Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.27.1 (RNase)
16,360 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogen administration to male Xenopus causes the cytoplasmic destabilization of the hepatic serum protein coding mRNAs, most notably, albumin, yet has little effect on mRNAs encoding intracellular proteins such as ferritin. This report describes an estrogen-inducible ribonuclease activity found in liver polysomes that degrades albumin mRNA 4 times faster in vitro than it degrades ferritin mRNA. This differential rate of degradation was observed upon incubation of polysome extract with free liver RNA, isolated liver mRNPs, or transcripts from plasmid vectors. A cleavage fragment consisting of a doublet of approximately 194 nucleotides in length was consistently observed upon digestion of transcripts for the full length or 5' half of albumin mRNA. The generation of this cleavage fragment was used as an assay to study properties of the polysome nuclease activity. The 194 doublet is produced by the action of a Mg(2+)-independent endonuclease. This distinguishes the Xenopus liver enzyme from the enzymes that degrade histone or c-myc mRNA in vitro. It is inactivated by 400 mM NaCl or heating at 90 degrees C, but not by placental ribonuclease inhibitor or N-ethylmaleimide. Finally, the polysomal nuclease activity does not degrade double-stranded RNA. We believe the estrogen-induced nuclease activity contains an enzyme(s) that may mediate hormone-regulated changes in mRNA stability in this tissue.
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PMID:Estrogen-induced ribonuclease activity in Xenopus liver. 193 72

Estrogen receptors (ER) from rat and rabbit uterine cytosol were examined for their sensitivity to ribonuclease (RNase). After RNase treatment, a major part of rabbit uterine ER was converted from the 7S to 3-4S form, and its binding to DNA-cellulose was increased by 40%. Similar treatment on rat uterine ER showed a shift from 7S to 4.5S, and the DNA-cellulose binding was stimulated by 20%. Measurement of endogenous RNase levels showed that lower RNase concentration in rabbit uterine cytosol coincided with larger stimulation of DNA-cellulose binding by exogenous RNase. These results indicate that a major part of 7S ER is susceptible to RNase, and cleavage of bound RNA seems to uncover additional binding sites for DNA. In contrast to the general thinking that 4S to 5S transformation is essential for nuclear binding, we have observed that RNase-treated rat uterine ER did not undergo such a transformation by warming at 25 degrees C, while DNA-cellulose binding of the receptors increased. Thus, temperature activation could occur independent of 4S to 5S transformation.
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PMID:Effect of ribonuclease on the physico-chemical properties of estrogen receptor. 241 Jun 67

The role of estradiol in the regulation of its cognate receptor in MCF-7 cells was investigated in this study. After treatment with 10(-9) M estradiol, the level of receptor protein was measured using an enzymeimmunoassay. By 6 h, the receptor protein declined by about 60% from a level of approximately 3.6 to 1.2 fmol/micrograms DNA. The level of receptor remained suppressed for 24-48 h. Similar results were obtained with an estrogen receptor (ER) binding assay. The steady state level of ER mRNA was determined by an RNase protection assay. Estrogen treatment resulted in a maximum suppression of mRNA by 6 h. Receptor mRNA remained depressed for 48 h. Transcription run on experiments demonstrated a transient decrease of about 90% in ER transcription after 1 h. By 3-6 h transcription increased approximately 2-fold and remained elevated for at least 48 h. These data suggest that estrogen down-regulates ER mRNA by inhibition of ER gene transcription at early times and by a posttranscriptional effect on receptor mRNA at later times.
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PMID:Regulation of the estrogen receptor in MCF-7 cells by estradiol. 321 58

Growth of hormone-dependent rat mammary tumors was arrested in vivo by N(6),O(2)'-dibutyryl cyclic adenosine 3',5'-monophosphate. Estrogen concentration did not change, but acid ribonuclease activity and synthesis increased during treatment with the dibutyryl cyclic nucleotide, as was shown during tumor regression due to hormonal deprivation. Growth arrest, thus, appears to derive from enhanced tissue catabolism.
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PMID:In vivo inhibition of growth of two hormone-dependent mammary tumors by dibutyryl cyclic AMP. 435 87

