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chip kit  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc chip kit
    <t>YAP</t> directly binds to the NADK promoter and activates its transcription. (A) Schematic illustration of the human NADK promoter region (−2000 to −0 bp relative to the transcription start site) showing putative YAP-binding sites and the design of a series of truncated NADK promoter luciferase reporter constructs. (B) <t>ChIP-qPCR</t> analysis demonstrating significant enrichment of the NADK promoter region in anti-YAP immunoprecipitates compared with IgG controls ( n = 3). (C) Luciferase reporter assays showing that YAP overexpression significantly enhances transcriptional activity driven by the −2000/0 and −1500/0 NADK promoter fragments, whereas further truncation to −1000/0 or −500/0 markedly attenuates YAP-induced activation, identifying the YAP-responsive region within the −1500 to −1000 bp interval ( n = 3). Data are presented as mean ± SEM. Unpaired Student's t -test or one-way ANOVA followed by Tukey's post hoc test for comparisons. *** P < 0.001. ChIP, Chromatin immunoprecipitation; IgG, immunoglobulin G; LUC, luciferase; Rluc, Renilla luciferase; NC, negative control.
    Chip Kit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1190 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/chip+plus+enzymatic+chromatin+ip+kit/SimpleChIP+Plus+Enzymatic+Chromatin+IP+Kit/pmc12962100-113-7-9
    Average 97 stars, based on 1190 article reviews
    chip kit - by Bioz Stars, 2026-09
    97/100 stars

    Images

    1) Product Images from "NMRK2–YAP–NADK axis preserves redox protection against myocardial ischemia/reperfusion injury"

    Article Title: NMRK2–YAP–NADK axis preserves redox protection against myocardial ischemia/reperfusion injury

    Journal: Redox Biology

    doi: 10.1016/j.redox.2026.104100

    YAP directly binds to the NADK promoter and activates its transcription. (A) Schematic illustration of the human NADK promoter region (−2000 to −0 bp relative to the transcription start site) showing putative YAP-binding sites and the design of a series of truncated NADK promoter luciferase reporter constructs. (B) ChIP-qPCR analysis demonstrating significant enrichment of the NADK promoter region in anti-YAP immunoprecipitates compared with IgG controls ( n = 3). (C) Luciferase reporter assays showing that YAP overexpression significantly enhances transcriptional activity driven by the −2000/0 and −1500/0 NADK promoter fragments, whereas further truncation to −1000/0 or −500/0 markedly attenuates YAP-induced activation, identifying the YAP-responsive region within the −1500 to −1000 bp interval ( n = 3). Data are presented as mean ± SEM. Unpaired Student's t -test or one-way ANOVA followed by Tukey's post hoc test for comparisons. *** P < 0.001. ChIP, Chromatin immunoprecipitation; IgG, immunoglobulin G; LUC, luciferase; Rluc, Renilla luciferase; NC, negative control.
    Figure Legend Snippet: YAP directly binds to the NADK promoter and activates its transcription. (A) Schematic illustration of the human NADK promoter region (−2000 to −0 bp relative to the transcription start site) showing putative YAP-binding sites and the design of a series of truncated NADK promoter luciferase reporter constructs. (B) ChIP-qPCR analysis demonstrating significant enrichment of the NADK promoter region in anti-YAP immunoprecipitates compared with IgG controls ( n = 3). (C) Luciferase reporter assays showing that YAP overexpression significantly enhances transcriptional activity driven by the −2000/0 and −1500/0 NADK promoter fragments, whereas further truncation to −1000/0 or −500/0 markedly attenuates YAP-induced activation, identifying the YAP-responsive region within the −1500 to −1000 bp interval ( n = 3). Data are presented as mean ± SEM. Unpaired Student's t -test or one-way ANOVA followed by Tukey's post hoc test for comparisons. *** P < 0.001. ChIP, Chromatin immunoprecipitation; IgG, immunoglobulin G; LUC, luciferase; Rluc, Renilla luciferase; NC, negative control.

