Characterization of the Nuclear Binding Sites (Acceptor Sites) for a Steroid Receptor

Spelsberg, Thomas C.; Goldberger, Amy; Hora, J.; Horton, Michael; Littlefield, Bruce A.

doi:10.1007/978-1-4612-4686-2_8

Cited by 5 publications

(4 citation statements)

References 52 publications

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“…Previous work from this laboratory has demonstrated that whole nuclei chromatin and nuclear matrix from the avian oviducts contains saturable, high-affinity binding sites for activated progesterone receptors (PR) ( − ). Pure genomic DNA did not display these high-affinity, saturable kinetics with PR or other steroid receptors ( − ). Other laboratories, studying other steroid receptor systems, have also reported specific receptor sites (acceptor sites) in the nuclear chromatin for a variety of steroid receptors (for reviews see refs 14−17 ).…”

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confidence: 99%

“…These sites displayed in vivo-like patterns of binding using seasonally active and inactive PR ( 2 , 7 , 10 , 12 ). Moreover, this binding by RBF displayed a genomic DNA specificity in the reconstituted complex by not binding to insect or bacterial genomic DNA ( , ). These data support that the RBF appears to be an essential protein component of progesterone receptor nuclear acceptor sites, or, at least, a component of a subset of these sites in the chromatin structure and that specific DNA elements may be required for these sites.…”

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Interactions of the Nuclear Matrix-Associated Steroid Receptor Binding Factor with Its DNA Binding Element in the c-myc Gene Promoter

et al. 2000

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Steroid receptor binding factor (RBF) was originally isolated from avian oviduct nuclear matrix. When bound to avian genomic DNA, RBF generates saturable high-affinity binding sites for the avian progesterone receptor (PR). Recent studies have shown that RBF binds to a 54 bp element in the 5'-flanking region of the progesterone-regulated avian c-myc gene, and nuclear matrix-like attachment sites flank the RBF element [Lauber et al. (1997) J. Biol. Chem. 272, 24657-24665]. In this paper, electrophoretic mobility shift assays (EMSAs) and S1 nuclease treatment are used to demonstrate that the RBF-maltose binding protei (MBP) fusion protein binds to single-stranded DNA of its element. Only the N-terminal domain of RBF binds the RBF DNA element as demonstrated by southwestern blot analyses, and by competition EMSAs between RBF-MBP and the N-terminal domain. Mass spectrometric analysis of the C-terminal domain of RBF demonstrates its potential to form noncovalent protein-protein interactions via a potential leucine-isoleucine zipperlike structure, suggesting a homo- and/or possible heterodimer structure in solution. These data support that the nuclear matrix binding site (acceptor site) for PR in the c-myc gene promoter is composed of RBF dimers bound to a specific single-stranded DNA element. The dimers of RBF are generated by C-terminal leucine zipper and the DNA binding occurs at the N-terminal parallel beta-sheet DNA binding motif. This complex is flanked by nuclear matrix attachment sites.

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confidence: 99%

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Interactions of the Nuclear Matrix-Associated Steroid Receptor Binding Factor with Its DNA Binding Element in the c-myc Gene Promoter

et al. 2000

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“…Its receptor plays an essential role in the mechanism of recognition and transduction of the hormonal signal (3,5,6,20,21,28,51,55). The hormone binds with high affinity to its specific receptor protein, which then becomes activated.…”

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Gene expression of steroid hormone receptors in brain and peripheral tissues relative to reproduction.

Kato¹,

Hirata²,

Hagihara³

et al. 1992

Acta Histochem. Cytochem

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“…In some systems, a requirement for protein synthesis during this lag period is required for the subsequent induction of the mRNA levels (3,4). A cascade model for steroid hormone action has been proposed whereby steroids rapidly regulate the expression of "early" (regulatory) genes during the lag phase (5)(6)(7)(8)(9). The products of these regulatory genes in turn regulate the expression of individual or whole groups of "late" structural genes.…”

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Rapid induction of the c-jun protooncogene in the avian oviduct by the antiestrogen tamoxifen.

Lau

Subramaniam

Rasmussen

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

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This report describes a rapid regulation of the expression of the c-jun protooncogene by the antiestrogen tamoxifen (Tam). The c-jun protooncogene codes for an important component of the AP-1 transcription factor complex, which regulates the expression of many unlinked genes. Repeated experiments have shown that Tam rapidly increases the steady-state c-jun mRNA levels in the avian oviduct but decreases the levels in the liver. The Tam effects are time- and dose-dependent. These results are supported by other studies that have demonstrated that 17 beta-estradiol decreases steady-state levels of c-jun protooncogene mRNA in oviducts of animals fully withdrawn from estradiol. The effect of Tam in the avian oviduct is in contrast to the reported effects of Tam on the expression of practically all other genes in the avian oviduct and other animal tissues. Transcription analyses using nuclear runoff experiments with oviduct nuclei demonstrate a decrease in the c-jun gene transcription within minutes after Tam treatment with a return to 75% of control values by 4 hr. The fact that Tam transiently decreases the transcription of the c-jun gene but increases the steady-state c-jun mRNA levels suggests that Tam must alter both transcriptional and post-transcriptional events. The results support a role of the c-jun protooncogene as a regulatory gene in the cascade model for steroid action whereby steroids rapidly regulate the regulatory genes, which in turn regulate many other structural genes.

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Characterization of the Nuclear Binding Sites (Acceptor Sites) for a Steroid Receptor

Cited by 5 publications

References 52 publications

Interactions of the Nuclear Matrix-Associated Steroid Receptor Binding Factor with Its DNA Binding Element in the c-myc Gene Promoter

Interactions of the Nuclear Matrix-Associated Steroid Receptor Binding Factor with Its DNA Binding Element in the c-myc Gene Promoter

Gene expression of steroid hormone receptors in brain and peripheral tissues relative to reproduction.

Rapid induction of the c-jun protooncogene in the avian oviduct by the antiestrogen tamoxifen.

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