Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.23 (beta-galactosidase)
 14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In in vitro tests with lysosomes isolated from the liver and kidneys of castrated rats of both sexes the action of testosterone and beta-estradiol in concentrations of 3.76.10(-4)M on the activity of beta-glucosidase, beta-galactosidase and acid phosphatase was investigated. Testosterone is shown to reduce the total and free activity of the membrane-bound enzymes and to increase the release from the matrix lysosomes. Estradiol proved less active than is testosteron. The renal lysosomes in vitro are more sensitive to the action of sex hormones than are hepatic lysosomes. In the interaction of testosterone and estradiol with lysosomal membranes a sex specificity was revealed.
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PMID:[The effects of testosterone and estradiol on the activity of lysosomal enzymes in rat liver and kidneys]. 9 95

An expression system that utilized yeast copper metallothionein promoter and ubiquitin fusion technology to express the human estrogen receptor gene in yeast is described. We have studied the biochemical and transcriptional regulatory properties of the human estrogen receptor. The biochemical properties of the yeast expressed receptors are identical to the receptors isolated from human tissue. Estradiol mediated activation of transcription by the receptor was studied by a reporter beta-galactosidase gene where expression was under the control of estrogen response elements. Using this expression system and a hyperpermeable yeast strain we have studied the effects of various antiestrogens on the regulation of estrogen receptor function. We demonstrate that tamoxifen and ICI 164,384 are capable of binding to the receptor but neither antiestrogen was able to block the estradiol mediated increase in transcription. In fact, both antiestrogens exerted weak agonist activity in this system.
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PMID:Human estrogen receptor regulation in a yeast model system and studies on receptor agonists and antagonists. 132 95

We examined the in vivo effect of estrogen, progesterone, RU 486, and pregnancy on the upstream regulatory region (URR) of human papillomavirus (HPV) 18 transgenic mice. The mice contain the bacterial reporter beta-galactosidase gene under control of the HPV 18 URR. Pregnant transgenic mice were sacrificed on various days of gestation and the level of URR activation was determined. Another group of female transgenic mice was ovariectomized at 4 to 6 weeks of age. Pellets of estradiol, progesterone, progesterone + RU 486, or placebo were implanted 1 to 2 weeks after ovariectomy. Mice were sacrificed after pellet implantation to examine acute and chronic effects. Marked increases in URR activation during pregnancy were observed. Progesterone was found to activate the URR acutely. Significantly higher activation was demonstrated at 24 hr in the progesterone group compared to placebo (P < 0.01). Activation with progesterone at 24 hr was significantly higher than at any other time point (P < 0.001). A trend toward decreasing activation over time was demonstrated in the progesterone group (r = -0.87, P = 0.0001). RU 486 does not block the activation of progesterone in our model. Estradiol activates the URR acutely compared to placebo (P = 0.034). This in vivo model demonstrates activation of the URR in response to exogenous estrogen, progesterone, and pregnancy. These data may have clinical implications for women who harbor high-risk HPV.
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PMID:Regulation of human papillomavirus type 18 in vivo: effects of estrogen and progesterone in transgenic mice. 926 63

The influence of estradiol on the delivery of plasmid DNA to estrogen receptor positive MCF-7 human breast cancer cells was studied by the use of a reporter assay and by histochemical staining. Continuous exposure to estradiol enhanced the lipofectamine-mediated delivery of both pSV40-luciferase and pCMV beta-galactosidase in a concentration-dependent manner. Estradiol increased both the amount of pCMV beta-galactosidase per cell and the total fraction of cells competent to receive the transgene. The efficiency of transgene delivery to MCF-7 cells was further improved by repeating the transfection procedure in the presence of estradiol. Although overall gene uptake was reduced in control cells when studies were performed at room temperature (as opposed to 37 degrees C), potentiation of gene uptake by estradiol was maintained. At a concentration of 100 microM, estradiol also enhanced delivery of the transgene to estrogen receptor negative MDA-MB-231 breast tumor cells, indicating that the potentiating effects of estradiol are not mediated through the estrogen receptor. These studies are the first to raise the possibility that gene delivery to breast tumor cells can be improved by estradiol in single- or repeated-treatment regimens.
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PMID:Estradiol enhances gene delivery to human breast tumor cells. 976 41

