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:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin-like growth factor 1 (IGF-1) is involved in the regulation of brain development and has been suggested as an autocrine stimulator of brain tumor cell proliferation. This study demonstrates the expression of IGF-1 in tumor tissue from human gliomas and one esthesioneuroblastoma. Using immunohistochemistry, expression of an IGF-1-like peptide was localized in tumor cells of 6 of the 9 gliomas examined as well as the esthesioneuroblastoma. From one anaplastic oligodendroglioma (which showed strong IGF-1 immunostaining) the IGF-1 transcripts were characterized after isolation of mRNA followed by amplification using the reverse transcriptase-polymerase chain reaction. Two IGF-1 complementary DNAs resulting from alternative splicing of the IGF-1 primary transcript were identified. These transcripts encode two different precursor proteins which correspond to Ea IGF-1 and Eb IGF-1. The significance of IGF-1 alternative mRNA splicing pathways remains to be determined.
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PMID:Characterization of insulin-like growth factor 1 in human primary brain tumors. 849 8

A cDNA encoding mouse butyrophilin was obtained by reverse transcriptase-coupled polymerase chain reaction (RT-PCR) using poly (A)+ RNA from lactating mouse mammary gland as a template and screening a cDNA library with the RT-PCR-amplified fragment as a probe. DNA sequencing and computer analysis revealed that it has a rather long 3'-untranslated sequence and that the carboxy-terminal cytoplasmic domain was well conserved between mouse and bovine butyrophilins. To elucidate the biological function of butyrophilin, the cytoplasmic region expressed as fusion protein with glutathione S-transferase (GST) was purified and incubated with the cell lysate of mouse mammary epithelial cell lines, COMMA-ID and HC11. A 150-kDa protein was shown to specifically associate with the cytoplasmic domain and the protein increased in amount when the cells were treated with basal medium supplemented with lactogenic hormones such as prolactin, insulin and glucocorticoid. N-terminal amino acid sequencing indicated that the protein is xanthine dehydrogenase/oxidase which has been cloned from mouse liver. Further, the cytoplasmic domain also bound xanthine dehydrogenase/oxidase from bovine milk fat globule membrane. These results suggest that butyrophilin might be physiologically associated with xanthine dehydrogenase/oxidase and might function in a complex form in milk fat secretion.
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PMID:Carboxy-terminal cytoplasmic domain of mouse butyrophilin specifically associates with a 150-kDa protein of mammary epithelial cells and milk fat globule membrane. 854 2

Syntaxin 1/HPC-1 is an integral membrane protein, which is thought to be implicated in the regulation of synaptic neurotransmitter release. We investigated syntaxin 1 expression in pancreatic beta cells and the functional role of syntaxin 1 in the insulin release mechanism. Expression of syntaxin 1A, but not 1B, was detected in mouse isolated islets by the reverse transcriptase-polymerase chain reaction procedure. An immunoprecipitation study of metabolically labeled islets with an anti-rat syntaxin 1/HPC-1 antibody demonstrated syntaxin 1A protein with an apparent molecular mass of approximately 35 kDa. Immunohistochemistry of the mouse pancreas demonstrated that syntaxin 1/HPC-1 was present in the plasma membranes of the islets of Langerhans. In order to determine the functional role of syntaxin 1 in pancreatic beta-cells, rat syntaxin 1A or 1B was overexpressed in mouse beta TC3 cells using the transient transfection procedure. Transfection of beta TC3 cells with either syntaxin 1 resulted in approximately 7-fold increases in their immunodetectable protein levels. Glucose-stimulated insulin release by syntaxin 1A-overexpressing cells was suppressed to about 50% of the level in control cells, whereas insulin release by syntaxin 1B-overexpressing and control cells did not differ. Next, we established stable beta TC3 cell lines that overexpressed syntaxin 1A and used them to evaluate the effect of syntaxin 1A on the regulatory insulin release pathway. Two insulin secretogogues, 4-beta-phorbol 12-myristate 13-acetate or forskolin, increased insulin release by untransfected beta TC3 cells markedly, but their effects were diminished in syntaxin 1A-overexpressing beta TC3 cells. Glucose-unstimulated insulin release and the proinsulin biosynthetic rate were not affected by syntaxin 1A overexpression, indicating a specific role of syntaxin 1A in the regulatory insulin release pathway. Finally, in vitro binding assays showed that syntaxin 1A binds to insulin secretory granules, indicating an inhibitory role of syntaxin 1A in insulin exocytosis via its interaction with vesicular proteins. These results demonstrate that syntaxin 1A is expressed in the islets of Langerhans and functions as a negative regulator in the regulatory insulin release pathway.
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PMID:Expression and functional role of syntaxin 1/HPC-1 in pancreatic beta cells. Syntaxin 1A, but not 1B, plays a negative role in regulatory insulin release pathway. 855 45

