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)

The detection of human papillomavirus (HPV) type 16 early genes: E7, E5, and the late gene: L1 was attempted in 42 uterine cervical neoplasia (35 cervical carcinomas and 7 cervical dysplasias) using the polymerase chain reaction (PCR) method. Consequently, E7 gene was detected in 19 (54.3%) of 35 carcinomas and in 5 (71.4%) of 7 dysplasias, E5 gene was detected in 7 (20.0%) of 35 carcinomas and in 5 (71.4%) of 7 dysplasias, L1 gene was detected in 18 (51.4%) of 35 carcinomas and in 5 (71.4%) of 7 dysplasias, respectively. In order to elucidate the transcriptional pattern of HPV type 16 in each of the clinical stages, the expression of mRNA for E7, E5 and L1 genes was examined in HPV DNA positive cases using the reverse transcriptase polymerase chain reaction (RT-PCR) method. E7 gene mRNA was detected in 18 (94.7%) of 19 cervical carcinomas, whereas E5 and L1 genes mRNAs were detected in only 4 (57.1%) of 7 and in one (5.6%) of 18 carcinomas respectively. In cervical dysplasias, E7, E5 and L1 genes mRNA were detected in all cases. E7, E5 and L1 genes were transcriptionally active in all dysplasias, whereas E5 and L1 genes were not always transcriptionally active in carcinomas. These results suggest that the HPV type 16 early gene E7 is present preferentially as integrated form and transcriptionally active in the carcinoma cell, and plays an important role in the development of malignancy. On the other hand, E5 and L1 genes are present and transcribed in the dysplasia cell but their transcriptional activity is less frequent in the carcinoma cell.
Hiroshima J Med Sci 1992 Dec
PMID:Occurrence and expression of human papillomavirus type 16 genes in uterine cervical carcinomas. 133 65

Paget's disease of bone is a disease of unknown etiology. The demonstration of viral-like particles on ultrastructural examination and the putative detection of viral antibodies and nucleic acids in the tissues suggest a possible viral association. The purpose of this study was to search for nucleic acid sequences homologous to measles virus using the recently described reverse transcriptase (RT) polymerase chain reaction (PCR) in situ hybridization (ISH) technique. After performing RT PCR ISH utilizing primers specific for the nucleocapsid region of the measles virus, an intense signal was evident in most measles-infected HeLa cells compared with a weak signal in few of these cells using standard cDNA-RNA ISH analysis. Amplified measles nucleic acid was detected in tissue from a patient who died of measles infection and was not detected in any of the 11 cases of Paget's disease of bone studied or in a giant cell tumor of bone that had tubuloreticular inclusions on electron microscopy. Therefore, these data suggest that infection by the measles virus is not associated with Paget's disease of bone.
Diagn Mol Pathol 1992 Dec
PMID:In situ analysis of Paget's disease of bone for measles-specific PCR-amplified cDNA. 134 74

Specific binding of radiolabelled FSH and LH to rat ovaries was demonstrated at the age of 7 days. However, when the biological response to LH and FSH was monitored by cAMP production in vitro, the FSH response appeared earlier than that of LH, on days 4 and 7, respectively. Cholera toxin stimulated cAMP production even in fetal ovaries, suggesting the presence of functional post-receptor machinery of cAMP production. Hence, the appearance of the functional gonadotropin receptor probably plays a key role in the onset of postnatal ovarian steroidogenesis. To test the effect of gonadotropin suppression during postnatal ovarian development, a potent GnRH antagonist was administered to neonatal animals between days 1-6 or 1-9 of life. The ovarian responsiveness to FSH developed even in the absence of normal gonadotropin levels, but that to LH was suppressed after the longer antagonist treatment. The temporal relationship between the onset of LHR gene expression, i.e. transcription, and translation to functional receptor protein was thereafter investigated using the reverse transcriptase-polymerase chain reaction (RT-PCR) technique. The measurements revealed the existence only of truncated versions of LHR mRNA in the fetal ovary from day 17 of gestation up to day 7 of postnatal life. With the onset of the receptor function around day 7, also larger mRNA transcripts, corresponding to the full-length receptor protein appeared. Our findings suggest that the LHR gene may be constitutively expressed in the ovary and a change in the alternative splicing pattern may cause the onset of translation of a functional receptor protein.
J Physiol Pharmacol 1992 Dec
PMID:Ontogeny of gonadotropin action in the rat ovary. 134 71

