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)

Serological analysis of the reverse transcriptase (RTase), purified from human osteosarcoma tissue, has shown that it is antigenically related to DNA polymerases from BEV and from RD-114. No cross-reactivity of the osteosarcoma RTase was observed with RTases purified from AMV, RLV, SiSV, GaLV and from human spleen of a patient with myelofibrosis.
Cancer Lett 1979 Aug
PMID:Serological characterization of a purified reverse transcriptase from osteosarcoma of a child. 9 61

Suramin--a well-known antitrypanosomal agent--was found to exert a strong inhibitory effect on the RNA-directed DNA polymerase (reverse transcriptase) activity of several oncornaviruses such as Moloney murine leukemia virus, murine Rauscher leukemia viruses, Moloney murine sarcoma virus and avian myeloblastosis virus. Inhibition of enzyme activity was obtained with both endogenous viral RNA and (A)n . oligo(dT) as the template-primer. Suramin effected a 50% inhibition of the reverse transcriptase activity of oncornaviruses at a concentration range of 0.1--1 microgram/ml. In this aspect it compared favorably to ethidium bromide, another trypanocide drug which is considered as one of the most powerful inhibitors of oncornaviral DNA polymerases. The inhibition of reverse transcriptase activity by suramin was competitive with the template-primer, (A)n . oligo(dT), suggesting that the drug may interact with the template-primer binding site of the enzyme.
Cancer Lett 1979 Nov
PMID:Suramin: a potent inhibitor of the reverse transcriptase of RNA tumor viruses. 9 62

The effects of bromodeoxyuridine (BrdUrd) incorporation into hepatocytes of carbon tetrachloride (CCl4)-induced regenerating liver of BALB/c mice on the induction of endogenous retroviruses was examined. From the nucliec acid hybridization studies, the maximum levels of hybridization were obtained for both N- and X-tropic BALB/c endogenous retrovirus specific [3H]-cDNAs with liver RNA from animals receiving BrdUrd at 40 and 44 h post-CCl4 treatment, and killed on the fourth day following BrdUrd injection. Media from NIH-3T3 (Swiss mouse) and mink cell cultures, infected with liver homogenates from animals treated as above, gave significant levels of reverse transcriptase activity. The observations made in the present study show that BrdUrd incorporation into cell DNA can cause induction of both N- and X-tropic endogenous retroviruses in BALB/c mouse hepatocytes in vivo, and such induction is probably a transient event.
Int J Cancer 1979 Oct 15
PMID:In vivo induction of endogenous retroviruses in BALB/c mouse hepatocytes by successive treatments with carbon tetrachloride and bromodeoxyuridine. 9 80

By optimal hormonal treatment the production of exogenously transmitted MMTV can be stimulated in vitro to different degrees, depending on cultivation conditions and origin of tumor cells. Moreover, after appropriate hormonal treatment, endogenous MMTV-Y can be rescued from primary cell cultures derived from dimethyl benzanthracene- and hormone-induced C57BL/10 mouse mammary adenocarcinoma, as determined by reverse transcriptase assay, distribution of 3H-uridine-labelled viral particles, immunofluorescence, and electron microscopy. On the contrary, all attempts to rescue MMTV-Y from cultures derived from urethane-induced C57BL/10 tumors failed. These data indicate that upon syncarcinogenic action of non-viral carcinogenes, estrogen and prolactin, the MMTV-Y genome can be expressed in mammary gland parenchymatous cells, which in turn may result in cell transformation. The full MMTV-Y gene expression occur after appropriate hormonal stimulation of the C57BL/10 mammary cancer cells in vitro.
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PMID:Hormone-responsive genes of the mouse mammary tumor virus. 9 6

In studying the immunogenicity of spleen cells and tumor cells in the generation, of cytotoxic T lymphocyte (CTL) in the allogeneic mixed lymphocyte culture (MLC) or mixed lymphocyte tumor cell culture (MLTC) reactions, we have found that the tumor cells not only appear to be poorly immunogenic, but are also immunosuppressive. This was shown by the ability of the tumor cells or their cell-free extracts to suppress standard MLC reactions. This suppression was acting mainly at the induction phase of the cytotoxic response. It could not interfere with the killing activity of the fully generated CTLs. In a Friend virus-induced leukemia FBL-3 system, at least two major components could be attributed to the cause of immunosuppression; one was of viral origin and the other was of non-viral origin. The viral component was sensitive to UV-irradiation and could be pelleted after ultracentrifugation at 100,000 g. The non-viral component was UV-resistant and was retained in the supernatant fraction after ultracentrifugation. Friend virus and 12 commonly found murine viruses have been excluded as the possible candidates causing the immunosuppression. The immunosuppressive viruses are very likely of endogenous origin and are defective in replication as shown by electromicroscopy, and by the virus focus-inducing and reverse transcriptase assays. These findings indicate that probably all tumor cells possess the immunosuppressive factor(s) which may account for their apparent lack of immunogenicity and the lack of proper immune responses in the tumor-bearing hosts.
Int J Cancer 1979 Nov 15
PMID:Suppression of T cell-mediated immunity by tumor cells: immunogenicity versus immunosuppression and preliminary characterization of the suppressive factors. 16 Aug 96

