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:3.1.30.2 (endonuclease)
18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have used DNA-mediated gene transfer to introduce a recombinant plasmid containing the human beta-globin gene (H beta 1) into cells of a mouse tissue culture line, Ltk-. DNA isolated from independent transfer lines was analyzed by restriction endonuclease digestion, gel electrophoresis, modified Southern blotting, and filter hybridization using H beta 1 as a probe. H beta 1 sequences were present in 80% of the lines at 1-30 copies per cell. Many of the lines gave a hybridization pattern indicative of H beta 1 sequences integrated into high molecular weight DNA. DNA from three cell lines, digested with several restriction enzymes, produced a pattern providing evidence for the presence of circular H beta 1 molecules in the murine recipient cells.
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PMID:DNA-mediated gene transfer of a circular plasmid into murine cells. 29 87

A 1.45 kb DNA sequence encoding the rat alpha 6 GABAA receptor subunit (nucleotides 33-1483) was cloned from a Sprague-Dawley rat brain cDNA library by PCR amplification. Dideoxy sequencing of two individual clones revealed that the nucleotide sequence differed at only one basepair (T480-->G) from that published previously. This difference altered the deduced amino acid sequence, producing a conservative amino acid substitution (His121-->Gln). A Gln residue is present at the same location in the bovine alpha 6 subunit. Restriction endonuclease analysis of the total PCR product demonstrated that this variant of the rat alpha 6 subunit was the only allele found in this particular rat brain library, the original allele was not present. These results were further verified by RNAse protection assays performed with RNA isolated from individual rat cerebella. alpha 6, beta 1, and gamma 2S subunits were transiently expressed in L929 cells for electrophysiological analysis. Whole-cell recordings obtained from the cells demonstrated that GABAA receptor channels with the expected GABA and benzodiazepine pharmacology were produced. Excised outside out single channel recordings from the same cells revealed that GABA elicited brief duration openings to a 33 pS main conductance level and to at least one smaller (approximately 21 pS) subconductance level. Thus this allelic variant of rat alpha 6 subunit could assemble with other subunits to form a functional GABAA receptor channel with similar properties to the original allelic form.
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PMID:Molecular and electrophysiological characterization of a allelic variant of the rat alpha 6 GABAA receptor subunit. 128 Dec 55

A rat genomic library was screened using a gastric H,K-ATPase beta-subunit cDNA probe, and two clones were identified. Restriction endonuclease mapping and Southern hybridization analyses indicated that each of these clones contains the entire H,K-ATPase beta-subunit gene. The nucleotide sequence was determined for the 8.75-kb transcription unit and 2.2 kb of the 5'-flanking region. The gene consists of seven exons and shows a high degree of similarity to the Na,K-ATPase beta 1-subunit gene. Primer extension and S1 nuclease protection analyses identified a major transcription initiation site 23 bases upstream of the translation start site and several minor transcription initiation sites located further upstream. The 5'-flanking region of the gene has two potential TATA sequences, each located 25-30 bases upstream of a transcription initiation site, and a number of potential promoter and regulatory elements. In addition, the 5'-flanking region contains nucleotide sequences that may regulate transcription through the formation of unusual DNA structures. These include a sequence that may form a triple helix and an adjacent sequence with the potential to form Z-DNA.
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PMID:Rat gastric H,K-ATPase beta-subunit gene: intron/exon organization, identification of multiple transcription initiation sites, and analysis of the 5'-flanking region. 166 70

Genomic DNA obtained from B lymphoblastoid cell line was digested with appropriate restriction endonuclease and hybridized with several probes specific for HLA-DQ gene. DNA probe which detects intron between DQ beta 1 and beta 2 domains suggested the intron insertion event of Alu-like repetitive sequence in DR7DQw2 haplotype. Southern hybridization with DQA1 3' untranslated (UT) region probe showed DQw2-type hybridization pattern in DR7LDQw3 haplotype. On the contrary, DQB1 3'UT region probe showed DQw3-type pattern in the same haplotype, which strongly supports the previous suggestion that recombination occurs between DQA1 and DQB1 genes in DR7DQw3 haplotype. 3'UT region probes of DQA1 and DQB1 genes failed to detect restriction fragment lenght polymorphism (RFLP) between DR4DQw3 and DR4DQw4 haplotypes. DNA sequencing of DQB1 genomic clone derived from KT3 cell line (DR4DQw4) revealed striking homology of beta 2 domain, 5'UT region, 3'UT region and intervening sequence between beta 1 and beta 2 domains in DR4DQw3 and DR4DQw4 haplotypes. This structural similarity suggests that DQw3 and DQw4 genes are generated from a common ancestral gene.
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PMID:[Diversity of the HLA-DQ gene]. 197 41

