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

---

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

The deleted in colorectal carcinomas (DCC) gene, located in human chromosome band 18q21, was identified as a potential tumor suppressor gene by Fearon et al. in 1990. The DCC gene encodes a protein which is highly similar to neural cell adhesion molecules and other related cell surface glycoproteins. In colorectal carcinoma, the expression of the DCC gene is reduced or absent in 88% of cases. We examined the expression of the DCC gene using reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. Its expression was reduced or absent in some leukemias. Our findings suggest the possibility that this gene may play a role in leukemogenesis.
...
PMID:[DCC gene and leukemia]. 151 58

Malignant lymphomas were observed in 38% (9 of 24) of simian immunodeficiency virus (SIV)-infected cynomolgus monkeys (Macaca fascicularis) 5 to 15 months after inoculation with SIV strain SMM3. Lymphomagenesis in the SIV-infected monkeys was not related directly to the SIV-infectious dose given. All SIV-infected animals developed severe immunodeficiency. No significant difference in immunodeficiency was observed between tumor-bearing and non-tumor-bearing animals. In contrast, no lymphomas were observed in a comparable group of HIV-2-infected monkeys, which did not develop immunodeficiency; nor did the noninfected control monkeys. All 9 SIV-related tumors were high-grade B-cell lymphoblastic or pleomorphic lymphomas with extranodal, disseminated growth. Most tumors showed marked infiltration by monocytes and CD8+ T lymphocytes. Occasional tumor infiltrating cells showed immunohistochemical reaction for SIV. The cells of two tumors were established in vitro and shown to be of B-cell phenotype. The tumor cell cultures showed no reverse transcriptase activity and no evidence of virus infection by electron microscopy. Our observations indicate that SIV-induced immunodeficiency in cynomolgus monkeys also mimics HIV infection and AIDS in humans with regard to increased lymphomagenesis and type of lymphomas.
...
PMID:Malignant lymphomas in cynomolgus monkeys infected with simian immunodeficiency virus. 170 62

Continuous cell lines could be reproducibly established by culturing spleen cells from adult mice injected with MLV-producer cells or directly infected with Mo-MLV with rIL-2, whereas the culture of normal splenic cells with rIL-2 induced only transient and limited proliferation resulting in no such lines. All of the lines showed morphological characteristics as LGL with Thy-1+,Lyt-1-,L3T4-,Lyt-2-,AsGM1+,FcR gamma+ phenotype without exception, and most of them exhibited typical NK-patterned cytotoxicity. Analysis of reverse transcriptase activity of the culture supernatants as well as Southern hybridization of the DNA from the lines using an Mo-MLV-specific cDNA probe indicated no evidence of retroviral replication or proviral integration, suggesting that the generation of cell lines reflected a reactive process and viral infection was not directly responsible. It was subsequently revealed that Thy-1+,Lyt-1+,Lyt-2- spleen cells from mice infected with Mo-MLV in vivo spontaneously produced surprising amounts of IL-3 in vitro, leading to the possibility that IL-3 was responsible for the generation of lines. The possibility was directly supported by the observation that continuous lines with identical characteristics could be generated completely in vitro by sequential stimulation with rIL-3 and rIL-2 from normal spleen cells without any involvement of Mo-MLV. The C beta gene of TCR was shown to be rearranged in all the lines examined, indicating the LGL lines were all genetically committed to T cell lineage. Unlike the situation in normal splenic populations expanded by rIL-2, where the expression of IL-2-R was progressively lost, constitutive expression of high-affinity-IL-2-R was observed in all the lines and thus, this was considered to explain the unlimited proliferation of them in response to rIL-2 alone. These results suggested the probable role of IL-3 in the regulation of growth and differentiation of a set of LGL committed to T cell lineage. The possible implications of the phenomenon in the regulation of hematopoiesis as well as in the control of Mo-MLV-induced leukemogenesis were discussed.
...
PMID:Generation of continuous large granular lymphocyte lines by interleukin 2 from the spleen cells of mice infected with Moloney leukemia virus. Involvement of interleukin 3. 244 1