    Techniques Used: Binding Assay, Luciferase, Construct, ChIP-qPCR, Over Expression, Activity Assay, Activation Assay, Chromatin Immunoprecipitation, Negative Control

    Related Articles

    Chromatin Immunoprecipitation:

    Article Title: Exosomes from chondrocytes overexpressing miR-214-3p facilitate M2 macrophage polarization and angiogenesis to relieve Legg Calvé-Perthes disease.
    Article Snippet: Objective: Legg-Calvé-Perthes disease (LCPD) is a partial or total necrosis of femoral head bone caused by blood supply disorder and its etiology is not clear.. Studies have revealed that microRNA-214-3p (miR-214-3p) plays a vital role in LCPD, however, its exact mechanism is still unclear.. In this study, we investigated the potential role of chondrocytes-derived exosomes carrying miR-214-3p (exos-miR-214-3p) in the pathogenesis of LCPD.

    Article Title: Grpel2 maintains cardiomyocyte survival in diabetic cardiomyopathy through DLST-mediated mitochondrial dysfunction: a proof-of-concept study
    Article Snippet: .. ChIP assays were performed using a ChIP Plus Enzymatic Chromatin IP Kit (9003, CST, USA) following the manufacturer’s protocols [ ]. ..

    Article Title: Grpel2 maintains cardiomyocyte survival in diabetic cardiomyopathy through DLST-mediated mitochondrial dysfunction: a proof-of-concept study.
    Article Snippet: .. ChIP assays were performed using a ChIP Plus Enzymatic Chromatin IP Kit (9003, CST, USA) following the manufacturer’s protocols [21]. ..

    Article Title: Impaired hepatic BMAL1-FGF21 signaling drives adverse metabolic outcomes of ketogenic diet.
    Article Snippet: Aims The ketogenic diet (KD) has gained popularity for its metabolic benefits; however, its effects vary markedly across physiological and pathological conditions.. This study aimed to determine the mechanisms underlying differential metabolic responses to KD.. Materials and Methods Db/db, liver-specific fibroblast growth factor 21 (FGF21) knockdown mice, and liverspecific brain and muscle aryl hydrocarbon receptor nuclear translocator-like 1 (BMAL1) knockout mice were treated with isocaloric KD for 8 weeks.

    Article Title: Period3 modulates the NAD + -SIRT3 axis to alleviate depression-like behaviour by enhancing NAMPT activity in mice.
    Article Snippet: .. ChIP assay was carried out using a simple ChIP Plus Enzymatic Chromatin IP Kit (Cell Signaling Technology, Beverly, MA, USA), following the manufacturer’s instructions. ..

    Article Title: An HBV‐Derived Peptide Poly6 as a Novel Candidate for Functional Cure Via IFN‐I–Mediated Epigenetic Regulation of cccDNA
    Article Snippet: .. ChIP assays were conducted using a ChIP Plus Enzymatic Chromatin IP kit (9003, CST, USA) according to the manufacturer's instruction. ..

    Article Title: Period3 modulates the NAD + -SIRT3 axis to alleviate depression-like behaviour by enhancing NAMPT activity in mice
    Article Snippet: .. ChIP assay was carried out using a simple ChIP Plus Enzymatic Chromatin IP Kit (Cell Signaling Technology, Beverly, MA, USA), following the manufacturer’s instructions. ..