Serum apolipoprotein AI (apoAI) levels correlate with the risk of developing atherosclerosis. Previous studies have suggested that dehydroepiandrosterone (DHEA) lowers high-density lipoprotein (HDL)-cholesterol levels. We investigated whether or not DHEA may lower HDL-cholesterol levels by suppressing apoAI gene transcription in hepatocytes. ApoAI mRNA levels, assessed by Northern blotting, were suppressed in HepG2 cells treated with DHEA (34%) (10 microg/mL) or testosterone (36%) (T, 1 microg/mL). Estradiol alone (E2, 1 microg/mL) had relatively little effect on apoAI mRNA levels, while E2 in combination with DHEA prevented a decrease in apoAI mRNA levels compared to DHEA alone. To determine whether these effects were due to changes in apoAI gene transcription, HepG2 cells were transfected with a plasmid carrying the full-length promoter of the rat apoAI gene ligated into a chloramphenicol acetyltransferase (CAT) reporter construct. The plasmid pCMV.SPORT-beta-gal was included in each transfection to normalize the data to transfection efficiency. Cells were then cultured in the presence or absence of DHEA (10 microg/mL), T (1 microg/mL), 17alpha-methyltestosterone (MTT, 1 microg/mL), 5alpha-dihydrotestosterone (DHT, 1 microg/mL), E2 (1 microg/mL), or a combination of DHEA plus E2, T plus E2, MTT plus E2, and DHT plus E2, for 24 hours. CAT activity, relative to beta-galactosidase activity, was reduced by 19.6%, 57.6%, 38.6%, and 54.6% with DHEA, T, DHT, and MTT addition, respectively. E2 increased CAT activity by 43.8%. When the androgens (ie, DHEA, T, DHT, or MTT) were combined with E2, apoAI promoter activity was suppressed. We conclude, therefore, that androgens downregulate apoAI promoter activity in the presence or absence of E2. However, the changes in mRNA levels do not always reflect changes in promoter activity, suggesting that these steroids may have additional post-transcriptional effects on steady-state apoAI mRNA levels. It remains to be established if the transcriptional effects we observed are mediated through an androgen response element.
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PMID:Effects of dehydroepiandrosterone on rat apolipoprotein AI gene expression in the human hepatoma cell line, HepG2. 1188 77

The functional impairment associated with atherogenic factors, including hypertension, constitutes a limitation to the ability of endothelial progenitor cells (EPCs) to repair. In addition, estrogens have been shown to play a role in reendothelialization after vascular injury. We investigated the effects of estrogens on differentiation and senescence of EPCs derived from bone marrow (BM-EPCs) in spontaneously hypertensive rats (SHR/Izm). Bone marrow (BM) cells were obtained from the tibias and femurs of age-matched, male SHR/Izm and Wistar-Kyoto rats (WKY/Izm). The number of differentiated, adherent BM-EPCs derived from SHR/Izm was significantly smaller than the number derived from WKY/Izm. 17beta-Estradiol (E2) significantly increased the number of adherent BM-EPCs from SHR/Izm, and this effect was significantly attenuated by pharmacological phosphatidylinositol 3-kinase (PI3-K) blockers. Immunoblotting analysis revealed that E2 treatment led to phosphorylation of Akt. Senescence, as assessed by acidic beta-galactosidase staining, occurred at a significantly greater rate in the BM-EPCs from SHR/Izm than in those from WKY/Izm, but E2 treatment dramatically delayed the senescence of BM-EPCs from SHR/Izm. A polymerase chain reaction (PCR)-ELISA based assay revealed that telomerase activity in BM-EPCs from SHR/Izm was significantly lower than in those from WKY/Izm, but that E2 treatment significantly augmented it. Both MTS and colony forming unit assay revealed that E2 treatment significantly augmented the functional activity in BM-endothelial cell (EC)-like cells from SHR/Izm compared to that in control BM-EC-like cells (no treatment). In conclusion, the differentiation of BM-EPCs derived from SHR/Izm was significantly decreased compared with that of BM-EPCs from WKY/Izm. In addition, the rate of senescence was significantly greater in the BM-EPCs from SHR/Izm than in those from WKY/Izm. Estrogen was shown to augment differentiation and delay the onset of senescence in BM-EPCs from SHR/Izm.
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PMID:Effect of estrogen on differentiation and senescence in endothelial progenitor cells derived from bone marrow in spontaneously hypertensive rats. 1641 50

A yeast (Saccharomyces cerevisiae)-based assay was developed and tested with steroids and chemicals (mostly pesticides). The induction of beta-galactosidase activity was strictly dependent on the presence of seabream (Sparus aurata) betaa estrogen receptor (sbERbetaa) and substances known to have estrogenic activity. 17beta-Estradiol (E(2)) and diethylstilbestrol (DES), both agonists, were most active and the antagonist tamoxifen (TAM) was 14-fold less active than E(2). Among the chemicals tested bisphenol-A was most active, followed by pentachlorophenol and naphthalene. Ligand-binding assays with recombinant sbERbetaa and sbERalpha revealed that sbERbetaa binds E(2) with 6.5-fold higher affinity than sbERalpha, confirming the selection of a high sensitive receptor for the yeast assay. DES, ICI 182,780, estrone and TAM had higher relative binding affinity to E2 in sbERalpha than sbERbetaa, although there was no difference in IC50 for these steroids between the two receptors. These results reveal the usefulness of using the yeast-based receptor assay for detecting chemical interaction with steroid receptors from contaminated samples.
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PMID:A yeast assay based on the gilthead sea bream (teleost fish) estrogen receptor beta for monitoring estrogen mimics. 1930 42