The Experts below are selected from a list of 25809 Experts worldwide ranked by ideXlab platform
Jeanpierre Cartron - One of the best experts on this subject based on the ideXlab platform.
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spleen focus forming virus Long Terminal Repeat insertional activation of the murine erythropoietin receptor gene in the t3cl 2 friend leukemia cell line
Journal of Biological Chemistry, 1991Co-Authors: Catherine Lacombe, S Chretien, V Lemarchandel, P Mayeux, Paulhenri Romeo, Sylvie Gisselbrecht, Jeanpierre CartronAbstract:Abstract We have characterized the structure of the erythropoietin receptor gene promoter in normal murine erythroid tissues and in Friend-induced tumor cells. Using primer extension analysis, we identified two distinct transcriptional start sites, which were located 2 base pairs apart in anemic spleens, fetal liver, Friend-induced tumoral spleens, and mouse erythro-leukemia cells. In contrast, transcription was initiated 37 base pairs upstream of the normal cap sites in T3Cl-2, a Friend virus-induced murine erythroleukemia cell line. Also, the erythropoietin receptor mRNA in T3Cl-2 was overexpressed when compared with other erythroleukemia cell lines. We found that abnormal transcription occurring in T3Cl-2 cells resulted from an erythropoietin receptor gene alteration. Indeed, one erythropoietin receptor allele was rearranged by insertion of a spleen focus-forming virus Long Terminal Repeat within the noncoding region of the first exon, 45 bases upstream of the ATG initiation codon and in the same 5'----3' orientation. The transcription of the rearranged allele was shown to be directed from the Long Terminal Repeat promoter, leading to a Long Terminal Repeat-erythropoietin receptor fusion transcript, whereas the normal erythropoietin receptor allele was weakly transcribed. Such altered receptor gene activation may provide a positive pressure in the development of tumorigenic erythroleukemia.
Cecilio López-galíndez - One of the best experts on this subject based on the ideXlab platform.
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Human Immunodeficiency Virus Type 1 Two-Long Terminal Repeat Circles: A Subject for Debate.
AIDS reviews, 2016Co-Authors: Isabel Olivares, Maria Pernas, Concepción Casado, Cecilio López-galíndezAbstract:HIV-1 infections are characterized by the integration of the reverse transcribed genomic RNA into the host chromosomes making up the provirus. In addition to the integrated proviral DNA, there are other forms of linear and circular unintegrated viral DNA in HIV-1-infected cells. One of these forms, known as two-Long Terminal Repeat circles, has been extensively studied and characterized both in in vitro infected cells and in cells from patients. Detection of two-Long Terminal Repeat circles has been proposed as a marker of antiretroviral treatment efficacy or ongoing replication in patients with undetectable viral load. But not all authors agree with this use because of the uncertainty about the lifespan of the two-Long Terminal Repeat circles. We review the major studies estimating the half-life of the two-Long Terminal Repeat circles as well as those proposing its detection as a marker of ongoing replication or therapeutic efficacy. We also review the characteristic of these circular forms and the difficulties in its detection and quantification. The variety of approaches and methods used in the two-Long Terminal Repeat quantification as well as the low reliability of some methods make the comparison between results difficult. We conclude that it is not possible to draw a clear supposition about the lifespan of two-Long Terminal Repeat circles and consequently they should not be used as a marker of ongoing replication without a careful analysis of the methods and results.
Myron Essex - One of the best experts on this subject based on the ideXlab platform.
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Diversity of the HIV-1 Long Terminal Repeat Following Mother-to-Child Transmission
Virology, 2000Co-Authors: Jason T. Blackard, Boris Renjifo, Wafaie W. Fawzi, Beth Chaplin, Gernard I. Msamanga, Myron EssexAbstract:A study of the human immunodeficiency virus Type 1 (HIV-1) 5' Long Terminal Repeat (LTR) was performed to determine the extent of variation found within the LTR from 19 mother-infant pairs in Tanzania and to assess whether the LTR is useful in distinguishing maternal sequences that were transmitted to infants. HIV-1 subtypes A, C, and D as well as intersubtype recombinant LTR sequences were detected in mothers and infants. The LTR subtype was 100% concordant between mothers and their infants. Diversity calculations showed a significant reduction in LTR variation in infants compared to their mothers. However, the overall magnitude of LTR variation was less than that found in the env gene from the same individuals. These data suggest a selective constraint active upon the 5' Long Terminal Repeat that is distinct from immune selective pressure(s) directed against HIV-1 structural genes. Detection of maternal LTR variants that were transmitted to infants may yield important information concerning nonstructural determinants of HIV-1 transmission from mother to infant.
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Transmission of human immunodeficiency type 1 viruses with intersubtype recombinant Long Terminal Repeat sequences.
Virology, 1999Co-Authors: Jason T. Blackard, Boris Renjifo, Davis Mwakagile, Monty Montano, Wafaie W. Fawzi, Myron EssexAbstract:Abstract Retroviruses such as human immunodeficiency virus type 1 (HIV-1) contain two RNA strands per virion, and recombination can occur frequently during reverse transcription. Recombination may occur between HIV-1 genomes of the same subtype or among genomes of two or more distinct subtypes present in an individual. In the current study, we found that recombinatorial events were not limited to viral structural genes such as gag and env, but rather, recombination could likewise occur within the 5′ Long Terminal Repeat (LTR). Intersubtype recombinant LTRs among HIV-1 subtypes A, C, and D were found in Tanzanian infants. By introducing novel LTR sequences, these recombinant LTR viruses may further increase the adaptive potential and fitness of HIV-1.