We used restriction endonuclease digestion of leukocyte DNA to assess the structural integrity of an N-acetylglucosamine beta 1----4 galactosyltransferase (GalTase)-associated (GTA) protein kinase gene in rheumatoid arthritis (RA) patients. This analysis provides evidence that the gross structure of the GTA protein kinase gene locus remains intact in patients with defective galactosylation and that this gene locus is polymorphic both in normal individuals and in patients with RA, although no polymorphisms unique to RA patients were observed. Initial data on the expression of this gene indicate that comparable levels of GTA protein kinase messenger RNA are present in the lymphocytes of normal individuals and RA patients, irrespective of whether lymphocytes were obtained from patients with decreased or normal levels of galactosylation.
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PMID:Polymorphism and expression of the galactosyltransferase-associated protein kinase gene in normal individuals and galactosylation-defective rheumatoid arthritis patients. 212 2

Poly(A)+-selected RNA prepared from cells or tissues that express a homogeneous population of either beta 1- or beta 2-adrenergic receptors was isolated and then microinjected into Xenopus laevis oocytes. Following microinjection, the expression of beta-adrenergic receptors was assessed by equilibrium radioligand binding analysis using the antagonist ligand [3H]dihydroalprenolol. The pharmacology of the newly- expressed beta-adrenergic receptors in oocyte membranes was the same as that of the original tissue used as a source of RNA. Hybridization of nick-translated cDNA of hamster beta 2-adrenergic receptor to poly(A)+-selected RNA from tissues containing beta 2-adrenergic receptors was to a mRNA species of 2.2 kilobases. In contrast, hybridization of the cDNA probe to poly(A)+-selected RNA from tissues containing beta 1-adrenergic receptors was to a mRNA species of 2.0 kilobases. A single-stranded fragment of hamster beta 2-adrenergic receptor cDNA corresponding to nucleotides 730-886 was isolated and uniformly radiolabeled. This region of the gene is predicted to encode for the entire second exofacial loop (L4-5), the entire fifth transmembrane-spanning region, and the first 5 amino acid residues of the third cytoplasmic loop (L5-6) of the beta 2-adrenergic receptor. Hybridization at 48 and 56 degrees C of poly(A)+-selected RNA prepared from sources that express either beta 1 or beta 2-adrenergic receptors to the antisense orientation strand of this region of the beta 2-adrenergic receptor cDNA was followed by S1 endonuclease digestion of nonhybridized sequences. At 48 degrees C, S1-resistant hybrids from both sources of RNA protected the probe from S1 endonuclease digestion. At 56 degrees C, however, only the RNA prepared from the source of beta 2-adrenergic receptors protected the probe from S1 endonuclease digestion. These results demonstrate that the mRNAs encoding for the structurally homologous beta 1- and beta 2-adrenergic receptors are distinct in the pharmacological specificity of their translation products and in their size and structure.
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PMID:Expression of mRNA of beta 1- and beta 2-adrenergic receptors in Xenopus oocytes results from structurally distinct receptor mRNAs. 245 28

Studies on mouse sperm-egg binding and fertilization have been suggested to involve the interaction of sperm-associated beta 1-4 galactosyltransferase with egg zona pellucida glycoproteins. A population of human males, whose sperm demonstrated an inability to penetrate ovulated zona pellucida-free hamster eggs in vitro, were examined for the level of activity of beta 1-4 galactosyltransferase. The level of enzyme activity was found to be reduced in human sperm isolated from this group of individuals compared with a known hamster penetration-positive group. Analysis of the deoxyribonucleic acid from these individuals by Southern hybridization with a putative human complementary deoxyribonucleic acid clone to beta 1-4 galactosyltransferase identified a unique allele lacking 0.8 and 0.4 kb restriction fragments on digestion with the endonuclease Taq I. These results represent the first evidence to suggest that mutations could be associated with the human gene for galactosyltransferase. Our data help to clarify one of the possible molecular mechanisms responsible for sperm-egg binding/penetration interactions.
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PMID:Identification of a deoxyribonucleic acid allelic variant for beta 1-4 galactosyltransferase expression associated with male sperm binding/penetration infertility. 256 20

