Modulation of the folate receptor type β gene by coordinate actions of retinoic acid receptors at activator Sp1/ets and repressor AP-1 sites

Hong, Hao; Qi, Huiling; Ratnam, Manohar

doi:10.1182/blood-2002-10-3174

Cited by 42 publications

(37 citation statements)

References 48 publications

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“…In the future, it will be of great interest to characterize this AP1 site, since AP1 proteins have been found to functionally cooperate with both Ets and Sp transcription factors in the regulation of several promoters (56,57).…”

Section: Discussionmentioning

confidence: 99%

The Role of Ets Transcription Factors in the Basal Transcription of the Translocator Protein (18 kDa)

et al. 2007

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The translocator protein (18kDa; TSPO), previously known as peripheral-type benzodiazepine receptor, is a high affinity cholesterol-and drug-binding mitochondrial protein involved in various cell functions including steroidogenesis, apoptosis, and proliferation. TSPO is highly expressed in secretory and glandular tissues, especially in steroidogenic cells, and its expression is altered in certain pathological conditions such as cancer and neurological diseases. In this study, we characterized the regulatory elements present in the region of the TPSO promoter extending from 515 to 805-bp upstream of the transcription start site, an area previously identified as being important for transcription. Promoter fragments extending 2.7-kb and 805-bp upstream of the transcription start site were able to direct enhanced green fluorescent protein expression to Leydig cells of the testis, theca cells of the ovary, and cells of the adrenal cortex in transgenic animals. This expression pattern perfectly mimicked endogenous TSPO expression. Functional characterization of the 515 to 805-bp region revealed the presence of one Specificity protein 1/Specificity protein 3 (Sp1/Sp3) and two vets erythroblastosis virus E26 oncogene homolog (Ets) binding sites that are important for transcriptional activity in both MA-10 mouse Leydig tumor cells and NIH/3T3 whole mouse embryo fibroblasts. GA-binding protein α (GABPα) -a member of the Ets family of transcription factorswas found to be associated with the endogenous TSPO promoter. We conclude that Sp1/Sp3 and members of the Ets family of transcription factors bind to specific binding sites in the TSPO promoter to drive basal TSPO gene transcription.

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Section: Discussionmentioning

confidence: 99%

The Role of Ets Transcription Factors in the Basal Transcription of the Translocator Protein (18 kDa)

et al. 2007

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“…However, it is increasingly evident that RA responsiveness is more complex than the conventional model of direct signaling exclusively through RARs. The RA responsiveness of several genes requires transcription factors other than the RARs (6,14,18,39).…”

Section: Discussionmentioning

confidence: 99%

“…An increasing body of evidence indicates that RA responsiveness is not mediated by retinoid receptors alone (6,14,18,39). Surprisingly, the CD18 proximal promoter, alone, accounts for one-half of the RA responsiveness.…”

mentioning

confidence: 99%

GA-Binding Protein and p300 Are Essential Components of a Retinoic Acid-Induced Enhanceosome in Myeloid Cells

Resendes

Rosmarin

2006

Molecular and Cellular Biology

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Expression of CD18, the ␤ chain of the leukocyte integrins, is transcriptionally regulated by retinoic acid (RA) in myeloid cells. Full RA responsiveness of the CD18 gene requires its proximal promoter, which lacks a retinoic acid response element (RARE). Rather, RA responsiveness of the CD18 proximal promoter requires ets sites that are bound by GA-binding protein (GABP). The transcriptional coactivator, p300, further increases CD18 RA responsiveness. We demonstrate that GABP␣, the ets DNA-binding subunit of GABP, physically interacts with p300 in myeloid cells. This interaction involves the GABP␣ pointed domain (PNT) and identifies p300 as the first known interaction partner of GABP␣ PNT. Expression of the PNT domain, alone, disrupts the GABP␣-p300 interaction and decreases the RA responsiveness of the CD18 proximal promoter. Chromatin immunoprecipitation and chromosome conformation capture demonstrate that, in the presence of RA, GABP␣ and p300 at the proximal promoter recruit retinoic acid receptor/retinoid X receptor from a distal RARE to form an enhanceosome. A dominant negative p300 construct disrupts enhanceosome formation and reduces the RA responsiveness of CD18. Thus, proteins on the CD18 proximal promoter recruit the distal RARE in the presence of RA. This is the first description of an RA-induced enhanceosome and demonstrates that GABP and p300 are essential components of CD18 RA responsiveness in myeloid cells.

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“…Forty-eight hours after transfection, cells were treated with vehicle, E 2 (10 nM) or E 2 (10 nM) plus Tam (1 mM) for 60 min, and then subjected to the crosslinking reaction using formaldehyde (1%). Chromatin immunoprecipitation (ChIP) assays were performed as described previously (Hao et al, 2003) with the following modifications. ChIP signals were measured by real-time PCR analysis of chromatinimmunoprecipitated products.…”

Section: Chromatin Immunoprecipitation Assaymentioning

confidence: 99%

Estrogen-induced and TAFII30-mediated gene repression by direct recruitment of the estrogen receptor and co-repressors to the core promoter and its reversal by tamoxifen

et al. 2007

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Estradiol (E 2 ) acts through the estrogen receptor (ER) to downregulate many genes, and tamoxifen (Tam) largely reverses this repression but the underlying mechanisms are unclear. Repression of the folate receptor (FR)-a P4 core promoter by ER is enhanced by E 2 and reversed by Tam. This effect was unaffected by inhibition of new protein synthesis and required the E/F and the DNA-binding domains of ER without direct binding of ER to DNA. The repression by E 2 /ER was not specific for either Sp1 or TATA elements but was loosely selective for the initiator and flanking sequence. Insertion of a response element or a relatively strong Sp1 cluster to recruit ER upstream of the core promoters caused a switch to activation by E 2 /ER that was inhibited by Tam. In nuclear extracts, association of ER with a biotinylated core promoter fragment was promoted by E 2 but Tam blocked this effect. Repression/ de-repression of the P4 promoter and endogenous FR-a expression by E 2 /Tam required SMRT and/or NCoR. ER associated with the chromosomal P4 promoter and SMRT and NCoR associated with it in an ER-dependent manner; these associations were favored by E 2 but disrupted by Tam, in the short term, without changes in ER expression. TAFII30 was required for optimal P4 promoter activity and for the repressive association of ER. E2 may thus maintain a low transcriptional status of genes by favoring direct TAFII30-dependent association of ER with the core promoter in a co-repressor complex containing SMRT and/or NCoR; this repression is overridden in target genes containing an upstream element that strongly recruits ER. In addition to suppressing the activation of classical E2 target genes, Tam may upregulate genes by passively dissociating the ER co-repressor complex.

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Modulation of the folate receptor type β gene by coordinate actions of retinoic acid receptors at activator Sp1/ets and repressor AP-1 sites

Cited by 42 publications

References 48 publications

The Role of Ets Transcription Factors in the Basal Transcription of the Translocator Protein (18 kDa)

The Role of Ets Transcription Factors in the Basal Transcription of the Translocator Protein (18 kDa)

GA-Binding Protein and p300 Are Essential Components of a Retinoic Acid-Induced Enhanceosome in Myeloid Cells

Estrogen-induced and TAFII30-mediated gene repression by direct recruitment of the estrogen receptor and co-repressors to the core promoter and its reversal by tamoxifen

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