Studies of recombinants between murine leukemia viruses (MuLVs) that cause thymic or erythroid leukemias have shown that enhancer sequences in the long-terminal repeats (LTRs) can determine the target tissues for pathogenesis. It has been inferred that the enhancers may specifically target viral expression into the cells that then become neoplastic. However, the neoplasms in those studies formed after latencies and contained ultimate viruses (called MCFs) that differed from the injected viruses in their enhancer sequences and envelope (env) genes. Transcriptional activities of LTRs from these proximal and ultimate viruses have not been thoroughly analyzed in different hematopoietic lineages. We present evidence that the enhancer of Friend spleen focus-forming virus (SFFV), an ultimate erythroleukemogenic retrovirus, contains an unstable 42-nucleotide direct repeat. Other ultimate erythroleukemogenic MuLVs (Friend MCFs) contain an enhancer nearly identical to that of SFFV both in its sequence and in its specific instability. The instability occurs in sequences that contain inverted repeats and we propose that it occurs by a simple reverse transcriptase hop mechanism. We constructed plasmids that contain the two forms of the SFFV LTR linked to the bacterial chloramphenicol acetyltransferase (CAT) gene, and we compared these in transient transfection assays with LTR-CAT plasmids constructed from Friend and Moloney MuLVs. The assays employed erythroleukemia cells, thymic lymphoma cells, and fibroblasts. The tropisms of expression correlated only weakly with tissue specificities of pathogenesis and each LTR was active in all cells. The SFFV 42-nucleotide duplication reduced expression in erythroid cells and increased expression in fibroblasts. We conclude that retroviral enhancers do not stringently direct gene expression into specific cell lineages, but on the contrary they are leaky and contain replicative instabilities that also may facilitate viral entrenchment throughout the host. These results have important implications for understanding murine retroviral evolution and the multi-step process of leukemogenesis.
...
PMID:An enhancer sequence instability that diversifies the cell repertoire for expression of a murine leukemia virus. 283 56

Rifamycin antibiotics, which inhibit RNA-directed DNA polymerase of Rauscher leuckemia virus, prevent the leukemogenic activity of the virus, and the effect of leukemogenesis correlates with the magnitude of inhibition of the purified enzyme. This inhibition of enzyme activity by rifamycin SV derivatives is due to a relatively tight binding between the enzymes and the inhibitors, yet the binding can be reversed by nonionic detergent. The results of this study suggest that RNA-directed DNA polymerase is essential for induction of leukemia by exogenous virus and correlate with the previous observation that the same derivatives block viral transformation in vitro.
...
PMID:RNA-directed DNA polymerase and virus-induced leukemia in mice. 412 70

An approach toward elucidation of the mechanisms of action of mammalian leukemia viruses has been made by the generation in tissue culture of recombinant viruses between a potent murine leukemia virus (MuLV), Rauscher-MuLV, and an endogenous xenotropic mouse type-C virus, BALB:virus-2, without known malignant potential. Using a double selection system devised to select against the temperature-sensitive (ts) lesion associated with a mutant of Rauscher-MuLV and the xenotropic host range of BALB:virus-2, recombinant viruses were obtained at frequencies ranging from 0.01 to 0.1%. Recombinant viruses were identified on the basis of the type specific antigenic determinants in the translational products of gag (p15, p12, p30, and p10 proteins), pol (reverse transcriptase), and env (gp70 glycoprotein) genes. By this approach, the partial genetic maps of a large number of recombinants were obtained. The fact that p10 of Rauscher-MuLV ts 25, the mutant utilized, was the only protein uniformly lacking in recombinant viruses, localized the lesion inhibiting gag precursor cleavage in this mutant at the carboxy terminus of its gag gene. The recombinant viruses demonstrated two host range phenotypes as defined by Fv-1 host cell restriction. In each case, NB-tropic recombinants possessed the p30 of BALB:virus-2 p30. Thus, it was possible to assign the site of Fv-1 action at, or closely linked, to the viral p30. The target within the viral genome of a second host restriction was also mapped. A serum factor, previously shown to specifically inactivate xenotropic virus infectivity, was demonstrated to exert its action on the viral env gene product. The system described here allows the generation of specific recombinant genotypes that should be useful in defining those regions of the viral genome involved in leukemogenesis.
...
PMID:Viral genes involved in leukemogenesis. I. Generation of recombinants between oncogenic and nononcogenic mouse type-C viruses in tissue culture. 615 14

