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

Five cDNA clones for TAXREB proteins that bind to the tax-responsive enhancer element of human T-cell leukemia virus type I (HTLV-I) were isolated from a Jurkat cell cDNA library. The beta-galactosidase fusion proteins of three of these clones specifically recognized the domain C within the enhancer. One of the three cDNAs, encoding TAXREB107, contained an open reading frame with 288 amino acid residues. RNA blot analysis showed that the level of mRNA for TAXREB107 increased transiently in Jurkat cells on treatment with TPA. Immunoblot analysis showed that polyclonal antibody against TAXREB107 specifically recognized a 34-kD protein in Jurkat cells. TAXREB107 may participate in tax-mediated trans-activation of transcription.
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PMID:Isolation of a cDNA clone encoding DNA-binding protein (TAXREB107) that binds specifically to domain C of the tax-responsive enhancer element in the long terminal repeat of human T-cell leukemia virus type I. 845 78

1,25-Dihydroxyvitamin D3 (calcitriol) at 100 nmol/l elicited morphological differentiation and expression of collagen IV in mouse F9 embryonal carcinoma cells, and its effect was enhanced and accelerated by dibutyryl-cAMP (db-cAMP). The RAR beta 2 promoter was also activated, as evidenced by an increase in beta-galactosidase activity in an F9 reporter cell line with a stably integrated RAR beta 2-lacZ construct. All three effects were slower and less extensive with calcitriol than with retinoic acid, even in the presence of db-cAMP. Activation of the RAR beta 2 promoter by calcitriol required its TRE sequence, whereas db-cAMP required the CRE. TPA also activated the RAR beta 2 promoter, requiring a functional TRE. Thus, in the RAR beta 2 promoter the TRE sequence, whose function has so far been unidentified, mediates the effects of calcitriol and TPA. RAR beta 2 promoter activation by calcitriol was blocked by inhibitors of protein kinase C indicating that calcitriol elicits its effect via protein kinase C. Therefore, calcitriol induces differentiation of F9 mouse embryonal carcinoma cells at least in part by a pathway different from the classical one operative with retinoic acids.
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PMID:Induction of mouse embryonal carcinoma cell differentiation and activation of the retinoic acid receptor beta 2 promoter by 1,25-dihydroxyvitamin D3. 896 Mar 71

Cytochemically detectable activity of endogenous beta-galactosidase was found at pH 6.0 in Swiss 3T3 cells after long-term incubation in low serum or in the presence of heparin concentrations known to reversibly inhibit cell proliferation. A high percentage of beta-galactosidase-positive cells were detected in U937 and HL60 cultures at the late stage of macrophage-like differentiation induced by TPA. Interestingly, a small number of beta-galactosidase-positive cells were found even in the growing Swiss 3T3 cultures. These positive cells expressed morphological features similar to those of senescent cells. Thus, the activity of beta-galactosidase at pH 6.0 cannot be considered an exclusive marker of senescent cells since it is expressed in other types of nonproliferating cells.
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PMID:Endogenous beta-galactosidase activity in continuously nonproliferating cells. 971 64

Oestrogens regulate the expression of genes both positively and negatively in a range of cell types. These effects are mediated via the oestrogen receptor (ER) and involve direct interactions between the ER and DNA response elements, as well as interactions between the ER and other nuclear proteins. We have examined the potential of the ERalpha to regulate the expression of reporter genes under the control of oestrogen response elements (EREs), NFkappaB response elements (NREs) or AP-1/TPA response elements (TREs) in HeLa cells and in human embryonic kidney (HEK-293) cells. Transiently transfected ERalpha was able to activate expression of beta-galactosidase under the control of EREs in an oestradiol (E2)-dependent manner in both HeLa and HEK-293 cells. The ERalpha was able to repress by 80% the TNF-mediated expression of beta-galactosidase under the control of NREs in an E2-dependent manner in HeLa cells but not in HEK-293 cells. ERalpha/E2 also induced a two-fold potentiation of TPA-mediated expression of beta-galactosidase under the control of TREs in HeLa cells but not in HEK-293 cells. These results suggest that the ERalpha is capable of regulating gene expression in a cell-specific manner. We further investigated the mechanisms by which the ERalpha regulates gene expression in these systems by co-expressing the ERalpha and the reporter gene constructs with known cofactors of the ERalpha. We have shown that expression of steroid receptor coactivator-1 alpha (SRC-1alpha) and receptor interacting protein-140 (RIP-140) have no effect on the capacity of the ERalpha to modulate NFkappaB reporter gene activity in HeLa cells. Furthermore, the expression of SRC-1alpha or RIP-140 does not enable the ERalpha to repress NFkappaB or to potentiate an AP-1 response in HEK-293 cells. This suggests that factors other than SRC-1alpha or RIP-140 are responsible for the cell-specific effects seen with ERalpha.
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PMID:The oestrogen receptor regulates NFkappaB and AP-1 activity in a cell-specific manner. 987 7

