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Results: 6

1.
Fig 4

Fig 4. From: CBP Mediates NF-?B-Dependent Histone Acetylation and Estrogen Receptor Recruitment to an Estrogen Response Element in the BIRC3 Promoter.

ER recruitment to the BIRC3 promoter requires E2, TNF-α and the NF-κB pathway. (A) ChIP assays for ER were carried out following treatment of MCF-7 cells with E2, TNF-α, or both for up to 60 min, and recruitment to the BIRC3 promoter was examined. (B) ER recruitment to BIRC3 was carried out by ChIP assay following 24 h of exposure to IκBα-DN and 45 min of treatment with E2, TNF-α, or both. *, P < 0.05 compared to treatment with E2 or TNF-α alone.

Madhumita Pradhan, et al. Mol Cell Biol. 2012 January;32(2):569-575.
2.
Fig 6

Fig 6. From: CBP Mediates NF-?B-Dependent Histone Acetylation and Estrogen Receptor Recruitment to an Estrogen Response Element in the BIRC3 Promoter.

Role of CBP in BIRC3 expression, ER recruitment, and histone acetylation around the ERE. (A) MCF-7 cells were transfected with siRNA for CBP, and regulation of BIRC3 mRNA by E2, TNF-α, or both was assessed by qPCR. (B) ER recruitment to the BIRC3 promoter was assessed by ChIP assays following transfection with siNeg, siER, or siCBP and treatment with E2 plus TNF-α for 15 min. Data are represented as a percentage of ER recruitment relative to the siNeg control. (C) Acetylated H3 and H4 at the ERE were examined following transfection with siNeg or CBP. *, P < 0.05, **, P < 0.01, and ***, P < 0.001, compared to the siNeg control. (D) ChIP assays for CBP or IgG were carried out after 15 min of treatment with E2, TNF-α, or both.

Madhumita Pradhan, et al. Mol Cell Biol. 2012 January;32(2):569-575.
3.
Fig 1

Fig 1. From: CBP Mediates NF-?B-Dependent Histone Acetylation and Estrogen Receptor Recruitment to an Estrogen Response Element in the BIRC3 Promoter.

Estradiol (E2) cannot induce expression of BIRC3 but potentiates regulation by proinflammatory cytokines. MCF-7 cells were treated for 2 h with increasing doses of TNF-α in the absence or presence of 10 nM E2 (A), 10 ng/ml IL-1β or IL-6 in the absence or presence of 10 nM E2 (B), increasing doses of E2 in the absence or presence of 10 ng/ml TNF-α (C), or 10 nM E2 and/or 10 ng/ml TNF-α in the absence or presence of 1 μM 4-hydroxytamoxifen (TAM) (D). BIRC3 mRNA was measured by qPCR, and fold change was calculated using the ΔΔCT method with 36B4 as an internal control. The data represent the means ± SEM for three independent replicates. *, P < 0.05 compared to treatment with either E2 or cytokine alone. nd, not detectable; ns, not significant.

Madhumita Pradhan, et al. Mol Cell Biol. 2012 January;32(2):569-575.
4.
Fig 5

Fig 5. From: CBP Mediates NF-?B-Dependent Histone Acetylation and Estrogen Receptor Recruitment to an Estrogen Response Element in the BIRC3 Promoter.

TNF-α and p65 cause enrichment of acetylated histones around the BIRC3 ERE. (A) AcH3 and AcH4 were examined by ChIP assay in MCF-7 cells treated with TNF-α for 15 min. Enrichment was calculated by first dividing the percentage of input for each AcH3 or AcH4 pulldown by the percentage of input for the total amount of H3 or H4, respectively, and second by comparing the ratio of acetylated to total histones in TNF-α-treated cells to that in vehicle-treated control cells. PCR was carried out using small amplicons that tile along the BIRC3 promoter. *, P < 0.05 compared to an untreated control. (B) Acetylation of H3 and H4 at the ERE was assessed following transfection with siNeg (control) or sip65 and treatment with or without TNF-α for 15 min. Fold change was calculated from the percentage of input for each pulldown and comparison to untreated siNeg controls for 3 independent experiments. **, P < 0.01 compared to untreated siNeg control. (C) p65 protein levels were examined by Western blotting in MCF-7 cells transfected with siNeg or sip65 for 48 h.

Madhumita Pradhan, et al. Mol Cell Biol. 2012 January;32(2):569-575.
5.
Fig 2

Fig 2. From: CBP Mediates NF-?B-Dependent Histone Acetylation and Estrogen Receptor Recruitment to an Estrogen Response Element in the BIRC3 Promoter.

The NF-κB pathway is required for enhanced BIRC3 expression by the combination of E2 and TNF-α. (A) BIRC3 mRNA expression was examined in MCF-7 cells following 24 h of exposure to adenoviral vectors for GFP (control) or a dominant-negative form of IκBα (IκBα-DN) and an additional 2 h of treatment with E2, TNF-α, or both. (B) MCF-7 cells were transiently transfected with a BIRC3 promoter reporter construct spanning bp −527 to +55 of the promoter, in which the NF-κB response elements (NF1 and NF3) were intact (−527) or mutated (mNF1/3). Dual-luciferase assays were carried out following 4 h of treatment with E2, TNF-α, or both. (C) ChIP assays were carried out for p65 following treatment of MCF-7 cells with E2, TNF-α, or both for various lengths of time. The fold-increase in p65 occupancy at the BIRC3 promoter was calculated from the percent input of each pulldown and then comparing each treatment to untreated controls from four independent experiments. *, P < 0.05 compared to treatment with TNF-α alone. nd, not detectable.

Madhumita Pradhan, et al. Mol Cell Biol. 2012 January;32(2):569-575.
6.
Fig 3

Fig 3. From: CBP Mediates NF-?B-Dependent Histone Acetylation and Estrogen Receptor Recruitment to an Estrogen Response Element in the BIRC3 Promoter.

The ability of estrogen to enhance BIRC3 expression requires an intact estrogen response element (ERE) and ER binding to DNA. (A) Schematic representation of the BIRC3 promoter showing the relative position of a putative ERE upstream of two functional NF-κB response elements (NF1 and NF3) (44). (B) MCF-7 cells were transfected with the BIRC3 promoter reporter construct in which the ERE was intact (−527), a region of the promoter containing the ERE was deleted (−247), or the ERE was mutated (mERE). Reporter activity was measured by dual-luciferase assay following 4 h of treatment with E2, TNF-α, or both. (C) Luciferase activity of the −527 promoter fragment, in which the ERE was intact (wild type [WT-ERE]) or mutated to a consensus ERE (Cons-ERE), was measured after 4 h of treatment with E2, TNF-α, or both. (D) BIRC3 mRNA levels were measured in MCF-7 cells treated with E2, TNF-α, or both in the absence or presence of an ER-DNA binding inhibitor, TPBM (20 μM). *, P < 0.05 compared to treatment with TNF-α alone. ns, not significant.

Madhumita Pradhan, et al. Mol Cell Biol. 2012 January;32(2):569-575.

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