Loss of responsiveness of an AP1-related factor, PEBP1, to 12-O-tetradecanoylphorbol-13-acetate after transformation of NIH 3T3 cells by the Ha-ras oncogene
- PMID: 2547991
- PMCID: PMC250957
- DOI: 10.1128/JVI.63.9.3669-3677.1989
Loss of responsiveness of an AP1-related factor, PEBP1, to 12-O-tetradecanoylphorbol-13-acetate after transformation of NIH 3T3 cells by the Ha-ras oncogene
Abstract
The function of the A element (nucleotides 5107 to 5130) of the polyomavirus enhancer is augumented in NIH 3T3 cells by a tumor-promoting phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA). One of its targets is an AP1 consensus sequence motif recognized by a nuclear factor, PEBP1. In Ha-ras-transformed NIH 3T3 cells, however, A element function was not enhanced by TPA treatment, and at the same time PEBP1 was not detected in the nuclear extract by a mobility shift assay. PEBP1 was not detected in either the extract from NIH 3T3 cells treated in vivo with a protein kinase inhibitor, staurosporine, or the extract from NIH 3T3 cells after treatment in vitro with phosphatase. These results suggest that PEBP1 is required to be properly phosphorylated for DNA binding and that it is underphosphorylated, possibly due to the downregulation of protein kinase C in Ha-ras-transformed cells. In addition, we observed that PEBP2, which bound to the A element adjacent to PEBP1, was converted to apparently related PEBP3 when conditions favored underphosphorylation.
Similar articles
-
[Signals and transcription factors].Gan To Kagaku Ryoho. 1989 Mar;16(3 Pt 2):509-15. Gan To Kagaku Ryoho. 1989. PMID: 2539780 Review. Japanese.
-
A tumor promoting phorbol ester, TPA, enhances polyomavirus DNA replication by activating the function of the viral enhancer.Oncogene. 1990 Jan;5(1):5-13. Oncogene. 1990. PMID: 2157181
-
Two overlapping sequence motifs within the polyomavirus enhancer are independently the targets of stimulation by both the tumor promoter 12-O-tetradecanoylphorbol-13-acetate and the Ha-ras oncogene.J Virol. 1989 Mar;63(3):1040-8. doi: 10.1128/JVI.63.3.1040-1048.1989. J Virol. 1989. PMID: 2536818 Free PMC article.
-
Effect of a dominant inhibitory Ha-ras mutation on mitogenic signal transduction in NIH 3T3 cells.Mol Cell Biol. 1990 Oct;10(10):5314-23. doi: 10.1128/mcb.10.10.5314-5323.1990. Mol Cell Biol. 1990. PMID: 2118993 Free PMC article.
-
AP1, a composite transcription factor implicated in abnormal growth control.Prog Growth Factor Res. 1989;1(2):69-77. doi: 10.1016/0955-2235(89)90001-x. Prog Growth Factor Res. 1989. PMID: 2518808 Review.
Cited by
-
Cell-shape regulation and matrix protein p52 content in phenotypic variants of ras-transformed rat kidney fibroblasts. Functional analysis and biochemical comparison of p52 with proteins implicated in cell-shape determination.Biochem J. 1991 Feb 1;273 ( Pt 3)(Pt 3):651-8. doi: 10.1042/bj2730651. Biochem J. 1991. PMID: 1996963 Free PMC article.
-
Growth inhibition and induction of differentiation of t(8;21) acute myeloid leukemia cells by the DNA-binding domain of PEBP2 and the AML1/MTG8(ETO)-specific antisense oligonucleotide.Proc Natl Acad Sci U S A. 1994 Nov 22;91(24):11723-7. doi: 10.1073/pnas.91.24.11723. Proc Natl Acad Sci U S A. 1994. PMID: 7972130 Free PMC article.
-
SL3-3 enhancer factor 1 transcriptional activators are required for tumor formation by SL3-3 murine leukemia virus.J Virol. 1991 Aug;65(8):4177-81. doi: 10.1128/JVI.65.8.4177-4181.1991. J Virol. 1991. PMID: 1649324 Free PMC article.
-
Identification of TAZ as a binding partner of the polyomavirus T antigens.J Virol. 2004 Nov;78(22):12657-64. doi: 10.1128/JVI.78.22.12657-12664.2004. J Virol. 2004. PMID: 15507652 Free PMC article.
-
An association of a simultaneous nuclear and cytoplasmic localization of Fra-1 with breast malignancy.BMC Cancer. 2006 Dec 28;6:298. doi: 10.1186/1471-2407-6-298. BMC Cancer. 2006. PMID: 17192200 Free PMC article.
References
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Molecular Biology Databases
Research Materials
Miscellaneous