Analysis of the expression of a number of known genes in cultured human cells has revealed UVB-induced changes that may be specific for melanocytic cells. The response of c-fos, p53 and HIV-LTR reporter constructs to UVB and UVC was reduced in MM96L melanoma cells compared to HeLa. Cell cycle arrest produced by UVA, gamma radiation, cisplatin or the antimetabolite deoxyinosine differed from that of UVB. Cell cycle analysis after multiple doses of UVB raised the possibility that UVB-induced pRb depletion could result in increased mutation and thus enhanced tumourigenesis of irradiated melanocytes in skin subjected to a defined pattern of UVB exposure. To extend the analysis of gene expression in cultured melanocytic cells to uncharacterised genes, promoter trap cell clones containing unknown genes 'tagged' by a beta-galactosidase reporter construct were generated from MM96L cells. Altered gene expression in clones treated with a panel of DNA-damaging agents was quantitated by measurement of beta-galactosidase activity. Of the clones containing 'tagged' endogenous promoters induced by UVB, 52% were induced only by UVB and not by other DNA-damaging agents (cisplatin, N-methyl-N-nitro-nitrsoguanidine, fotemustine). One third of the clones were also activated by TPA suggesting that general DNA damage responses involving PKC are activated less frequently than unique pathways of gene activation. Overall, 60% of the 50 clones that responded to the panel of agents were induced by only one of the agents, indicating that a high proportion of genes are induced by agent-specific mechanisms. In the long term, promoter trapping may allow the full repertoire of UVB-inducible genes to be characterised.
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PMID:UVB-specific regulation of gene expression in human melanocytic cells: cell cycle effects and implication in the generation of melanoma. 992 Apr 26

The expression of human placental aromatase is transcriptionally regulated through the promoter region of exon 1a (I.1) of the gene. We examined the transcriptional regulation by using human choriocarcinoma-derived JEG-3 cells which also express aromatase mRNA transcribed under the control of the placenta-specific promoter of the exon 1a. Aromatase in the cells was induced by forskolin (cAMP) and phorbol ester (TPA) in both levels of the activity and the mRNA. However, any elements responsible for the cAMP-responsiveness have not yet identified. To identify and characterize the specific elements, CAT assay of the placenta-specific promoter was performed. We reconstructed an 11.5 kb gene structure consisting of exons 1a (I.1), 1b (I.4), 1c (I.3), and 1d (PII) and their proximal promoter regions to mimic the native structure of human aromatase gene and performed a promoter assay by the transient expression of a CAT reporter carrying the mini-gene structure. The construct was transcribed from exon 1a in JEG-3 cells and exon 1b in HepG2 cells to produce tissue-specific mRNAs from the exons 1-CAT hybrid gene, indicating that the mini-gene structure contained promoter regions essential for the tissue-specific expression. However, unexpectedly exons 1-CAT hybrid mRNA in JEG-3 cells was not induced by forskolin. Then, we prepared JEG-3 cells transformed by incorporation of the exons 1-CAT hybrid gene into the chromosomal DNA. The cells stably expressed the hybrid reporter gene which was transcribed from exon 1a and induced by forskolin and TPA. These results suggest that enhancers on the promoter regions of exons 1b, 1c, and 1d might interact with a transcriptional machinery of exon 1a in the induction by forskolin and TPA. Finally, a beta-galactosidase gene connected with the 11.5 kb gene structure was introduced into mouse eggs to produce transgenic mice. The hybrid gene was transcribed from exon 1c in the gonadal tissues of all lines of the transgenic mice in accordance with the tissue-specificity of human aromatase gene, whereas it was not transcribed from exon 1a, but from exons 1b and 1c in the all placentae. The results suggest that the mouse placenta might lack in the transcriptional elements or factors essential for the placenta-specific expression of human aromatase gene.
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PMID:Unique regulation of expression of human aromatase in the placenta. 1462 29