Adenovirus E1A-mediated negative control of genes activated during F9 differentiation.
نویسندگان
چکیده
منابع مشابه
Adenovirus 12S E1A gene represses differentiation of F9 teratocarcinoma cells.
The F9 teratocarcinoma cell line differentiates in vitro after treatment with retinoic acid and cAMP and has been a widely used model system for the study of the molecular events that are responsible for cellular commitment and differentiation during early development. Previous experiments have suggested intriguing parallels between the control of gene expression during F9 cell differentiation ...
متن کاملAdenovirus infection of differentiated F9 cells results in a global shut-off of differentiation-induced gene expression.
Previous experiments have demonstrated a link between transcriptional regulatory mechanisms acting during F9 cell differentiation and transcription control by the adenovirus E1A gene. We have isolated a number of differentiation-specific genes by cDNA cloning to determine if E1A exerts a coordinated control over differentiation specific gene expression. The mRNAs encoded by these cDNAs were und...
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We describe a retroviral mediated gene transfer system that facilitates the transfer of heterologous genes into primary epithelial cells. Using a series of retroviral vectors containing the genes coding for the 12S and 13S mRNAs from the E1A region of adenovirus type 5 and the hygromycin resistance gene as a selectable marker, we demonstrate that, when packaged as helper virus-free amphotropic ...
متن کاملpRB-E2F1 complexes are resistant to adenovirus E1A-mediated disruption.
Disruption of pRB-E2F interactions by E1A is a key event in the adenoviral life cycle that drives expression of early viral transcription and induces cell cycle progression. This function of E1A is complicated by E2F1, an E2F family member that controls multiple processes besides proliferation, including apoptosis and DNA repair. Recently, a second interaction site in pRB that only contacts E2F...
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ژورنال
عنوان ژورنال: Molecular and Cellular Biology
سال: 1989
ISSN: 0270-7306,1098-5549
DOI: 10.1128/mcb.9.7.3109