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mouse anti pp53 s392  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc mouse anti pp53 s392
    Mouse Anti Pp53 S392, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 175 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse anti pp53 s392/product/Cell Signaling Technology Inc
    Average 93 stars, based on 175 article reviews
    mouse anti pp53 s392 - by Bioz Stars, 2026-06
    93/100 stars

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    Mechanisms of PD-L1 regulation in lung cancer. PD-L1 expression in tumor cells is regulated at multiple levels. The <t>p53–p21</t> axis can negatively influence PD-L1 transcription, while oncogenic pathways such as PI3K/AKT and JAK/STAT promote its up-regulation. Epigenetic mechanisms play a critical role: histone acetylation and methylation dynamically regulate chromatin accessibility, and DNA methylation (e.g., via DNMT1) can repress or activate PD-L1 transcription depending on context. Collectively, these mechanisms contribute to PD-L1-mediated immune evasion and tumor survival.
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    Mechanisms of PD-L1 regulation in lung cancer. PD-L1 expression in tumor cells is regulated at multiple levels. The p53–p21 axis can negatively influence PD-L1 transcription, while oncogenic pathways such as PI3K/AKT and JAK/STAT promote its up-regulation. Epigenetic mechanisms play a critical role: histone acetylation and methylation dynamically regulate chromatin accessibility, and DNA methylation (e.g., via DNMT1) can repress or activate PD-L1 transcription depending on context. Collectively, these mechanisms contribute to PD-L1-mediated immune evasion and tumor survival.

    Journal: Cancers

    Article Title: Regulation of PD-L1 Expression by SAHA-Mediated Histone Deacetylase Inhibition in Lung Cancer Cells

    doi: 10.3390/cancers17172919

    Figure Lengend Snippet: Mechanisms of PD-L1 regulation in lung cancer. PD-L1 expression in tumor cells is regulated at multiple levels. The p53–p21 axis can negatively influence PD-L1 transcription, while oncogenic pathways such as PI3K/AKT and JAK/STAT promote its up-regulation. Epigenetic mechanisms play a critical role: histone acetylation and methylation dynamically regulate chromatin accessibility, and DNA methylation (e.g., via DNMT1) can repress or activate PD-L1 transcription depending on context. Collectively, these mechanisms contribute to PD-L1-mediated immune evasion and tumor survival.

    Article Snippet: pp53 (Phospho-p53) , CST , 12571 , 1:1000.

    Techniques: Expressing, Methylation, DNA Methylation Assay