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)

Human T-cell leukemia virus (HTLV-I, HTLV-II) rex protein function is required for the cytoplasmic expression of incompletely spliced viral transcripts encoding structural proteins. The effect is mediated by a cis-acting rex-response element (RRX) which is located near the 3' end of all viral mRNAs. We show that rex polypeptides of HTLV-I and HTLV-II expressed in Escherichia coli are capable of specifically binding RRX-containing transcripts of both viruses in cell-free assays. Binding analyses with deletion variants of rex proteins revealed a domain with RNA-binding activity in the first 77 N-terminal amino acids. Removal of a basic peptide of 19 amino acids from the N terminus abrogated RNA binding, whereas a beta-galactosidase fusion protein containing this peptide bound to the RRX. These results suggest that direct binding of rex protein to the RRX is important for rex-mediated regulation of viral gene expression and that a short stretch of positively charged amino acids contributes to the specific binding of rex to its target RNA.
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PMID:In vitro binding of human T-cell leukemia virus rex proteins to the rex-response element of viral transcripts. 190 3

The Syrian Hamster kidney cell line (BHK-21) was stably transfected with a plasmid vector containing the lacZ bacterial gene under the control of a HTLV-I-LTR promoter. In these cells termed pA18G-BHK-21, this lacZ construct is inducible by the tax protein produced by a tax expression vector. It was also shown that beta-galactosidase synthesis was detected within 48 h after cocultivation of pA18G-BHK-21 cells with HTLV-I (HUT-102, MT2, C91/PL, 2060) or HTLV-II (MoT strain) -producing cells. The number of positive cells was directly related to the number of HTLV-I or -II-infected cells seeded. In addition, the LTR transactivation observed in coculture with HTLV-I-infected cells was specifically inhibited by sera containing antibodies directed against HTLV-I proteins, but not, or only weakly, by sera containing HTLV-II antibodies. Conversely, beta-galactosidase expression induced by HTLV-II-infected cells was inhibited by sera of HTLV-II-infected individuals, but not, or only weakly, by HTLV-I-positive sera. Irrespective of the inducer cell, sera from uninfected people did not inhibit LTR-driven expression of the lacZ gene in pA18G-BHK-21 cells cocultivated with HTLV-producing cells. This assay may thus be employed profitably for the detection and quantification of both HTLV-producing cells and HTLV-specific antibodies.
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PMID:Identification of HTLV-I- or HTLV-II-producing cells by cocultivation with BHK-21 cells stably transfected with a LTR-lacZ gene construct. 773 Apr 34

A set of recombinant plasmids containing different fragments of HTLV-I env gene has been constructed on the basis of pUR290-pUR292 vectors. The hybrid proteins containing different fragments of ENV predecessor in the C-terminal of beta-galactosidase differed in stability in Escherichia coli cells. The presence of N-terminal of ENV predecessor in recombinant proteins considerably decreases their resistance to proteases of the bacterial cell. Elimination of this fragment led to obtaining of the recombinant plasmid pESG coding for the high level of synthesis of the env-specific hybrid polypeptide (up to 30% of the total cellular protein). This 134 Kda protein is able to interact efficiently with the HTLV-I positive sera and may be used in the diagnostic test-systems for identification of the HTLV-I infected patients.
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PMID:[Expression of the gene for the gp46 surface glycoprotein from the human T-cell leukemia virus type I (HTLV-I) in bacteria]. 806 80

A set of recombinant plasmids containing sequences of HTLV-I viral gag-gene has been constructed on the basis of pUR290-pUR292 vector plasmids. The resulting hybrid proteins containing different fragments of GAG-precursor in the C-end of beta-galactosidase differed to a large extent in stability in Escherichia coli cells. The presence of an N-end fragment of GAG-precursor in the recombinants decreases drastically their resistance to bacterial proteases. Elimination of the fragment resulted in obtaining the recombinant plasmid pGdN coding for high rate synthesis (up to 30% of total cellular protein) of gag-specific hybrid polypeptide in Escherichia coli HB101 cells. This 145 kDa protein efficiently interacts with HTLV-I positive sera. It can be used in diagnostic test-systems for indicating HTLV-I infected persons.
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PMID:[Expression of the gag-precursor of the human T-cell leukemia virus type I in Escherichia coli: study of the stability and antigenic properties of virus-specific hybrid proteins]. 828 46

We have analyzed the effect of transfection into murine NIH/3T3 cells of the human dsRNA-activated kinase PKR on the expression of the beta-galactosidase reporter gene, placed under control of the HIV1 or the HTLV-I LTR. beta-Galactosidase expression is stimulated when the reporter plasmids are cotransfected with wild-type PKR but inhibited when cotransfected with a catalytically inactive mutant PKR. In the case of HIV1, beta-galactosidase expression was not stimulated when cotransfection was carried out with PKR harboring mutations in the dsRNA binding domains, indicating that stimulation depends on the classical mode of PKR activation through dsRNA binding. In contrast, the dsRNA binding mutants of PKR could still partially stimulate beta-galactosidase expression from the HTLV-I LTR, suggesting that PKR activation in this case may involve different/additional mechanisms. These results show that, in addition to the known down-regulation of protein synthesis through elF2 phosphorylation, PKR can also positively stimulate gene expression in vivo, most probably through phosphorylation of a substrate distinct from elF2.
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PMID:Human PKR transfected into murine cells stimulates expression of genes under control of the HIV1 or HTLV-I LTR. 855 71

Replication-defective recombinant adenovirus, Adex4SRLacZL, was used as a vector for transferring exogenous genes in mouse zona pellucida-free eggs at the pronuclear stage. The vector contained the E. coli LacZ reporter gene under the control of the SR alpha promoter (SV40 early promoter-fused HTLV-I LTR), and the expression of the reporter gene was examined during preimplantation development in culture. Histochemical staining of the embryos for beta-galactosidase activity showed that the exogenous LacZ gene as expressed in 98% of the embryos at the morula-blastocyst stages. As in the microinjection method, the exogenous genes could be pursued from the 2-cell stage. Neither apparent morphological changes nor cytotoxic effects were observed. Both the percentages of embryos expressing reporter genes and the rate of development to the blastocyst stage were higher in the adenovirus vector-treated embryos than in the microinjected ones. These results suggest that the adenovirus vector system is a useful tool in investigating the genetic control of early mammalian development.
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PMID:Gene transfer and expression in mouse preimplantation embryos by recombinant adenovirus vector. 857 42

We generated several lines of mice transgenic for the lacZ reporter gene under the control of an HTLV-I LTR. Two different LTR were used; one was isolated from a case of Adult T-cell Leukemia (ATL), the other from a case of Tropical Spastic Paraparesis (TSP/HAM). These LTR differed at 18 nucleotide positions. The pattern of expression of the transgene, studied at the RNA level by RT-PCR, was the same regardless of the origin of the promoter. The beta-galactosidase activity was detected primarily in the central nervous system, in the parenchyma, the choroid plexus and the ependymal cells along the ventricles. In parenchyma, double labelling experiments showed that the cells expressing beta-galactosidase were neurons. These results show that choroid plexus cells and ependymal cells, as well as some neurons, are permissive for the activity of the HTLV-I promoter. The origin of the LTR had not influence on the pattern of expression of the reporter gene.
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PMID:Analysis of the expression directed by two HTLV-I promoters in transgenic mice. 902 6