Insulin and insulin-like growth factors (IGF-I and -II) are members of a family of growth factors which are known to be developmentally regulated during preimplantation mouse embryogenesis. The physiological actions of the insulin family of growth factors are mediated by interactions with specific cell surface receptors that are detectable on the cells of preimplantation mouse embryos. Mouse embryonic stem (ES) cells are totipotent cells derived directly from the inner cell mass of the blastocyst. ES cells have the ability to differentiate into all three germ layers and have unlimited growth potential under certain culture conditions. The great advantage of ES cells is the ability to obtain large amounts of tissue for biochemical studies as compared with preimplantation embryos. To examine in greater detail the biological actions of the insulin family of growth factors, the expression of their cognate receptors on ES cells was examined. ES cells were cultured in DMEM medium supplemented with leukemia inhibitory factor (LIF) to maintain the undifferentiated state. Receptor expression was evaluated at the mRNA level using the reverse transcription polymerase chain reaction (RT-PCR), and at the protein level by radioactive labeled ligand-receptor binding assay. Using RT-PCR, mRNAs of all three growth factor receptors were detected in ES cells. Messenger RNA from ES cells was reverse transcribed into cDNA by AMV reverse transcriptase at 42 degrees C for 1 hr. The reverse transcription reaction was amplified with Taq polymerase and specific primers for insulin, IGF-I, or IGF-II receptors by PCR. RT-PCR and the control plasmid cDNA PCR products were resolved electrophoretically on 3% agarose gels. Each amplified PCR product showed the predicted correct size.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mouse embryonic stem cells express receptors of the insulin family of growth factors. 856 62

Insulin-like growth factors IGF-I and IGF-II are potent inducers of oligodendrocyte development. Because IGF-I is produced, in some cases, by the same cells that respond to it (autocrine/paracrine action), we examined the possibility that IGF-I is expressed by developing oligodendroglial cells. We employed a sensitive method, reverse transcriptase-polymerase chain reaction (RT-PCR), to detect IGF-I mRNA in purified populations of oligodendroglial cells isolated from rat brain during the period of oligodendrocyte development. Cells were purified by fluorescence activated cell sorting (FACS), using antibodies to the cell surface antigenic markers O4 and galactocerebroside (GC). RNA was isolated from the sorted cells, reverse-transcribed, and PCR-amplified, using a strategy that recognizes IGF-I mRNA but not DNA. The amplified band was identified as IGF-I by size, hybridization to an IGF-I-specific antisense probe, and restriction analysis. IGF-I mRNA was detected in O4-positive/GC-negative oligodendrocyte precursors and, more weakly, in GC-positive oligodendrocytes. IGF-I mRNA could be detected reproducibly in RNA extracted from 100-cell samples of O4-positive cells, making it unlikely that the mRNA was derived from contaminants in the FACS-sorted cell populations. We conclude that IGF-I is expressed by developing oligodendroglia. Autocrine expression of IGF-I by developing oligodendroglial cells suggests that oligodendrocyte development is, in part, autoregulatory.
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PMID:Developing oligodendroglia express mRNA for insulin-like growth factor-I, a regulator of oligodendrocyte development. 856 38

The ATP-sensitive potassium channel of insulin-secreting pancreatic beta-cells is a complex of Kir6.2, a member of the inwardly rectifying potassium channel superfamily, and the sulfonylurea receptor. We have isolated cDNA clones encoding rat Kir6.2. Co-expression of rat Kir6.2 and sulfonylurea receptor in human embryonic kidney cells generated a potassium current with the properties of the beta-cell ATP-sensitive potassium channel. A quantitative reverse transcriptase-polymerase chain reaction assay indicated that Kir6.2 and sulfonylurea receptor mRNAs were abundantly expressed in rat islets and that expression of Kir6.2 mRNA was reduced by >70% in islets from Zucker diabetic fatty male rats, whereas there was no significant change in sulfonylurea receptor mRNA levels. Thus, decreased expression of Kir6.2 could contribute to the beta-cell dysfunction which characterizes diabetes mellitus in this animal model.
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PMID:Rat inwardly rectifying potassium channel Kir6.2: cloning electrophysiological characterization, and decreased expression in pancreatic islets of male Zucker diabetic fatty rats. 860

