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p300 150 inhibitor c646  (MedChemExpress)


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    MedChemExpress p300 150 inhibitor c646
    P300 150 Inhibitor C646, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 131 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p300/C646/pm42575452-54-9-19
    Average 97 stars, based on 131 article reviews
    p300 150 inhibitor c646 - by Bioz Stars, 2026-10
    97/100 stars

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    other:

    Article Title: Gemcitabine-induced β4 integrin drives cancer progression and gemcitabine resistance in pancreatic cancer.
    Article Snippet: IQ1, a specific inhibitor of the p300/-catenin interaction, was obtained from MedChemExpress (#HY10593).

    Article Title: Identification of A p300-SP1-BRD4 Transcriptional Axis as a Key Driver of AR Hyperactivation in Polycystic Ovarian Syndrome.
    Article Snippet: Treatments include the p300-selective inhibitors C646 (10 u m , HY-13823, MCE, USA) and A-485 (0, 0.1, 0.5, 1, 5, 10 u m , HY107455, MCE, USA), p300 agonist CTPB (5 u m , HY-124960, MCE, USA), and the SP1-selective inhibitor Plicamycin (Plica, 100 n m , HY-A0122).



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    <t>P300</t> interacts with and regulates H4K12la to modulate cellular energy metabolism in PD models. (A) RT‐qPCR analysis of P300, GCN5, HBO1, HDAC6, TIP60 mRNA expression in SN4741 cells treated with or without MPP + (N = 3). (B) Western blotting analysis and quantification of P300 protein levels in SN4741 cells treated with or without MPP + (N = 3). (C) Co‐IP assays showing reciprocal binding between P300 and H4K12la in MPP + ‐treated SN4741 cells (N = 3). (D) Representative immunofluorescence images showing the co‐localization of P300 (red) and H4K12la (green) in the nucleus of SN4741 cells, and (E) the quantitative analysis of co‐localization. DAPI (blue) stains nuclei (N = 3). Scale bar, 50 µm. (F) Predicted molecular docking model of the interaction between P300 and H4K12la, generated using the STRING database, indicating the presence of six hydrogen bonds. (G) Western blotting analysis of H4K12la and HIF‐1α protein levels in SN4741 cells treated with MPP + in the presence or absence of the indicated concentrations of A‐485 (N = 3). (H) Intracellular ATP levels in SN4741 cells treated with MPP + and/or A‐485 (N = 3). Data are presented as mean ± SEM. ns, not significant, * p < 0.05, ** p < 0.01, and *** p < 0.001. Statistical significance was determined by one‐way ANOVA or Student's t‐test as appropriate. “N” refers to the number of biologically independent experiments.
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    <t>P300</t> interacts with and regulates H4K12la to modulate cellular energy metabolism in PD models. (A) RT‐qPCR analysis of P300, GCN5, HBO1, HDAC6, TIP60 mRNA expression in SN4741 cells treated with or without MPP + (N = 3). (B) Western blotting analysis and quantification of P300 protein levels in SN4741 cells treated with or without MPP + (N = 3). (C) Co‐IP assays showing reciprocal binding between P300 and H4K12la in MPP + ‐treated SN4741 cells (N = 3). (D) Representative immunofluorescence images showing the co‐localization of P300 (red) and H4K12la (green) in the nucleus of SN4741 cells, and (E) the quantitative analysis of co‐localization. DAPI (blue) stains nuclei (N = 3). Scale bar, 50 µm. (F) Predicted molecular docking model of the interaction between P300 and H4K12la, generated using the STRING database, indicating the presence of six hydrogen bonds. (G) Western blotting analysis of H4K12la and HIF‐1α protein levels in SN4741 cells treated with MPP + in the presence or absence of the indicated concentrations of A‐485 (N = 3). (H) Intracellular ATP levels in SN4741 cells treated with MPP + and/or A‐485 (N = 3). Data are presented as mean ± SEM. ns, not significant, * p < 0.05, ** p < 0.01, and *** p < 0.001. Statistical significance was determined by one‐way ANOVA or Student's t‐test as appropriate. “N” refers to the number of biologically independent experiments.
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    <t>P300</t> interacts with and regulates H4K12la to modulate cellular energy metabolism in PD models. (A) RT‐qPCR analysis of P300, GCN5, HBO1, HDAC6, TIP60 mRNA expression in SN4741 cells treated with or without MPP + (N = 3). (B) Western blotting analysis and quantification of P300 protein levels in SN4741 cells treated with or without MPP + (N = 3). (C) Co‐IP assays showing reciprocal binding between P300 and H4K12la in MPP + ‐treated SN4741 cells (N = 3). (D) Representative immunofluorescence images showing the co‐localization of P300 (red) and H4K12la (green) in the nucleus of SN4741 cells, and (E) the quantitative analysis of co‐localization. DAPI (blue) stains nuclei (N = 3). Scale bar, 50 µm. (F) Predicted molecular docking model of the interaction between P300 and H4K12la, generated using the STRING database, indicating the presence of six hydrogen bonds. (G) Western blotting analysis of H4K12la and HIF‐1α protein levels in SN4741 cells treated with MPP + in the presence or absence of the indicated concentrations of A‐485 (N = 3). (H) Intracellular ATP levels in SN4741 cells treated with MPP + and/or A‐485 (N = 3). Data are presented as mean ± SEM. ns, not significant, * p < 0.05, ** p < 0.01, and *** p < 0.001. Statistical significance was determined by one‐way ANOVA or Student's t‐test as appropriate. “N” refers to the number of biologically independent experiments.
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    <t>P300</t> interacts with and regulates H4K12la to modulate cellular energy metabolism in PD models. (A) RT‐qPCR analysis of P300, GCN5, HBO1, HDAC6, TIP60 mRNA expression in SN4741 cells treated with or without MPP + (N = 3). (B) Western blotting analysis and quantification of P300 protein levels in SN4741 cells treated with or without MPP + (N = 3). (C) Co‐IP assays showing reciprocal binding between P300 and H4K12la in MPP + ‐treated SN4741 cells (N = 3). (D) Representative immunofluorescence images showing the co‐localization of P300 (red) and H4K12la (green) in the nucleus of SN4741 cells, and (E) the quantitative analysis of co‐localization. DAPI (blue) stains nuclei (N = 3). Scale bar, 50 µm. (F) Predicted molecular docking model of the interaction between P300 and H4K12la, generated using the STRING database, indicating the presence of six hydrogen bonds. (G) Western blotting analysis of H4K12la and HIF‐1α protein levels in SN4741 cells treated with MPP + in the presence or absence of the indicated concentrations of A‐485 (N = 3). (H) Intracellular ATP levels in SN4741 cells treated with MPP + and/or A‐485 (N = 3). Data are presented as mean ± SEM. ns, not significant, * p < 0.05, ** p < 0.01, and *** p < 0.001. Statistical significance was determined by one‐way ANOVA or Student's t‐test as appropriate. “N” refers to the number of biologically independent experiments.
