Regulation of expression of mouse mammary tumor virus through sequences located in the hormone response element: involvement of cell-cell contact and a negative regulatory factor

Härtig, E.; B, Nierlich; Mink, Sigrun; Nebl, Gabriele; Cato, Andrew C. B.

doi:10.1128/jvi.67.2.813-821.1993

Cited by 27 publications

(5 citation statements)

References 43 publications

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“…These elements are not discussed here since a short fragment of the promoter, lacking the sequences in question, exhibits complete regulation: repression in the absence of hormones and strong hormonal induction dependent on NFI and OTF1. However, other reports suggest the existence of negative regulatory elements in the region between the two blocks of HREs [117][118][119]. In genomic footprinting experiments we have not obtained evidence for the existence of such repressor binding sites in human mammary tumor cells lines (see below and [120]).…”

Section: Other Elementscontrasting

confidence: 59%

Chromatin structure and the regulation of gene expression: remodeling at the MMTV promoter

Beato

1996

J Mol Med

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The role of the various levels of chromatin organization in the control of eukaryotic gene expression is discussed on the basis of recent advances in our understanding of chromatin structure in well-defined model systems. Particular attention is devoted to the precise structure and the possible functions of positioned nucleosomes and to the enzymatic mechanism of nucleosome remodeling. Some of the principles involved are illustrated with genomic footprinting results obtained with the mouse mammary tumor virus promoter, the nucleosomal organization of which is remodeled following transcriptional induction by steroid hormones. In this system a positioned nucleosome is responsible for transcriptional repression prior to hormone administration and participates in hormonal induction by facilitating the functional interaction among transcription factors on the promoter.

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Section: Other Elementscontrasting

confidence: 59%

Chromatin structure and the regulation of gene expression: remodeling at the MMTV promoter

Beato

1996

J Mol Med

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“…The tissue tropism of MMTV may be mediated by the combined action of hormone receptors and of modulatory factors bound to cis-acting elements. By functional assays in tissue culture cells, several positive and negative regulatory elements have been identified in the 5Ј part of the LTR (21,29,41,49,50,52,81). Moreover, the involvement of regions located outside of the HRE in the tissue-specific expression of MMTV was defined by the generation of transgenic mice (reviewed in reference 26) and by the analysis of cloned MMTV variant proviruses, isolated from T-cell lymphomas, with alterations in the U3 region of their LTRs (40,47).…”

mentioning

confidence: 99%

Tissue-specific and ubiquitous factors binding next to the glucocorticoid receptor modulate transcription from the mouse mammary tumor virus promoter

Cavin¹,

Buetti²

1995

J Virol

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Steroid hormones complexed with their receptors play an essential role in the regulation of mouse mammary tumor virus (MMTV) transcription. However, the need for additional tissue-specific regulatory factors is suggested by the lack of virus expression in liver, in which glucocorticoid receptors are highly abundant, and by the tissue-specific transcription of reporter genes linked to an MMTV long terminal repeat in transgenic mice. In this study, we characterized two distal-region regulatory elements, DRa and DRc, which, together with the distal glucocorticoid receptor binding site (DRb), increased transcription from the MMTV promoter in permissive cells. This was demonstrated by transfection of these sequences (DRa, DRb, and DRc) in different combinations with the natural MMTV promoter in mouse fibroblasts and mammary epithelial cells, followed by quantitative S1 nuclease mapping of the transcripts. We further showed by DNase I footprinting, methylation interference, and gel retardation assays with various nuclear extracts from permissive or nonpermissive tissues and cell lines that the factors binding to the DRa site are distinct and tissue-specific whereas those binding to DRc are ubiquitous.

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“…20,21 In the MMTV long terminal repeat (LTR), a complex array of binding sites exists for the hormone receptors located between −202 and −59 upstream of the start of transcription that mediates hormonal induction of the provirus. 22‐23 These HREs, when separated from the MMTV LTR promoter and cloned in front of an otherwise hormone‐insensitive gene such as bacterial chloramphenicol acetyltransferase (CAT), confer hormone inducibility upon this gene. 24‐26 Clone 1471.1 cells containing a stable MMTV‐CAT construct were cultured in the presence of increasing concentrations of corticosterone for 48 h. AED did not induce independent transcription of the CAT gene (data not presented).…”

Section: Resultsmentioning

confidence: 99%

Steroid Hormone Regulation of Antiviral Immunity

Padgett

Loria

Sheridan

2000

Annals of the New York Academy of Sciences

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A BSTRACT : Recent observations in both humans and animals have demonstrated that stress is immunomodulatory and can alter the pathogenesis of microbial infections to the extent that it may be adverse to health. Stress disrupts homeostasis, and the body responds through endocrine and nervous system interactions in an effort to re-establish the health of the host. However, the resulting physiologic changes associated with stress, such as the rise in serum glucocorticoids (GCs), are implicated in suppression of antiviral immunity. Therefore, it would be of significance to counterregulate stress-mediated immunosuppression during viral infection to improve immune responses and limit virus-mediated damage. The data in this study focus upon the antiglucocorticoid influence of a native steroid hormone that has been shown to augment immune function and protect animals against lethal viral infections. Androstenediol (5-androstene-3 ␤ ,17 ␤ -diol, AED), a metabolite of dehydroepiandrosterone (DHEA), confers protection against lethal infection with influenza A virus. The protective activity appears to counterbalance the function of the regulatory GCs because AED prevents GC-mediated suppression of IL-1, TNF-␣ , and IL-2 secretion. Furthermore, AED inhibits GC-induced transcription of a GC-sensitive reporter gene.

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Regulation of expression of mouse mammary tumor virus through sequences located in the hormone response element: involvement of cell-cell contact and a negative regulatory factor

Cited by 27 publications

References 43 publications

Chromatin structure and the regulation of gene expression: remodeling at the MMTV promoter

Chromatin structure and the regulation of gene expression: remodeling at the MMTV promoter

Tissue-specific and ubiquitous factors binding next to the glucocorticoid receptor modulate transcription from the mouse mammary tumor virus promoter

Steroid Hormone Regulation of Antiviral Immunity

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