John F. Mcdonald - One of the best experts on this subject based on the ideXlab platform.
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Long Terminal Repeat retrotransposons of Mus musculus
Genome Biology, 2004Co-Authors: Eugene M Mccarthy, John F. McdonaldAbstract:Background Long Terminal Repeat (LTR) retrotransposons make up a large fraction of the typical mammalian genome. They comprise about 8% of the human genome and approximately 10% of the mouse genome. On account of their abundance, LTR retrotransposons are believed to hold major significance for genome structure and function. Recent advances in genome sequencing of a variety of model organisms has provided an unprecedented opportunity to evaluate better the diversity of LTR retrotransposons resident in eukaryotic genomes. Results Using a new data-mining program, LTR_STRUC, in conjunction with conventional techniques, we have mined the GenBank mouse ( Mus musculus ) database and the more complete Ensembl mouse dataset for LTR retrotransposons. We report here that the M. musculus genome contains at least 21 separate families of LTR retrotransposons; 13 of these families are described here for the first time. Conclusions All families of mouse LTR retrotransposons are members of the gypsy -like superfamily of retroviral-like elements. Several different families of unrelated non-autonomous elements were identified, suggesting that the evolution of non-autonomy may be a common event. High sequence similarity between several LTR retrotransposons identified in this study and those found in distantly-related species suggests that horizontal transfer has been a significant factor in the evolution of mouse LTR retrotransposons.
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Long Terminal Repeat retrotransposons of Oryza sativa.
Genome Biology, 2002Co-Authors: Eugene M Mccarthy, Gao Lizhi, John F. McdonaldAbstract:Background: Long Terminal Repeat (LTR) retrotransposons constitute a major fraction of the genomes of higher plants. For example, retrotransposons comprise more than 50% of the maize genome and more than 90% of the wheat genome. LTR retrotransposons are believed to have contributed significantly to the evolution of genome structure and function. The genome sequencing of selected experimental and agriculturally important species is providing an unprecedented opportunity to view the patterns of variation existing among the entire complement of retrotransposons in complete genomes. Results: Using a new data-mining program, LTR_STRUC, (LTR retrotransposon structure program), we have mined the GenBank rice (Oryza sativa) database as well as the more extensive (259 Mb) Monsanto rice dataset for LTR retrotransposons. Almost two-thirds (37) of the 59 families identified consist of copia-like elements, but gypsy-like elements outnumber copia-like elements by a ratio of approximately 2:1. At least 17% of the rice genome consists of LTR retrotransposons. In addition to the ubiquitous gypsy- and copia-like classes of LTR retrotransposons, the rice genome contains at least two novel families of unusually small, noncoding (non-autonomous) LTR retrotransposons. Conclusions: Each of the major clades of rice LTR retrotransposons is more closely related to elements present in other species than to the other clades of rice elements, suggesting that horizontal transfer may have occurred over the evolutionary history of rice LTR retrotransposons. Like LTR retrotransposons in other species with relatively small genomes, many rice LTR retrotransposons are relatively young, indicating a high rate of turnover.
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Evidence for the recent horizontal transfer of Long Terminal Repeat retrotransposon
Proceedings of the National Academy of Sciences of the United States of America, 1999Co-Authors: I. King Jordan, Lilya V. Matyunina, John F. McdonaldAbstract:The evolutionary dynamics existing between transposable elements (TEs) and their host genomes have been likened to an “arms race.” The selfish drive of TEs to replicate, in turn, elicits the evolution of host-mediated regulatory mechanisms aimed at repressing transpositional activity. It has been postulated that horizontal (cross-species) transfer may be one effective strategy by which TEs and other selfish genes can escape host-mediated silencing mechanisms over evolutionary time; however, to date, the most definitive evidence that TEs horizontally transfer between species has been limited to class II or DNA-type elements. Evidence that the more numerous and widely distributed retroelements may also be horizontally transferred between species has been more ambiguous. In this paper, we report definitive evidence for a recent horizontal transfer of the copia Long Terminal Repeat retrotransposon between Drosophila melanogaster and Drosophila willistoni.
Masabumi Shibuya - One of the best experts on this subject based on the ideXlab platform.
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Unregulated expression of the erythropoietin receptor gene caused by insertion of spleen focus-forming virus Long Terminal Repeat in a murine erythroleukemia cell line.
Molecular and Cellular Biology, 1991Co-Authors: Masayuki Hino, Arinobu Tojo, Y Misawa, H Morii, Fumimaro Takaku, Masabumi ShibuyaAbstract:A murine erythroleukemia (MEL) cell line, F5-5, expressed 10,000 binding sites for erythropoietin (EPO) per cell, 10-fold more than was expressed by other murine erythroleukemia cell lines and normal erythroid progenitors. Northern (RNA) and Southern blot analyses revealed overexpression of mRNA for the EPO receptor (EPOR) and rearrangement of one of the EPOR gene alleles in F5-5 cells, respectively. Molecular cloning of F5-5-derived cDNA encoding EPOR revealed that the 5' noncoding region of the EPOR cDNA corresponds to the 3' Long Terminal Repeat sequence of the polycythemic strain of Friend spleen focus-forming virus (F-SFFVP). The aberrant EPOR transcripts containing the 3' Long Terminal Repeat sequence were mainly expressed in F5-5 cells. The same integration upstream of the EPOR gene was also observed in other subclones and the parent cell line. It is possible that overexpression of EPOR by viral promoter insertion will confer growth advantage to an F-SFFVP-infected erythroid progenitor cell, leading to positive clonal selection through further leukemogenic steps.
