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Journal ArticleDOI

Non-function of a Moloney murine leukaemia virus regulatory sequence in F9 embryonal carcinoma cells

TLDR
Evidence is presented which supports the hypothesis that certain M-MuLV regulatory sequences do not function in EC cells and that viral gene expression is not observed even at early times.
Abstract
Moloney murine leukaemia virus (M-MuLV) infection of embryonal carcinoma (EC) cells results in the integration of proviral DNA into the host cell genome, but not in virus production. One suggested explanation for the lack of viral gene expression in EC cells has been methylation of the integrated viral DNA. However, subsequent reports indicated that integration of the M-MuLV DNA occurs soon after infection, but that viral DNA methylation occurs considerably later. Nevertheless, viral gene expression is not observed even at early times. One possible explanation is that certain M-MuLV regulatory sequences do not function in EC cells. We now present evidence which supports this hypothesis.

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Citations
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Journal ArticleDOI

Progress toward human gene therapy

TL;DR: The most well-known models involve alteration of mutant target genes by gene transfer with recombinant pathogenic viruses in order to express new genetic information and to correct disease phenotypes.
Journal ArticleDOI

Genetically modified skin fibroblasts persist long after transplantation but gradually inactivate introduced genes.

TL;DR: In this article, the authors used retroviral vectors carrying genes encoding human adenosine deaminase and neomycin phosphotransferase to produce therapeutic proteins in animals.
Journal ArticleDOI

TRIM28 mediates primer binding site-targeted silencing of murine leukemia virus in embryonic cells.

TL;DR: It is shown that RNAi-mediated knockdown of TRIM28 in EC and ES cells relieves the restriction and that TRIM 28 is bound to the PBS in vivo when restriction takes place and added to the growing body of evidence that many TRIM family proteins are involved in retroviral restriction.
Book ChapterDOI

The intracisternal A-particle gene family: structure and functional aspects.

TL;DR: This chapter reviews the various aspects of research on intracisternal type A particles—expression in early development, genomic sequences as chromosomal genes and transposable elements, general molecular biology, and proteins as neoantigen in autoimmune diabetes.
Journal ArticleDOI

Negative regulation of viral enhancers in undifferentiated embryonic stem cells.

TL;DR: It is proposed that the undifferentiated cells contain a trans-acting regulatory factor (or factors) that reduces transcription by interacting with viral enhancers and results in inactivation of the SV40 early promoter in these cells.
References
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Journal ArticleDOI

Recombinant genomes which express chloramphenicol acetyltransferase in mammalian cells.

TL;DR: A series of recombinant genomes which directed expression of the enzyme chloramphenicol acetyltransferase (CAT) in mammalian cells provided a uniquely convenient system for monitoring the expression of foreign DNAs in tissue culture cells.
Journal ArticleDOI

A lymphocyte-specific cellular enhancer is located downstream of the joining region in immunoglobulin heavy chain genes

TL;DR: It is proposed that this tissue-specific enhancer contributes to the activation of somatically rearranged immunoglobulin variable region genes and possibly to abnormal expression of other genes (e.g. c-myc) that become translocated to its domain of influence.
Journal ArticleDOI

A tissue-specific transcription enhancer element is located in the major intron of a rearranged immunoglobulin heavy chain gene

TL;DR: The DNA sequences derived from the germ line JH-C mu region are found to be required for accurate and efficient transcription from a functionally rearranged VH promoter, and the Ig gene enhancer appears to act in a tissue-specific manner.
Book

RNA tumor viruses

TL;DR: This book contains 12 selections of retroviral diseases and some of the titles are: Genome Structure;Genetics of Retroviruses;Functions and Origins of Retoviral Transforming Genes;Human T-cell RetrovIRuses;Replications of Retrospective Viruses; and Endogenous Viruses.
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