A significantly higher MuLV expression was demonstrated in cells of MNU-induced leukemia of mice compared to corresponding cells of untreated control animals by reverse transcriptase activity and XC cell assay. These positive findings were verified by determination of indirect immunofluorescence test to look for intracytoplasmic MuLV p30. The problem is discussed whether these viruses play a role in chemical leukemogenesis.
...
PMID:Demonstration of C-type viruses in N-methyl-N-nitroso urea (MNU)-induced leukemia of mice by reverse transcriptase activity and XC assay. 615 22

Moloney leukemia virus (MoLV) induces lymphomas in BALB/c mice which either involve an immature thymic T-cell subpopulation or a splenic mature T-cell subpopulation. To investigate further the possible virological and immunological differences in these lymphomas, several lymphoma cell lines were derived. Although the majority of these cell lines expressed only the parental MoLV, one lymphoma cell line (5F4) was found which expressed only a defective virus. 5F4 virions lacked detectable reverse transcriptase activity and by immunoprecipitation lacked a serologically detectable reverse transcriptase. The lack of reverse transcriptase did not appear to be due to a deletion in the viral genome. Intracellularly 5F4 cells synthesized normal gag gene precursors but had little, if any, detectable Pr180gag-pol or an altered precursor. These results suggest that the defect of the 5F4 virus is associated with the inability to translate the appropriate precursor for reverse transcriptase. The possible origin of the detective 5F4 virus was also examined by competition radioimmunoassays. These results demonstrate that the type-specific proteins, gp71 and p12, are serologically identical to those of the endogenous ecotropic virus and distinct from the MoLV proteins. Competition assays of 5F4 cell extracts further demonstrated the lack of any detectable MoLV type-specific proteins, although the tumor was presumably induced by MoLV. The significance of these observations to leukemogenesis is discussed.
...
PMID:Characterization of a unique defective type C virus associated with a Moloney leukemia virus-induced splenic T-cell lymphoma cell line. 615 81

In order to investigate the genetic background of leukemogenesis of two brothers with acute myelogenous leukemia (AML), they and their family members were studied genetically, immunologically, virologically, and cytogenetically. Their parents were first cousins once removed and had the same or a very close type of human leukocyte antigen (HLA) and blood groups. In all five non-leukemic family members the immunoglobulin G (IgG) level was elevated, and in two healthy siblings the IgM level was beyond the normal range. The RNA reverse transcriptase activity in serum of the younger brother (Case 2) with AML was elevated. A cytogenetic study of the family revealed polymorphism of 1qh+. Based on these findings, we discuss the genetic and environmental factors of familial leukemia.
...
PMID:Familial acute myelogenous leukemia associated with RNA virus and polymorphism of 1qh+. 616 26

We have determined the sequence of a cloned DNA fragment 1108 base pairs long which corresponds to the 3' end of the Moloney murine leukemia provirus. The clone was obtained as the primary product of reverse transcription and begins with the Moloney "strong stop" sequence, then extends towards the 5' end of the provirus. Our sequence: (i) proves that reverse transcriptase switches templates during minus strand synthesis; (ii) defines the limits of the 515-base-pair repeats which occupy both ends of the integrated provirus; (iii) shows that the structure of the proviral repeats has strong analogy to bacterial insertion sequences, indicating that the Moloney provirus is a transposon; (iv) identifies the putative promotor for genomic transcription within these repeats; (v) shows that the presumed origin of second strand synthesis, which lies just outside the 3' repeat, has tertiary structure analogous to single-stranded bacteriophage origins of replication; (vi) solves the amino acid sequence of most of pI5E, the carboxy-terminal product of the env gene; (vii) allows detailed mapping of the mink cell focus-forming virus substitution locus in a central location within the gp70 region of the env gene; and (viii) identifies a long open translation frame to the right of the env gene (R gene) which could be involved in leukemogenesis.
...
PMID:Nucleotide sequence of Moloney leukemia virus: 3' end reveals details of replications, analogy to bacterial transposons, and an unexpected gene. 625 54


1 2 3 4 5 6 Next >>

---