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    p300 150 inhibitor c646  (MedChemExpress)
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    <t>P300</t> interacts with and regulates H4K12la to modulate cellular energy metabolism in PD models. (A) RT‐qPCR analysis of P300, GCN5, HBO1, HDAC6, TIP60 mRNA expression in SN4741 cells treated with or without MPP + (N = 3). (B) Western blotting analysis and quantification of P300 protein levels in SN4741 cells treated with or without MPP + (N = 3). (C) Co‐IP assays showing reciprocal binding between P300 and H4K12la in MPP + ‐treated SN4741 cells (N = 3). (D) Representative immunofluorescence images showing the co‐localization of P300 (red) and H4K12la (green) in the nucleus of SN4741 cells, and (E) the quantitative analysis of co‐localization. DAPI (blue) stains nuclei (N = 3). Scale bar, 50 µm. (F) Predicted molecular docking model of the interaction between P300 and H4K12la, generated using the STRING database, indicating the presence of six hydrogen bonds. (G) Western blotting analysis of H4K12la and HIF‐1α protein levels in SN4741 cells treated with MPP + in the presence or absence of the indicated concentrations of A‐485 (N = 3). (H) Intracellular ATP levels in SN4741 cells treated with MPP + and/or A‐485 (N = 3). Data are presented as mean ± SEM. ns, not significant, * p < 0.05, ** p < 0.01, and *** p < 0.001. Statistical significance was determined by one‐way ANOVA or Student's t‐test as appropriate. “N” refers to the number of biologically independent experiments.
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    P300 Inhibitor A 485, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    <t>P300</t> interacts with and regulates H4K12la to modulate cellular energy metabolism in PD models. (A) RT‐qPCR analysis of P300, GCN5, HBO1, HDAC6, TIP60 mRNA expression in SN4741 cells treated with or without MPP + (N = 3). (B) Western blotting analysis and quantification of P300 protein levels in SN4741 cells treated with or without MPP + (N = 3). (C) Co‐IP assays showing reciprocal binding between P300 and H4K12la in MPP + ‐treated SN4741 cells (N = 3). (D) Representative immunofluorescence images showing the co‐localization of P300 (red) and H4K12la (green) in the nucleus of SN4741 cells, and (E) the quantitative analysis of co‐localization. DAPI (blue) stains nuclei (N = 3). Scale bar, 50 µm. (F) Predicted molecular docking model of the interaction between P300 and H4K12la, generated using the STRING database, indicating the presence of six hydrogen bonds. (G) Western blotting analysis of H4K12la and HIF‐1α protein levels in SN4741 cells treated with MPP + in the presence or absence of the indicated concentrations of A‐485 (N = 3). (H) Intracellular ATP levels in SN4741 cells treated with MPP + and/or A‐485 (N = 3). Data are presented as mean ± SEM. ns, not significant, * p < 0.05, ** p < 0.01, and *** p < 0.001. Statistical significance was determined by one‐way ANOVA or Student's t‐test as appropriate. “N” refers to the number of biologically independent experiments.
    P300 Cbp Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    <t>P300</t> interacts with and regulates H4K12la to modulate cellular energy metabolism in PD models. (A) RT‐qPCR analysis of P300, GCN5, HBO1, HDAC6, TIP60 mRNA expression in SN4741 cells treated with or without MPP + (N = 3). (B) Western blotting analysis and quantification of P300 protein levels in SN4741 cells treated with or without MPP + (N = 3). (C) Co‐IP assays showing reciprocal binding between P300 and H4K12la in MPP + ‐treated SN4741 cells (N = 3). (D) Representative immunofluorescence images showing the co‐localization of P300 (red) and H4K12la (green) in the nucleus of SN4741 cells, and (E) the quantitative analysis of co‐localization. DAPI (blue) stains nuclei (N = 3). Scale bar, 50 µm. (F) Predicted molecular docking model of the interaction between P300 and H4K12la, generated using the STRING database, indicating the presence of six hydrogen bonds. (G) Western blotting analysis of H4K12la and HIF‐1α protein levels in SN4741 cells treated with MPP + in the presence or absence of the indicated concentrations of A‐485 (N = 3). (H) Intracellular ATP levels in SN4741 cells treated with MPP + and/or A‐485 (N = 3). Data are presented as mean ± SEM. ns, not significant, * p < 0.05, ** p < 0.01, and *** p < 0.001. Statistical significance was determined by one‐way ANOVA or Student's t‐test as appropriate. “N” refers to the number of biologically independent experiments.
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    https://www.bioz.com/product/p300/p300+Rabbit+mAb/pm41791566-70-13-14
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    mouse anti p300 antibody  (Santa Cruz Biotechnology)
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    <t>P300</t> interacts with and regulates H4K12la to modulate cellular energy metabolism in PD models. (A) RT‐qPCR analysis of P300, GCN5, HBO1, HDAC6, TIP60 mRNA expression in SN4741 cells treated with or without MPP + (N = 3). (B) Western blotting analysis and quantification of P300 protein levels in SN4741 cells treated with or without MPP + (N = 3). (C) Co‐IP assays showing reciprocal binding between P300 and H4K12la in MPP + ‐treated SN4741 cells (N = 3). (D) Representative immunofluorescence images showing the co‐localization of P300 (red) and H4K12la (green) in the nucleus of SN4741 cells, and (E) the quantitative analysis of co‐localization. DAPI (blue) stains nuclei (N = 3). Scale bar, 50 µm. (F) Predicted molecular docking model of the interaction between P300 and H4K12la, generated using the STRING database, indicating the presence of six hydrogen bonds. (G) Western blotting analysis of H4K12la and HIF‐1α protein levels in SN4741 cells treated with MPP + in the presence or absence of the indicated concentrations of A‐485 (N = 3). (H) Intracellular ATP levels in SN4741 cells treated with MPP + and/or A‐485 (N = 3). Data are presented as mean ± SEM. ns, not significant, * p < 0.05, ** p < 0.01, and *** p < 0.001. Statistical significance was determined by one‐way ANOVA or Student's t‐test as appropriate. “N” refers to the number of biologically independent experiments.
    Mouse Anti P300 Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p300/p300+Antibody/pm41703985-74-21-29
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    Image Search Results


