The interaction of a c-Jun/Fos related protein factor with the U3 sequences of the mouse mammary tumor virus LTR

Siddique, H.; Sarkar, Nurul H.

doi:10.1016/s0006-291x(05)80216-5

Cited by 5 publications

(2 citation statements)

References 33 publications

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“…At least three negative regulatory elements have been described between Ϫ861 and Ϫ364 (41). An AP-1 site has also been described between position Ϫ766 and Ϫ737 (45). We identified in this work a consensus STAT5-binding site between positions Ϫ923 and Ϫ914 of the MMTV-LTR and showed the involvement of this sequence in the IL-2 positive regulation of the promoter activity, but not in the IL-2 inhibitory effect on DEXinduced MMTV transactivation.…”

Section: Role Of Coactivators In Il-2 Inhibition Of Gc-induced P2grsupporting

confidence: 53%

Interleukin-2 Inhibits Glucocorticoid Receptor Transcriptional Activity through a Mechanism Involving STAT5 (Signal Transducer and Activator of Transcription 5) but Not AP-1

Biola

Lefèbvre

Perrin-Wolff

et al. 2001

Molecular Endocrinology

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Cytokines and glucocorticoids (GCs) signaling pathways interfere with each other in the regulation of apoptosis and gene expression in the immune system. Interleukin-2 (IL-2), through the Janus kinase/signal transducers and activators of transcription (Jak/STAT) and mitogen-activated protein kinase (MAPK) pathways, activates STAT5 and activated protein-1 (AP-1) transcription factors, respectively, which are known to repress glucocorticoid receptor (GR) activity, at least in part, through protein-protein interactions. In this work, we have analyzed the mechanisms whereby IL-2 down-regulates the GC-induced transactivation of the mouse mammary tumor virus long terminal repeat (MMTV-LTR) in murine CTLL-2 T lymphocytes. Mutagenesis studies revealed that the MMTV-LTR STAT5 binding site (-923/-914) was not required for IL-2-mediated inhibition but identified both glucocorticoid response elements (GREs) and the -104/+1 region as critical elements for this negative response. The DNA binding activities of transcription factors required for GC-mediated activation of the MMTV-LTR promoter and that bind to the -104/+1 region (nuclear factor-1, Oct-1) were not affected by IL-2 treatment. Overexpression of wild-type STAT5B enhanced the effect of IL-2 on MMTV-LTR activity, and a dominant negative form of STAT5B (Y699F) abolished the IL-2-mediated MMTV-LTR inhibition, whereas AP-1 activation had no effect in this system. Direct interaction between liganded GR and STAT5 was observed in CTLL-2 cells in a STAT5 phosphorylation-independent manner. Overexpression of nuclear coactivators CBP (CREB-binding protein) or SRC-1a (steroid receptor coactivator 1a) did not blunt IL-2 inhibitory effects. We suggest that the STAT5-repressive activity on the GC-dependent transcription may involve direct interaction of STAT5 with GR, is dependent on the promoter context and STAT5 activation level, and occurs independently of coactivators levels in T cells.

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Section: Role Of Coactivators In Il-2 Inhibition Of Gc-induced P2grsupporting

confidence: 53%

Interleukin-2 Inhibits Glucocorticoid Receptor Transcriptional Activity through a Mechanism Involving STAT5 (Signal Transducer and Activator of Transcription 5) but Not AP-1

Biola

Lefèbvre

Perrin-Wolff

et al. 2001

Molecular Endocrinology

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“…; 17 contains numerous binding sites for many transcription factors 34–3745–47 These transcription factors have been shown to interact with GR and alter GR–induced MMTV promoter activity through influencing the chromatin structure of the promoter. For example, HNF3 has been shown to associate with GR,48 facilitate GR-DNA binding49–52 and alter the chromatin structure of the MMTV LTR 34.…”

Section: Discussionmentioning

confidence: 99%

Bacillus anthracis Lethal Toxin Represses MMTV Promoter Activity through Transcription Factors

Kang

Marketon

Johnson

et al. 2009

Journal of Molecular Biology

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We have recently shown that the anthrax lethal toxin (LeTx) selectively represses nuclear hormone receptors. In the current studies, we found that LeTx repressed activation of the MMTV promoter related to over-expression of the transcription factors, HNF3, Oct1 and c-Jun. LeTx transcriptional repression was associated with a decrease in protein levels of these transcription factors in a lethal factor (LF) protease activity dependent manner. Early administration of LeTx antagonists partially or completely abolished the repressive effects of LeTx. In contrast to the rapid cleavage of MAPKKs by LeTx, the degradation of these transcription factors occurred at a relatively late stage after LeTx treatment. In addition, LeTx repressed phorbol 12-myristate 13-acetate (PMA) -induced MMTV promoter activity and PMA-induction of endogenous c-Jun protein. Collectively, these findings suggest that transcription factors are intracellular targets of LeTx and expand our understanding of the molecular action of LeTx at a later stage of low-dose exposure.

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The glucocorticoid receptor precludes the binding of a transcriptional repressor protein to the long terminal repeat of the mouse mammary tumor virus

Kmiec

1993

Mol Cell Biochem

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The long terminal repeat (LTR) of the mouse mammary tumor virus was used as a template to examine the dual binding parameters of the glucocorticoid-receptor (GR) and a repressor protein termed Inhibitory Factor 1 (IF1). The receptor binds specifically to the glucocorticoid response element and precludes the binding of IF1 to its juxtaposed binding site within the LTR. When the two DNA targets are separated by the insertion of an additional 52 base pairs, coincident binding of both proteins is observed. Gel retention assays reveal three distinct nucleoprotein complexes. The first complex consists of the receptor and the LTR, the second is comprised of IF1 and DNA and the third is a multiprotein-DNA complex consisting of the GR, IF1 and DNA, migrating at a higher molecular weight position. The inhibition of IF1 binding by the presence of prebound GR leads to the repression of transcription of juxtaposed genes. The GR may act to block access of a sequence, used by the cell to titrate repressor proteins and facilitate the onset of gene expression.

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The interaction of a c-Jun/Fos related protein factor with the U3 sequences of the mouse mammary tumor virus LTR

Cited by 5 publications

References 33 publications

Interleukin-2 Inhibits Glucocorticoid Receptor Transcriptional Activity through a Mechanism Involving STAT5 (Signal Transducer and Activator of Transcription 5) but Not AP-1

Interleukin-2 Inhibits Glucocorticoid Receptor Transcriptional Activity through a Mechanism Involving STAT5 (Signal Transducer and Activator of Transcription 5) but Not AP-1

Bacillus anthracis Lethal Toxin Represses MMTV Promoter Activity through Transcription Factors

The glucocorticoid receptor precludes the binding of a transcriptional repressor protein to the long terminal repeat of the mouse mammary tumor virus

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