enhancement of transcription rather than an alteration of post-transcriptional processing. At different times after BUdR treatment, similar increases in virus-specific RNA concentration occur in both nucleus and cytoplasm. After 48 h of BUdR treatment, nuclear virus-specific RNA increased 99-fold, from 29 copies per cell to 2,880 copies per cell, whereas cytoplasmic virus-specific RNA increased 47-fold from 85 copies per cell to 4,000 copies per cell. Decay rates of virus-specific RNA in the presence of actinomycin D were similar in the presence or absence of BUdR, indicating that BUdR does not stabilize virus-specific RNA. In BUdR-treated cells the t1/2 of virus-specific RNA was 170 min either in the continued presence of BUdR or after the removal of BUdR, and 150 min in untreated cells. The size distribution of nuclear virus-specific RNA sequences, after denaturation with dimethyl sulfoxide, was similar in untreated and BUdR-treated cells, suggesting similar nuclear processing of viral RNA in both untreated and BUdR-treated cells. The accumulation of nuclear precursors to 38S virus-specific RNA was not observed at steady-state levels in untreated or BUdR-treated cells. Similar species of virus-specific RNA (14S 24S, 38S, and 70S) were present in the total cellular RNA of untreated and BUdR-treated cells. Additionally, virus-specific RNA was present in purified polyribosomes of untreated cells. Finally, direct analysis of the amount of radiolabeled virus-specific RNA in nuclear RNA pulse-labeled for 30 min with [3H]uridine was performed by the method of Coffin et al. (J. Mol. Biol. 86:373-396, 1977) for quantitative determination of pulse-labeled virus-specific RNA. It was found that labeled virus-specific RNA comprised 0.0035 to 0.004% of the total pulse-labeled nuclear RNA of cells treated for 48 h with BUdR. This 50-fold increase in radiolabeled virus-specific RNA may full- account for the 40-fold increase in steady-state levels of virus-specific RNA observed after 48 h of BUdR treatment.
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PMID:Induction of endogenous guinea pig retrovirus by 5-bromodeoxyuridine: amplification of virus-specific RNA. 56 98


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