    P300 interacts with and regulates H4K12la to modulate cellular energy metabolism in PD models. (A) RT‐qPCR analysis of P300, GCN5, HBO1, HDAC6, TIP60 mRNA expression in SN4741 cells treated with or without MPP + (N = 3). (B) Western blotting analysis and quantification of P300 protein levels in SN4741 cells treated with or without MPP + (N = 3). (C) Co‐IP assays showing reciprocal binding between P300 and H4K12la in MPP + ‐treated SN4741 cells (N = 3). (D) Representative immunofluorescence images showing the co‐localization of P300 (red) and H4K12la (green) in the nucleus of SN4741 cells, and (E) the quantitative analysis of co‐localization. DAPI (blue) stains nuclei (N = 3). Scale bar, 50 µm. (F) Predicted molecular docking model of the interaction between P300 and H4K12la, generated using the STRING database, indicating the presence of six hydrogen bonds. (G) Western blotting analysis of H4K12la and HIF‐1α protein levels in SN4741 cells treated with MPP + in the presence or absence of the indicated concentrations of A‐485 (N = 3). (H) Intracellular ATP levels in SN4741 cells treated with MPP + and/or A‐485 (N = 3). Data are presented as mean ± SEM. ns, not significant, * p < 0.05, ** p < 0.01, and *** p < 0.001. Statistical significance was determined by one‐way ANOVA or Student's t‐test as appropriate. “N” refers to the number of biologically independent experiments.

