ArticleNucleic acids research1991
A novel nuclear inhibitor I-92 regulates DNA binding activity of octamer binding protein p92 during the cell cycle.
Article in Nucleic acids research, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- The enhancer in the long control region of human papillomavirus type 16 is up-regulated by PEF-1 and down-regulated by Oct-1.Journal of virology · 1995Article
- Third colloquium on cellular signal transduction: cell-cycle signalling. German Cancer Research Centre Heidelberg, 14 January 1994.Journal of cancer research and clinical oncology · 1994Article
- Tissue restricted expression and chromosomal localization of the YB-1 gene encoding a 42 kD nuclear CCAAT binding protein.Nucleic acids research · 1992Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear DNA binding protein p92 is a sequence specific octamer binding protein with identical molecular weight as the ubiquitous octamer binding protein Oct-1. It binds to octamer related sequences from the enhancer of human papillomavirus type 18. The activity and intracellular distribution of p92 is regulated by extracellular signals. In serum starved Hela-fibroblast hybrid cells p92 is localized to the cytosol. Serum stimulation leads to nuclear import of p92. In fractions of asynchronously growing cells, which were separated according to cell cycle phases into G1, S, and G2 populations by centrifugal elutriation, p92 DNA binding is confined to S phase. In binding site blots however, p92 DNA binding activity is also present in G1 and G2. In G1 and G2 DNA binding activity of p92 is masked by a novel nuclear inhibitor I-92. The cyclic association of p92 with its inhibitor I-92 provides a new mechanism of regulating S phase dependent activity of a sequence specific DNA binding protein.
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