A plasmacytoid leukemia (PL) has caused mortalities in chinook salmon (Oncorhynchus tshawytscha) reared in seawater netpens in western British Columbia, Canada, since 1988. Kidney or eye tissues from 11 of 13 fish from netpens with clinical PL had reverse transcriptase (RT) activity. This RT activity was associated with virus particles of retrovirus morphology and buoyant density. In a transmission experiment, PL-positive donor fish tissues also had RT activity and virus particles of retrovirus morphology and buoyant density, as did recipient fish tissues following development of the disease 6 weeks postinjection with a tissue homogenate from the donor fish. Kidney and spleen tissues from fish that developed PL following injection with an inoculum that was passed through a 0.22-micron filter, in a separate experiment (M. L. Kent and S. C. Dawe. Further evidence for a viral etiology in the plasmacytoid leukemia of chinook salmon Oncorhynchus tshawytscha. Dis. Aquat. Org., in press, 1992), also exhibited RT activity. The virus particles observed by electron-microscopic examination of tissues or sucrose fractions from PL-positive fish were enveloped and were about 110-nm diameter with a central electron-dense core. Polypeptides of about M(r) 120,000, 80,000, 42,000, 27,000, 25,000, 22,000, and 19,000 were observed when purified virus particles were examined by polyacrylamide gel electrophoresis analysis. Many infectious neoplasms of animals, including fishes, are caused by retroviruses. The evidence in this study shows the presence of a retrovirus in chinook salmon with PL and further suggests a retroviral etiology of the disease. We are tentatively calling this virus salmon leukemia virus.
Cancer Res 1992 Dec 01
PMID:A retrovirus in chinook salmon (Oncorhynchus tshawytscha) with plasmacytoid leukemia and evidence for the etiology of the disease. 138 64

BL/VL3 radiation leukemia virus (RadLV) is a thymotropic, highly leukemogenic murine leukemia virus (MuLV) which is unable to replicate in vitro in mouse fibroblasts. We have previously reported that the U3 long terminal repeat region of its genome is responsible for this block (E. Rassart, Y. Paquette, and P. Jolicoeur, J. Virol. 62:3840-3848, 1988). By using hybrids of permissive and resistant cells infected with BL/VL3 RadLV or fibrotropic MuLV, we found that the resistant phenotype was dominant. Investigation to determine at which step of the virus cycle the block operates revealed that integration, transcription, and translation of the BL/VL3 viral genome occurred at normal levels in nonpermissive cells. The BL/VL3 RadLV Pr65gag proteins made in nonpermissive cells were also myristylated and located at the membrane, and the levels of their cleaved products were similar to those of fibrotropic MuLV. However, processing of BL/VL3 RadLV Pr85env was impaired in nonpermissive cells. Virions were not released into the culture medium of nonpermissive cells, as measured by reverse transcriptase activity and by content in p30 or gp70 protein and as documented by lower levels of budding particles seen by electron microscopy. These results indicate that BL/VL3 RadLV replication is blocked at a late stage of the virus cycle, i.e., at virion assembly. Interestingly, these BL/VL3 RadLV-infected nonpermissive fibroblasts were resistant to superinfection by fibrotropic Moloney MuLV, and this resistance also occurred at a late step of the Moloney virus cycle. Since this block is dominant, it appears that the U3 long terminal repeat region of the BL/VL3 viral genome has the ability to induce a cellular suppressor factor(s), thus bringing intracellular immunity against itself and against other ecotropic MuLVs.
J Virol 1992 Dec
PMID:U3 long terminal repeat-mediated induction of intracellular immunity by a murine retrovirus: a novel model of latency for retroviruses. 143 13