    Journal: Advanced Science

    Article Title: H4K12 Lactylation Impairs Dopaminergic Neuron Energy Metabolism via the HIF‐1α/NDUFS1 Pathway in Parkinson's Disease

    doi: 10.1002/advs.78220

    Figure Lengend Snippet: P300 interacts with and regulates H4K12la to modulate cellular energy metabolism in PD models. (A) RT‐qPCR analysis of P300, GCN5, HBO1, HDAC6, TIP60 mRNA expression in SN4741 cells treated with or without MPP + (N = 3). (B) Western blotting analysis and quantification of P300 protein levels in SN4741 cells treated with or without MPP + (N = 3). (C) Co‐IP assays showing reciprocal binding between P300 and H4K12la in MPP + ‐treated SN4741 cells (N = 3). (D) Representative immunofluorescence images showing the co‐localization of P300 (red) and H4K12la (green) in the nucleus of SN4741 cells, and (E) the quantitative analysis of co‐localization. DAPI (blue) stains nuclei (N = 3). Scale bar, 50 µm. (F) Predicted molecular docking model of the interaction between P300 and H4K12la, generated using the STRING database, indicating the presence of six hydrogen bonds. (G) Western blotting analysis of H4K12la and HIF‐1α protein levels in SN4741 cells treated with MPP + in the presence or absence of the indicated concentrations of A‐485 (N = 3). (H) Intracellular ATP levels in SN4741 cells treated with MPP + and/or A‐485 (N = 3). Data are presented as mean ± SEM. ns, not significant, * p < 0.05, ** p < 0.01, and *** p < 0.001. Statistical significance was determined by one‐way ANOVA or Student's t‐test as appropriate. “N” refers to the number of biologically independent experiments.

    Article Snippet: The primary antibodies used in this study were as follows: GAPDH Monoclonal antibody (60004‐1‐Ig; ProteinTech, China), Pan‐Kla (PTM‐1401RM; PTM Biolabs, China), H4K12la (PTM‐1411RM; PTM Biolabs, China), H3K18la (PTM‐1406RM; PTM Biolabs, China), H3K23la (PTM‐1413RM; PTM Biolabs, China), H3K9la (PTM‐1419RM; PTM Biolabs, China), H3K14la (PTM‐1414RM; PTM Biolabs, China), H3 (PTM‐1001RM; PTM Biolabs, China), TH (MAB318; Sigma‐Aldrich, USA), HIF‐1α (PA1‐16601; Thermo Fisher Scientific, USA), NDUFS1 (PTM‐20288; PTM Biolabs, China), ATPB (A5769; ABclonal Biotechnology, China), P300 (sc‐48343; Santa Cruz Biotechnology, USA), β‐actin (4970; Cell Signaling Technology, USA), IBA1 (RT1316; BUABIO, China), HK2 (66974‐1‐Ig; ProteinTech, China), LDHA ( R24822 ; Zenbio, China).

    Techniques: Quantitative RT-PCR, Analysis, Expressing, Western Blot, Co-Immunoprecipitation Assay, Binding Assay, Immunofluorescence, Docking Assay, Generated