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    <t>YAP</t> directly binds to the NADK promoter and activates its transcription. (A) Schematic illustration of the human NADK promoter region (−2000 to −0 bp relative to the transcription start site) showing putative YAP-binding sites and the design of a series of truncated NADK promoter luciferase reporter constructs. (B) <t>ChIP-qPCR</t> analysis demonstrating significant enrichment of the NADK promoter region in anti-YAP immunoprecipitates compared with IgG controls ( n = 3). (C) Luciferase reporter assays showing that YAP overexpression significantly enhances transcriptional activity driven by the −2000/0 and −1500/0 NADK promoter fragments, whereas further truncation to −1000/0 or −500/0 markedly attenuates YAP-induced activation, identifying the YAP-responsive region within the −1500 to −1000 bp interval ( n = 3). Data are presented as mean ± SEM. Unpaired Student's t -test or one-way ANOVA followed by Tukey's post hoc test for comparisons. *** P < 0.001. ChIP, Chromatin immunoprecipitation; IgG, immunoglobulin G; LUC, luciferase; Rluc, Renilla luciferase; NC, negative control.
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    <t>YAP</t> directly binds to the NADK promoter and activates its transcription. (A) Schematic illustration of the human NADK promoter region (−2000 to −0 bp relative to the transcription start site) showing putative YAP-binding sites and the design of a series of truncated NADK promoter luciferase reporter constructs. (B) <t>ChIP-qPCR</t> analysis demonstrating significant enrichment of the NADK promoter region in anti-YAP immunoprecipitates compared with IgG controls ( n = 3). (C) Luciferase reporter assays showing that YAP overexpression significantly enhances transcriptional activity driven by the −2000/0 and −1500/0 NADK promoter fragments, whereas further truncation to −1000/0 or −500/0 markedly attenuates YAP-induced activation, identifying the YAP-responsive region within the −1500 to −1000 bp interval ( n = 3). Data are presented as mean ± SEM. Unpaired Student's t -test or one-way ANOVA followed by Tukey's post hoc test for comparisons. *** P < 0.001. ChIP, Chromatin immunoprecipitation; IgG, immunoglobulin G; LUC, luciferase; Rluc, Renilla luciferase; NC, negative control.
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    Image Search Results


    YAP directly binds to the NADK promoter and activates its transcription. (A) Schematic illustration of the human NADK promoter region (−2000 to −0 bp relative to the transcription start site) showing putative YAP-binding sites and the design of a series of truncated NADK promoter luciferase reporter constructs. (B) ChIP-qPCR analysis demonstrating significant enrichment of the NADK promoter region in anti-YAP immunoprecipitates compared with IgG controls ( n = 3). (C) Luciferase reporter assays showing that YAP overexpression significantly enhances transcriptional activity driven by the −2000/0 and −1500/0 NADK promoter fragments, whereas further truncation to −1000/0 or −500/0 markedly attenuates YAP-induced activation, identifying the YAP-responsive region within the −1500 to −1000 bp interval ( n = 3). Data are presented as mean ± SEM. Unpaired Student's t -test or one-way ANOVA followed by Tukey's post hoc test for comparisons. *** P < 0.001. ChIP, Chromatin immunoprecipitation; IgG, immunoglobulin G; LUC, luciferase; Rluc, Renilla luciferase; NC, negative control.

    Journal: Redox Biology

    Article Title: NMRK2–YAP–NADK axis preserves redox protection against myocardial ischemia/reperfusion injury

    doi: 10.1016/j.redox.2026.104100

    Figure Lengend Snippet: YAP directly binds to the NADK promoter and activates its transcription. (A) Schematic illustration of the human NADK promoter region (−2000 to −0 bp relative to the transcription start site) showing putative YAP-binding sites and the design of a series of truncated NADK promoter luciferase reporter constructs. (B) ChIP-qPCR analysis demonstrating significant enrichment of the NADK promoter region in anti-YAP immunoprecipitates compared with IgG controls ( n = 3). (C) Luciferase reporter assays showing that YAP overexpression significantly enhances transcriptional activity driven by the −2000/0 and −1500/0 NADK promoter fragments, whereas further truncation to −1000/0 or −500/0 markedly attenuates YAP-induced activation, identifying the YAP-responsive region within the −1500 to −1000 bp interval ( n = 3). Data are presented as mean ± SEM. Unpaired Student's t -test or one-way ANOVA followed by Tukey's post hoc test for comparisons. *** P < 0.001. ChIP, Chromatin immunoprecipitation; IgG, immunoglobulin G; LUC, luciferase; Rluc, Renilla luciferase; NC, negative control.

    Article Snippet: ChIP assays were performed using a commercial ChIP kit (CST 9005S) to assess the binding of YAP to the NADK promoter.

    Techniques: Binding Assay, Luciferase, Construct, ChIP-qPCR, Over Expression, Activity Assay, Activation Assay, Chromatin Immunoprecipitation, Negative Control