Non-producer (NP) human cells induced by the Kirsten sarcoma virus were characterized. These morphologically altered NP cells produced neither infectious virus nor complement-fixing antigens of the murine sarcoma-leukemia virus complex. The NP cells did not release RNA-dependent DNA polymerase and type-C virus particles with a density of approximately 1.15 g/ml in sucrose gradients by 3H-uridine labelling. The NP cells produced tumors when transplanted subcutaneously into athymic nude mice. The tumor cells re-established in culture resembled the orginal NP cells, were confirmed as human cells by karyological analysis and were also found to be "non-producer". The sarcoma virus genome in NP cells could be rescued not only by co-cultivation with "helper virus"-releasing cells but also by superinfection with helper type-C viruses. Murine (Rauscher, Ki-MuLV, AT-124 and two other xenotropic viruses), feline, RD-114 and Simian (woolly monkey and baboon) type-C viruses possessed the ability to rescue the sarcoma genome from NP cells but not AKR leukemia virus. In addition, the feline leukemia virus titer obtained by the rescuing technique in NP cells was the same as those obtained in feline embryo and NP cells by CF induction assay.
Int J Cancer 1975 Nov 15
PMID:Characterization of non-producer human cells induced by Kirsten sarcoma virus. 17 Dec 29

The oncornaviruses share several biological, biochemical, and structural properties that distinguish them from other RNA viruses. Rous sarcoma virus, a representative of avian oncornaviruses, manifests two major functions: cell transformation and virus replication. Both functions are independent, and are expressed separately in defective viruses. The virus has a 60-70S RNA, composed of 35 S subunits. It appears that each subunit of viral RNA carries the same genetic information and, furthermore, that 10% of this information is coding for cell transformation. Without this 10% the virus can still replicate. The RNA genome is expressed when the virus penetrates a sensitive cell, provided the virus carries an active reverse transcriptase. Virus-transformed cells possess a DNA form of the viral genome. The viral DNA is infectious, and can lead, upon transfection of permissive cells, to the production of a new viral progeny. We have established that the minimum molecular weight of the viral DNA is 6 X 10(6) daltons, and that this DNA is covalently bound to the chromosomal DNA. Also by examining the frequency of transfection events in the DNA-treated cells we suggest that transfection is a single-hit phenomenon. It follows that viral DNA of 6 X 10(6) daltons carries all the genetic information to code for the virus production. It seems likely that the transfection mechanism giving rise to transforming viruses is different from that producing nontransforming segments. In general terms, the experimental data indicate that certain RNAs and DNAs could accomplish malignant transformation if they are able to penetrate into the cell and give rise to the DNA forms which could be integrated into the cellular genome.
Bull Cancer
PMID:[DNA form of the genome of oncornaviruses]. 17 70

Bone-marrow cells from two leukemic children were co-cultivated with the leukemic children A 7573. In early passages, C-type oncornaviruses were released as detected by extracellular reverse transcriptase assay. Co-cultivation of the infected canine cells with the non-producing cell lines R-970-5 (human) or K-NRK (rat) both transformed by Kirsten mouse sarcoma virus (MSV) yielded a new pseudotype of MSV that could transform rat embryo, rabbit SIRC and human kidney cells but not mouse embryo cells. The focur formation could be inhibited by an antiserum to the simian sarcoma virus but not by a serum directed against murine leukemia virus. A cell line derived from a focus of transformed cells became a highe virus is related to the simian sarcoma virus. It is concluded that the leukemic bone-marrow cells produce a C-type oncornavirus that can serve as a helper virus to the defective MSV.
Int J Cancer 1977 Jan
PMID:Detection of human C-type "helper" viruses in human leukemic bone marrow with murine sarcoma virus-transformed human and rat non-producer cells. 18 71

The expression of Thy 1.2 (theta C3H) antigen was measured on the membranes of normal and neoplastic RIII and C3H mammary cells. Competitive inhibition assays revealed that the average membrane content of Thy 1.2 in mammary tissues was about equal to that of lymph node cells. Higher percentages of Thy 1.2-positive cells than mammary tumor virus (MuMTV)-positive cells were observed by immunofluorescence, which suggested that not all the Thy 1.2-positive cells recovered from tumors were also MuMTV-positive. Established tissue culture cell lines C3H and RIII MT expressed lower levels of Thy 1.2 than did cells from mammary tumors. Treatment with the synthetic gluco-corticoid dexamethasone increased the average Thy 1.2 expression in cultured mammary tumor cells as well as the levels of RNA-directed DNA polymerase. Since the percentages of Thy 1.2-positive cells also were greater in steroid-treated cultures, while fewer cells were needed to absorb a standard amount of anti-Thy 1.2 activity, it was concluded that dexamethasone enhanced membrane Thy 1.2 expression as well as MuMTV production by the cultured cells.
J Natl Cancer Inst 1977 Jun
PMID:Expression of Thy 1 antigen in normal and neoplastic mammary cells of mice. 19 40

Simian sarcoma virus, type 1 (SSV-1)-transformed non-producer cell lines were established by infection of normal marmoset fibroblast cells (HF) with limiting dilutions of SSV-1. Four focus-derived cell lines were identified as non-producers by assay of culture fluids for focus-forming activity and by the mixed culture cytopathogenicity test with XC cells. Further studies failed to detect production of type-C virus by 3H-uridine labelling, reverse transcriptase assay or electron microscopy. The non-producer cell lines, designated HF/SSV-NPI, IV, V, and VI, appeared morphologically transformed and cloned in soft agar with the same efficiency as HF/SSV-1 virus-producing transformed cells. Expression of either cytoplasmic or cell surface virus-related antigens was not detected by immunofluorescence or serum cytotoxicity tests. The presence of sarcoma genome in the transformed non-producer cell lines was demonstrated by rescue of focus-forming activity following superinfection with non-transforming helper virus or by cocultivation with helper-virus-producing cell lines. The SSV-1-transformed non-producer primate cells provide a useful tool for future studies.
Int J Cancer 1977 Jul 15
PMID:Establishment of simian sarcoma virus, type 1 (SSV-1)-transformed non-producer marmoset cell lines. 19 78


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