The expression of insulin receptor mRNA was examined in rat pancreatic islet cells by single-cell reverse transcriptase (RT)-polymerase chain reaction (PCR). Single cells from disaggregated islets were individually isolated in a microcapillary pipet, and the beta-cells were identified by amplification of the mRNA for insulin. We found that in single beta-cells, the mRNA for the insulin receptor was also expressed. The fraction of single islet cells expressing both insulin receptor and insulin mRNAs corresponds closely to the fraction of beta-cells in the disaggregated islet cell preparation. These results indicate that normal beta-cells have the potential to express authentic insulin receptors. Immunohistochemical analysis was insufficiently sensitive for assaying insulin receptor protein; however, insulin receptor substrate 1 (IRS-1) was readily immunolocalized in islet beta-cells. Since IRS-1 links several cell surface receptors, including those for insulin and IGF-I, to distal signal transduction pathways, our observations indicate that hormonal regulation of islet beta-cells potentially involves the same signal transduction pathway that mediates insulin and growth factor signaling in peripheral insulin target tissue cell types.
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PMID:Expression of insulin receptor mRNA and insulin receptor substrate 1 in pancreatic islet beta-cells. 863 42

Alternative splicing of the 36-base pair exon 11 of the human insulin receptor gene results in the synthesis of two insulin receptor isoforms with distinct functional characteristics (the isoform containing exon 11 has lower insulin binding affinity and lower internalization rate). Altered expression of these insulin receptor isoforms has been previously demonstrated in skeletal muscle of patients with non-insulin-dependent diabetes mellitus (NIDDM). However, this observation was not confirmed by other studies and is still a matter of controversy; furthermore, it is not known whether it represents a primary event or is secondary to hyperinsulinaemia and insulin resistance. In order to address this issue in patients with pure non-genetically determined hyperinsulinaemia, we examined the alternative splicing of insulin receptor mRNAs in skeletal muscle of eight patients with surgically confirmed insulinoma and insulin resistance and in eight healthy subjects, using the reverse transcriptase-polymerase chain reaction technique. The insulinoma patients displayed a significant increase in the expression of the insulin receptor isoform containing exon 11 (75.7 +/- 2.3%) when compared with normal subjects (57.9 +/- 1.5%); furthermore, this increase was positively correlated with plasma insulin concentration and negatively correlated with in vivo insulin sensitivity (glucose clamp). In conclusion, the increased expression of the insulin receptor isoform with lower insulin binding affinity in patients with primary non-genetically determined hyperinsulinaemia supports a role for insulin in the regulation of alternative splicing of insulin receptor pre-mRNA and suggests that in NIDDM an altered receptor isoform distribution might be secondary to the ambient hyperinsulinaemia rather than representing a primary defect.
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PMID:Chronic primary hyperinsulinaemia is associated with altered insulin receptor mRNA splicing in muscle of patients with insulinoma. 863 75

Among glycosaminoglycans, dermatan sulfate (DS) is the strongest inhibitor of DNA synthesis in adult rat hepatocytes in primary culture stimulated with insulin and epidermal growth factor. Hyaluronate also inhibited DNA synthesis, whereas chondroitin-6 sulfate, 4-sulfate or heparin had no effect on DNA synthesis in hepatocytes. Analysis of growth regulatory factors in hepatocyte culture medium treated with DS revealed that interleukin-1 (IL-1) was released into the medium. IL-1 beta mRNA was detected in DS-treated hepatocytes by reverse transcriptase-polymerase chain reaction, but not in untreated hepatocytes. For a marked inhibition of DNA synthesis, more than 10 hr of exposure to DS before cultured hepatocytes started DNA synthesis, was required. Similarly, more than 10 hr was required after the addition of DS before IL-1 beta mRNA was detected. These findings suggest that DS in the medium induced the production of IL-1 beta which, in turn, reduced DNA synthesis in hepatocytes.
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PMID:Release of interleukin-1 beta by dermatan sulfate suppresses hepatocyte growth. 866 99

A macromolecular fraction was isolated from ovine bone marrow and designated the active fraction (AF). Two distinct enzymatic activities were detected in the AF: (1) a RNA-dependent RNA polymerase, and (2) a reverse transcriptase. RNA polymerase uses an endogenous RNA molecule of the AF as the template while the product of this RNA polymerase reaction forms the template for the reverse transcriptase. Synthetic reactions are initiated exclusively upon the exposure of the in vitro system to one of the external proteins, selected at random, ovalbumin or insulin. Ovalbumin specific (OS) and insulin specific (IS) AF fractions were prepared. OS-AF binds 14C-ovalbumin and the IS-AF binds 14C-insulin, but not vice versa. Reverse transcription activity of OS-AF is stimulated only upon its exposure to ovalbumin and not to insulin while the reverse is true for the activity associated with IS-AF. Indirect evidence indicates that the enzymes which synthesize nucleic acids are closely associated with the antigen receptor on the B-lymphocyte plasma membrane, the mlgM, and that the antigen binding to its receptor helps in the activation of these enzymes.
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PMID:Reverse transcription in a macromolecular complex of ovine bone marrow: possible involvement in the antigen receptor mediated signal transduction process. 868 97


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