ArticleJournal of virology1992
Induction of E1A-responsive negative factors for transcription of the fibronectin gene in adenovirus E1-transformed rat cells.
Article in Journal of virology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Proteasomal inhibition potentiates drugs targeting DNA topoisomerase II.Biochemical pharmacology · 2016Article
- KSHV regulation of fibulin-2 in Kaposi's sarcoma: implications for tumorigenesis.The American journal of pathology · 2011Article
- Human papillomavirus type 16 E7 oncoprotein represses transcription of human fibronectin.Journal of virology · 2000Article
- Cloning and characterization of a GC-box binding protein, G10BP-1, responsible for repression of the rat fibronectin gene.Molecular and cellular biology · 1998Article
- Induction of Sp1 in differentiating human embryonal carcinoma cells triggers transcription of the fibronectin gene.Molecular and cellular biology · 1998Article
- Sp1-mediated transactivation of LamC1 promoter and coordinated expression of laminin-gamma1 and Sp1 in human hepatocellular carcinomas.The American journal of pathology · 1997Article
- DNA binding proteins from keloid fibroblasts form unique complexes with the human fibronectin promoter.Gene expression · 1996Article
- Transcription factor TFIID is a direct functional target of the adenovirus E1A transcription-repression domain.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- G10BP, an E1A-inducible negative regulator of Sp1, represses transcription of the rat fibronectin gene.Molecular and cellular biology · 1995Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The level of fibronectin (FN) gene expression is very high in resting rat 3Y1 cells but greatly decreased in adenovirus E1-transformed cells. To study the mechanism of this down-regulation, nuclear factors binding to the 5'-flanking region of the FN gene were analyzed by gel retardation assay and DNase I footprinting. Nuclear factors that were present in the transformed cells but nearly absent in resting 3Y1 cells interacted with multiple sites of the promoter region. Oligonucleotide competition with the FN promoter-chloramphenicol acetyltransferase (CAT) reporter constructs (pFCAT) for these factors in the transformed cells indicated that all of them had a negative effect on FN gene expression. Of them, a factor(s) (G10BP) binding to the G10 stretch from positions -239 to -230 and to two GC boxes consisting of the G10 stretch with one internal C residue insertion from positions -105 to -95 and -54 to -44 had the strongest repressive activity. Introduction of substitutive mutations into these G-rich sequences resulted in the increase in CAT activity of pFCAT in the transformed cells. The recognition sequences of G10BP and Sp1 overlap in two GC boxes. G10BP has stronger affinity for heparin and GC boxes than does Sp1, suggesting that G10BP may repress FN gene transcription by displacing Sp1.
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