Estrogen has been shown to affect ventromedial hypothalamic (VMH) nerve cell nucleoli in ovariectomized rats, by causing an increase in the number of electron-dense aggregates associated with nucleoli. In order to characterize these nucleolus-associated structures and other nuclear components, we examined the ultrastructure of ventromedial hypothalamic nucleoli and nuclei revealed by enzyme digestions (pepsin, RNase and DNase) in resinless thin sections. Digestion by pepsin did not cause obvious alterations in the morphology of the nucleolus or its related structures. Pepsin treatment followed by RNase, however, reduced the density of the nucleolus, while that of the nucleolus-associated structure and other related structures remained unchanged. Conversely pepsin treatment followed by DNase, reduced the density of nucleolus-associated and other chromatin structures, but had no effect on the density of the nucleolus. Pepsin treatment followed by RNase and then DNase treatment, reduced the density of the nucleolus and nucleolus-associated structures. A residual nucleolus and nucleolus-associated structure remained after this treatment. Stereo viewing of resinless sections shows that the nucleolus, its associated structures, and other related structures, are associated with fine filaments that may comprise the nuclear matrix. The nucleolus-associated structure containing DNA may direct RNA synthesis at an increased rate in estrogen-treated hypothalamic cells.
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PMID:Ultrastructure and enzyme digestion of nucleoli and associated structures in hypothalamic nerve cells viewed in resinless sections. 623 97

Estrogen administration to rats diminishes all apoproteins and lipoproteins from plasma. In contrast, some inbred strains of mice raise their plasma apoB and LDL levels by more than 2-fold (Srivastava et al, 1993, Eur. J. Biochem. 216, 527-538). Further studies with 13 inbred strains of mice given 3 micrograms beta-estradiol/g body weight/day for 5 consecutive days suggest that some mouse strains increased their apoB and LDL levels and some did not. To examine the mechanism of influence of genetic factors on apoB regulation, two strains, C57L and C57BL, that increased their VLDL- and LDL-cholesterol, and 2 strains, BALB and C3H, that did not, were chosen. Estrogen increased plasma apoB levels selectively in the strains C57L and C57BL, termed as 'responders,' but did not change in BALB and C3H, termed as 'non-responders.' One of the mechanisms for increased plasma apoB levels could be through increased production of apoB-containing particles. This possibility was investigated. ApoB and REPR mRNA were quantified by RNase protection assay, and apoB-100 mRNA by apoB mRNA editing assay. Hepatic apoB mRNA increased by 30% in 'non-responders,' but decreased by 20% in the 'responders.' However, apoB-100 mRNA increased relative to apoB-48 mRNA in all the 4 strains by 50%. The mRNA for RNA editing protein (REPR) decreased in all strains, suggesting that apoB-100 mRNA increased as a result of decreased apoB mRNA editing activity. These results suggest that:(a) modulation of apoB mRNA by estrogen was strain-specific;(b) increased apoB100 mRNA in inbred strains of mice were caused by decreased apoB mRNA editing activity; and (c) the differences in the plasma apoB levels among 'responder' and 'nonresponder' strains of mice occur through mechanisms other than the apoB mRNA editing.
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PMID:Increased apoB100 mRNA in inbred strains of mice by estrogen is caused by decreased RNA editing protein mRNA. 762 51

Insulin-like growth factors (IGFs) I and II are two single-chain polypeptide hormones that are structurally related to each other and to proinsulin. Among the large number of growth factors involved in ovarian physiology, IGF-I and IGF-II are considered to be important progression factors for ovarian follicular development. To explore the ovarian expression of IGF-I, IGF-II and their receptor genes, a solution hybridization/RNase protection assay, was used. IGF-I mRNA was seen in the granulosa cells, and IGF-II mRNA in the theca-interstitial compartment. To study the hormonal regulation of the IGF-I and IGF-II gene, immature (21-day-old) hypohysectomized rats were treated with FSH (10 micrograms/day), GH (150 micrograms/day) and diethylstilbestrol (DES subcutaneous implant/5 days). Estrogen differentially regulated ovarian IGF-I and IGF-II gene expression. In concert with GH, estrogen up-regulated ovarian IGF-I mRNA, but significantly decreased hepatic IGF-I gene expression. Both IGF receptors (type I and type II) as well as the insulin receptor gene, were expressed in both ovarian cells. The expression of the type I IGF receptor gene (but not the type II IGF gene) was up-regulated by FSH and estrogen in vivo. In conclusion, these studies may serve to better understand the auto paracrine role of IGF, and their receptors in the pathophysiology of follicle recruitment, oocyte maturation and potentially embryo development.
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PMID:Regulation of the genes for insulin-like growth factor (IGF) I and II and their receptors by steroids and gonadotropins in the ovary. 762 58