Telokin is a protein which consiste of the C-terminal portion of smooth muscle myosin light chain kinase (MLCK) (M. Ito, R. Dabrowska, V. Guerriero, Jr., and D. J. Hartshone (1989) J. Biol. Chem. 264, 13971-13974). In this study, the chicken gizzard telokin cDNA and gene were cloned and analyzed. The telokin cDNA coded 157 amino acid residues which were completely identical to the C-terminal portion of the amino acid sequence of chicken gizzard MLCK. The telokin gene was coded in a 6.3-kb EcoRI genomic fragment and it consisted of three exons. The 5'-leader sequence of the telokin cDNA and genomic sequence revealed that the telokin gene was included in the MLCK gene and the transcription started in the intronic sequence of the MLCK gene. The analysis of the telokin gene suggests that the telokin expression was under the control of an independent promotor. Northern blotting and the reverse transcriptase-polymerase chain reaction methods revealed that telokin was expressed not only in chicken gizzard but also in chicken heart, lung, intestine, and skeletal muscle although the levels of the expression in the latter were much less than that in the gizzard.
Arch Biochem Biophys 1992 Dec
PMID:Molecular cloning of the chicken gizzard telokin gene and cDNA. 144 62

The differentiation status of Sternberg-Reed (SR) cells is still not well defined, primarily because of their scarcity in tumor biopsies of Hodgkin's disease (HD). In this study we have determined the genomic differentiation status of SR cells by quantitation of recombinase activating gene (RAG) expression. RAG genes are selectively transcribed in immature lymphoid cells. In B cells they are silent after genomic rearrangement has occurred, whereas in T cells they are downregulated during positive selection of double-positive thymocytes into single-positive cells. RNA from tumor biopsies either with numerous (11 cases) or a with few SR cells (16 cases) was assessed by a sensitive reverse transcriptase polymerase chain reaction (RT-PCR) and the results compared with established positive and negative controls. In all except two cases levels of RAG expression were within the range of those determined in negative controls. In both positive cases and in the positive control RAG mRNA was further quantitated by competitive PCR. In cases with abundant SR cells RAG expression was still below that observed in 10(-2) dilutions of positive controls. These results suggest that SR cells are derived from lymphoid cells, more differentiated than the pre-B or common thymocyte stage, which have already undergone genomic rearrangement. They show the value of assessing RAG expression by RT-PCR in the characterization of lymphoid malignancies.
Blood 1992 Dec 01
PMID:Expression of human recombination activating genes (RAG-1 and RAG-2) in Hodgkin's disease. 145 Apr 11

The aim of the present study was to determine whether mRNA for the three endothelin peptides (endothelin-1, endothelin-2, and endothelin-3) and the two known receptor subtypes (ETA and ETB) was present in human endometrium at different stages of the menstrual cycle (menstrual, early and mid-proliferative, and early, mid-, and late secretory). Endometrium was obtained from women undergoing surgery for benign disease, and total RNA was extracted using a guanidinium isothiocyanate method. mRNA for endothelin peptide and receptor was detected using the reverse transcriptase-polymerase chain reaction with nested oligonucleotide primers. mRNA for endothelin-1, endothelin-2, and endothelin-3 was demonstrated throughout the menstrual cycle, and three splice variants of mRNA encoding endothelin-3 were found in all samples. The ratio of ETA to ETB receptor mRNA was found to change throughout the menstrual cycle. In the proliferative phase, amplified cDNA product was almost exclusively confined to the ETA receptor, whereas an increase in the amplified product of the ETB receptor cDNA was seen in the secretory and menstrual phases. These studies show that mRNA for endothelin-1, endothelin-2, and endothelin-3 is present in human endometrium at all stages of the menstrual cycle and suggest that different physiological actions of the endothelin peptides may be mediated through changes in the ratio of the ETA and ETB receptor subtypes.
J Clin Endocrinol Metab 1992 Dec
PMID:Presence of messenger ribonucleic acid for endothelin-1, endothelin-2, and endothelin-3 in human endometrium and a change in the ratio of ETA and ETB receptor subtype across the menstrual cycle. 146 62