This paper describes a technique of DNA amplification in vitro and its application on detection of sickle cell (Hb S) gene. Genomic DNA was microextracted from dried blood specimen of the first patient with sickle cell trait in China. Target DNA sequence was amplified by the polymerase chain reaction (PCR) with the primers beta 1 (5'-ACACAACTGTGTTCACTAGC-3') and beta 2 (5'-CAACTTCATCCACGTTCACC-3') that primed amplification of an 110-base-pair (bp) segment of beta globin gene. The amplified DNA was digested with a restriction endonuclease Mst II, which has a recognition site at codon 6 in the normal beta globin gene, and cleaved the normal amplified beta globin DNA into two fragments of 54bp and 56 bp which was as an overlap band in agarose gel electrophoresis, while the 110bp fragment amplified from DNA of sickle cell mutation remained uncleaved owing to a single base substitution (A----T) at codon 6 in the mutation. DNA amplification method is rapid, sensitive and simple, and does not require radioactive probes. Besides, the PCR amplification can be carried out on the DNA extracted from dried blood samples. So the technique is very useful for gene diagnosis and carrier screening of genetic disease.
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PMID:[Detection of sickle cell gene by analysis of amplified DNA sequences]. 264 Jan 44

Type 1 diabetes results from the destruction of insulin-producing pancreatic beta cells. Genetic and environmental factors are implicated in the beta cell destruction. As environmental factors affecting the induction of type 1 diabetes, diabetogenic viruses, chemicals, toxins, and diet are likely candidates as either primary injurious agents of beta cells or triggering agents for the induction of autoimmunity. Regarding viruses as a triggering factor of type 1 diabetes, there are at least two different pathogenic mechanisms in virus-induced diabetes: cytolytic infection of beta cells, leading to their destruction, and triggering of autoimmunity, leading to the autoimmune-mediated destruction of beta cells. Since there is no correlation between the induction of antibodies to Coxsackie B viruses and the presence of islet cell autoantibodies in patients with type 1 diabetes, the induction of diabetes by Coxsackie B viruses may be due to cytolytic infection of beta cells rather than an autoimmune response. In contrast, rubella virus and cytomegalovirus (CMV) do appear to be somehow associated with autoimmune type 1 diabetes since there is a strong correlation between the presence of islet cell autoantibodies and persistent infections. Regarding genetic factors, there are distinct markers related to the susceptibility to Coxsackie B4 virus-associated type 1 diabetes and CMV-associated type 1 diabetes. Four specific DNA restriction endonuclease fragments (BamHI-DQ-beta 6.6, TaqI-DR-beta 4.3, TaqI-DR-beta 2.5 and TaqI-DR-beta 1.5 kb) are related to the susceptibility to Coxsackie B4 virus-associated type 1 diabetes while six specific DNA restriction endonuclease fragments (BamHI-DQ-alpha 12.5, -beta 3.7 and -beta 3.2 kb, TaqI-DQ-alpha 7.2, -beta 7.2 and -beta 5.4 kb) are related to the susceptibility to CMV-associated type 1 diabetes.
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PMID:Viruses as a triggering factor of type 1 diabetes and genetic markers related to the susceptibility to the virus-associated diabetes. 268 Mar 67

Incubation of DDT1 MF-2 hamster vas deferens cells with beta-adrenergic agonists results in a time- and concentration-dependent decreases in both beta-adrenergic receptor (beta AR) responsiveness and receptor number. Receptor mRNA levels were quantified by DNA-excess solution hybridization by using a 170-nucleotide single-stranded probe derived from the hamster beta 2AR cDNA. RNA blot analysis of poly(A)+-selected RNA with the solution probe revealed a 2.2-kilobase species. Digestion of the RNA/solution probe mixture with S1 endonuclease revealed a single species of RNA (170 bases) that was protected by the solution probe. DDT1 MF-2 cells were found to contain 0.38 pg of beta AR mRNA per microgram of total cellular RNA. Incubation (16 hr) with isoproterenol decreased beta AR mRNA levels in cells by 40%. This agonist-induced decrease in receptor mRNA levels was found to be dependent on the time of incubation and the dose of agonist. The decrease in beta AR mRNA was half-maximal at 0.1-0.5 microM isoproterenol. The beta-adrenergic antagonists CGP 20712A (beta 1-selective) and ICI 118,551 (beta 2-selective) blocked in a dose-dependent fashion the ability of isoproterenol to effect receptor mRNA levels. The beta 2-adrenergic antagonist displayed a potency 25-fold greater than that of the beta 1-adrenergic antagonist, in agreement with the subtype of receptor (beta 2) expressed by these cells. For down-regulated cells in which receptor mRNA levels declined in response to agonist, the addition of the antagonist ligand (-)-propranolol (1 microM) was able to restore receptor mRNA levels to 90% of the control value within 12 hr. Full recovery of steady-state beta AR mRNA was achieved within 60 hr. These studies provide a molecular explanation for the down-regulation of GTP-binding regulatory protein (G protein)-linked cell-surface receptors that accompanies desensitization.
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PMID:Down-regulation of beta-adrenergic receptors: agonist-induced reduction in receptor mRNA levels. 289 21


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