Estrogen-mediated accumulation of the avian apolipoprotein (apo) II mRNA is in part due to its stabilization. To identify the biochemical activity responsible for this effect, radiolabeled, capped, and polyadenylated apoII mRNA was incubated in vitro in liver cytosolic extracts from roosters who received either estrogen (estrogen-treated extract) or the vehicle (control extract) parenterally. The mRNA was very stable in estrogen-treated extract but was rapidly degraded in control extract. The RNA was degraded predominantly by endonuclease rather than exonuclease activity. The addition of the estrogen-treated extract to the control extract prevented the degradation of the mRNA in trans. This biochemical activity was heat labile and was also destroyed by proteinase K but not by micrococcal nuclease, indicating that estrogen treatment resulted in the expression of a protein in the liver that stabilized the apoII mRNA by inhibiting its nucleolytic degradation. This mRNA stabilization factor was labile around 60 degrees C, whereas the RNase remained stable up to 80 degrees C. Studies on mRNA protein interaction showed that both control and estrogen-treated extracts contain mRNA-binding (mRNP) proteins that bind apoII mRNA. An increased binding to apoII mRNA by a subset of these proteins was observed with estrogen-treated extract as compared with the control extract. This activity, although it afforded complete protection from nucleolytic degradation to apoII and apo A1 mRNAs, appeared to provide less protection to mRNAs encoding chicken serum albumin and vitellogenin, suggesting differential stabilization of mRNAs. These studies indicate that a cytosolic mRNA-stabilization factor, providing apoII mRNA complete protection from nucleolytic degradation, is expressed in the avian liver upon estrogen treatment. This appears to be the first time that a biochemical activity responsible for hormone-mediated stabilization of mRNAs and estrogen induction of mRNA binding by specific mRNPs have been identified and partially characterized in vitro.
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PMID:In vitro characterization of an estrogen-regulated mRNA stabilizing activity in the avian liver. 877 38

Expression of steroidogenic factor 1 (SF-1/Ad4BP) is essential for gonadal differentiation. We have assessed whether expression of SF-1 in the gonads of rat fetuses was altered following maternal treatment with diethylstilbestrol (DES, a synthetic oestrogen) or 4-octylphenol (OP, a xenoestrogen). Pregnant rats were injected subcutaneously with DES (500 microg/kg), OP (600 mg/kg) or vehicle (oil, control) on days 11.5 and 15.5 post coitum (p.c.) and fetal rat testes were recovered on day 17.5 p.c. The level of expression of SF-1 was determined by RNase protection assay and immunocytochemistry. In both DES- and OP-exposed fetuses immunoexpression of SF-1 was reduced in Sertoli and interstitial cells when compared with controls. In parallel, a significant decrease occurred in the total amount of SF-1 mRNA (P < 0.05) in fetal testes but not in fetal ovaries. These results suggest that: (a) Sertoli cell-derived oestradiol may be important in the physiological regulation of SF-1 in the fetal testis; and (b) one mechanism by which inappropriate exposure to oestrogens might alter the genetic cascade that ensures normal development of the testis is via altered expression of SF-1.
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PMID:Maternal oestrogen/xenoestrogen exposure alters expression of steroidogenic factor-1 (SF-1/Ad4BP) in the fetal rat testis. 909 4

Estrogen protects against developing premature coronary artery disease. However, the mechanism of protective effects of estrogen still remains poorly understood. One mechanism by which estrogen can have protective effects appears to be through modulation of plasma lipoproteins. We showed that the mouse can be used as animal model to study estrogen-mediated synthesis and secretion of lipoproteins since, unlike the rat, the mouse does not up-regulate LDL receptors (Srivastava et al. [4]). Since inbred strains of mice differ in their genetic background and show differing responsiveness to dietary lipids, we examined how various inbred strains of mice respond to estradiol administration, and whether some mouse strains show responses similar to rats. 17beta-estradiol was administered to male mice from 15 different inbred strains, and the changes in plasma levels of lipids, apoB, apoAI, and apoE were examined. Total cholesterol decreased in all but one strain, apoAI levels decreased in all but 3 strains while apoB levels and apoB/apoAI ratios increased in all but 2 strains, suggesting that in contrast to rats, the apoB-containing lipoproteins increased relative to HDL in all strains of mice examined. Basal and estradiol-induced changes in total cholesterol were significantly correlated with changes in apoAI, but not apoB, reflecting the predominance of HDL over other lipoproteins in mouse plasma. The effects of estrogen on plasma apoE levels varied among various inbred strains of mice tested. Plasma apoE levels increased in seven strains treated with estrogen, and remained unchanged in the rest. To examine whether changes of plasma apoproteins are associated with the changes in the respective hepatic mRNA levels, apoAI, B and E mRNA were quantified by RNase protection assay. Hepatic apoE mRNA did not show correlation with either basal or post treatment plasma apoE levels in any of the strains. Similarly, most of the mouse strains did not show correlation of plasma apoAI and apoB levels with the corresponding hepatic mRNA levels. These results suggest that estrogen regulates plasma lipoprotein concentrations primarily by posttranscriptional mechanisms, and there were strain-related differences in the estrogen-mediated regulation of lipoprotein metabolism.
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PMID:Regulation of lipoprotein metabolism by estrogen in inbred strains of mice occurs primarily by posttranscriptional mechanisms. 927 67


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