Anti-CREBBP 抗体

• IHC-P

Lab

Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-CREBBP antibody (AB2832)

IHC image of CREBBP staining in human pancreas formalin fixed paraffin embedded tissue section, performed on a Leica Bond^TM system using the standard protocol F. The section was pre-treated using heat mediated antigen retrieval with sodium citrate buffer (pH6, epitope retrieval solution 1) for 20 mins. The section was then incubated with ab2832, 5μg/ml, for 15 mins at room temperature and detected using an HRP conjugated compact polymer system. DAB was used as the chromogen. The section was then counterstained with haematoxylin and mounted with DPX.

For other IHC staining systems (automated and non-automated) customers should optimize variable parameters such as antigen retrieval conditions, primary antibody concentration and antibody incubation times.

• ICC/IF

Supplier Data

Immunocytochemistry/ Immunofluorescence - Anti-CREBBP antibody (AB2832)

Immunofluorescent analysis of HeLa cells, labeling CREBBP with ab2832 (right) compared with a negative control without ab2832 (left). Cells were formalin fixed, permeabilized with 0.1% Triton X-100 for 5-10 minutes, and blocked with 3% BSA-PBS for 30 minutes at room temperature. Cells were incubated with anti-KAT3A/CBP diluted 1/100 in 3% BSA/PBS overnight at 4°C. Actin was stained using Alexa Fluor 554 (red) and nuclei were stained with DAPI (blue). The nuclear localization of KAT3A/CBP can be observed (green).

• ICC/IF

Supplier Data

Immunocytochemistry/ Immunofluorescence - Anti-CREBBP antibody (AB2832)

Immunofluorescent analysis of MCF-7 cells, labeling CREBBP with ab2832 (right) compared with a negative control without ab2832 (left). Cells were formalin fixed, permeabilized with 0.1% Triton X-100 for 5-10 minutes, and blocked with 3% BSA-PBS for 30 minutes at room temperature. Cells were incubated with anti-KAT3A/CBP diluted 1/100 in 3% BSA/PBS overnight at 4°C. Actin was stained using Alexa Fluor 554 (red) and nuclei were stained with DAPI (blue). The nuclear localization of KAT3A/CBP can be observed (green).

• IHC-P

Supplier Data

Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-CREBBP antibody (AB2832)

Immunohistochemical analysis of FFPE mouse colon tissue, labeling CREBBP with ab2832 (right) compared with a negative control without ab2832 (left). Heat antigen retrieval performed with 10mM Sodium Citrate (pH 6) for 8-15 minutes. Tissue blocked with 3% H2O2-methanol for 15 minutes at room temperature. Incubation with ab2832 diluted 1/2000 in 3% BSA-PBS overnight at 4°C. Counterstaining with hematoxylin.

• ICC/IF

Supplier Data

Immunocytochemistry/ Immunofluorescence - Anti-CREBBP antibody (AB2832)

Immunofluorescent analysis of NIH-3T3 cells, labeling CREBBP with ab2832 (right) compared with a negative control without ab2832 (left). Cells were formalin fixed, permeabilized with 0.1% Triton X-100 for 5-10 minutes, and blocked with 3% BSA-PBS for 30 minutes at room temperature. Cells were incubated with anti-KAT3A/CBP diluted 1/100 in 3% BSA/PBS overnight at 4°C. Nuclei were stained with DAPI (blue).

• WB

Unknown

Western blot - Anti-CREBBP antibody (AB2832)

ab2832 using HeLa cell lysate. ab2832 using HeLa cell lysate.

All lanes:

Western blot - Anti-CREBBP antibody (ab2832)

Predicted band size: 265 kDa

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• WB

CiteAb

Western blot - Anti-CREBBP antibody (AB2832)

Western Blotting using Anti-CREBBP antibody, ab2832. Publication image from Solier, S. et al., 2023, Nature, 37100912. Legend direct from paper.

Pharmacological inactivation of mitochondrial copper(II) attenuates inflammation in vivo.a, Western blots of copper-signalling effectors in SPMs from mice treated with LPS. Macrophages of several mice were pooled (4–7 mice per condition). b, Western blots of copper-signalling effectors in SPMs from mice subjected to CLP. Macrophages of several mice were pooled (7–8 mice per condition). H3 is a sample processing control. c, Western blots of copper-signalling effectors in AMs from K18-hACE2 mice infected with SARS-CoV-2. Macrophages of several mice were pooled (10 mice per condition). H3 is a sample processing control. d, Average body temperature of mice treated as indicated (n = 6–9 mice per group). e, GO term analysis of downregulated genes in lung tissues of SARS-CoV-2 infected K18-hACE2 mice treated with LCC-12 (0.5 mg/kg). f, RNA-seq analysis of gene expression in lung tissues of SARS-CoV-2-infected K18-hACE2 mice treated with LCC-12 (0.5 mg/kg) (n = 8 mice per group). Inflammatory signature genes highlighted. Dashed lines, adjusted P value = 0.05. g, Illustration of copper-signalling. Cell plasticity involves upregulation of the cell surface marker CD44, which mediates endocytosis of metal-bound hyaluronates. In the presence of copper(II), NADH reacts with H2O2 to replenish NAD+ in mitochondria, an enzyme cofactor involved in the biosynthesis ofαKG and acetyl-CoA. These co-substrates of iron-dependent demethylases and acetyl-transferases are required for epigenetic and transcriptional programming of inflammation and the regulation of cell plasticity. Pharmacological inactivation of mitochondrial copper(II) blocks NAD(H) redox cycling, leading to distinct epigenetic states and transcriptional profiles. Targeting copper(II) interferes with cell plasticity in immune and cancer cells. For a – c gating strategy of SPMs and AMs see Methods and Supplementary Information. For d 2-way ANOVA. Mean values ± s.e.m. For e and f differential gene expression was assessed with the limma/voom framework. GO enrichment was assessed with the enrichGO method from clusterProfiler. P-values were corrected for multiple testing with the Benjamini-Hochberg procedure.Source data

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