NF kappa B is a potent mediator of specific gene expression in human monocytes and has been shown to play a role in transcription of the HIV-1 genome in promonocytic leukemias. There is little information available on the response of NF kappa B to cytokines in normal human monocytes. We have used a 32P-labeled oligonucleotide derived from human immunodeficiency virus (HIV-1) long terminal repeat, which contains a tandem repeat of the NF kappa B binding sequence, as a probe in a gel retardation assay to study this transcription factor. Using this assay, we have detected NF kappa B in extracts of nuclei from normal human monocytes. Treatment of normal monocytes with 12-0-tetradecanoyl phorbol-13-acetate (TPA) for 4-24 h caused the complete disappearance of NF kappa B from nuclear extracts of monocytes. A similar result was obtained with the mature monocytic leukemia cell line THP-1. The constitutive transcription factor SP1 was unaffected by addition of TPA. The disappearance of NF kappa B from the nucleus was concentration dependent between 10 and 50 ng/ml of phorbol ester. In THP-1 cells, TPA also induced a new, faster-migrating NF kappa B species not induced in monocytes. Protein kinase C inhibitor staurosporine, but not cyclic nucleotide-dependent protein kinase inhibitor HA-1004, also dramatically reduced constitutive levels of nuclear NF kappa B. Finally, TPA addition to monocytes infected with HIV-1 inhibited HIV-1 replication, as determined by reverse transcriptase assays, in a concentration-dependent manner. These results are in striking contrast to the increase in nuclear NF kappa B and HIV-1 replication induced by phorbol esters in promonocytic leukemia cells U937 and HL-60, and emphasize the importance of studying cytokine regulation of HIV-1 in normal monocytes.
J Leukoc Biol 1992 Dec
PMID:Phorbol ester reduces constitutive nuclear NF kappa B and inhibits HIV-1 production in mature human monocytic cells. 146 36

Estrogen is required for oocyte maturation and embryonic development in vivo; however, the mechanism involved is not clear. Since the effect of estrogen is mediated through the estrogen receptor (ER), we examined the ontogeny and expression of the ER gene in mouse oocytes and embryos of various gestational stages using the highly sensitive reverse transcriptase-polymerase chain reaction (RT-PCR) technique. Total RNA, extracted from 40 ovulated oocytes, 2-cell embryos, morulae, and blastocysts, was reverse transcribed into cDNA. A pair of primers flanking the 453-bp region encoding the hormone-binding domain of ER was used for 30 cycles of PCR. The identity of the amplified product was confirmed by sizing and Southern blot hybridization. The results indicated that ER gene is expressed in unfertilized oocytes and cumulus-oocyte complexes. The amount of ER mRNA decreases in 2-cell embryos, coincident with degradation of maternal mRNA. No ER transcript can be detected in the morulae or blastocyst stage when the embryonic genome has been activated. Postimplantation embryos do not contain detectable ER mRNA until gestation day 8. The levels of ER mRNA increase from day 10 to day 18 of gestation. These data suggest that estrogen, secreted by granulosa cells, may directly influence oocyte growth and maturation in vivo. Since estrogen is known to stimulate the production of growth factors in mouse uteri, the absence of ER mRNA in periimplantation embryos suggests that the effects of estrogen on early embryogenesis may be indirect, i.e., through estrogen-regulated growth-promoting factors produced by the reproductive tract. In mid- and late-post-implantation embryos which contain ER mRNA, estrogen may affect embryonic development through the receptor-mediated mechanisms.
Mol Reprod Dev 1992 Dec
PMID:Expression of estrogen receptor gene in mouse oocyte and during embryogenesis. 147 72


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