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Ping-Yao Zeng

Researcher at Wistar Institute

Publications -  6
Citations -  954

Ping-Yao Zeng is an academic researcher from Wistar Institute. The author has contributed to research in topics: Chromatin immunoprecipitation & Histone. The author has an hindex of 6, co-authored 6 publications receiving 906 citations. Previous affiliations of Ping-Yao Zeng include Central South University & University of Pennsylvania.

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Journal ArticleDOI

Signaling Kinase AMPK Activates Stress-Promoted Transcription via Histone H2B Phosphorylation

TL;DR: This work found that AMPK activates transcription through direct association with chromatin and phosphorylation of histone H2B at serine 36, placing AMPK-dependent H2 B Ser36 phosphorylated in a direct transcriptional and chromatin regulatory pathway leading to cellular adaptation to stress.
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In vivo dual cross-linking for identification of indirect DNA-associated proteins by chromatin immunoprecipitation.

TL;DR: Cross-Linking Transcriptional Cofactors The chromatin immunoprecipitation (ChIP) assay, essential for studying such processes as transcriptional regulation, DNA replication, and DNA repair, relies on cross-linking transcriptional cofacts.
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During Lytic Infection Herpes Simplex Virus Type 1 Is Associated with Histones Bearing Modifications That Correlate with Active Transcription

TL;DR: Analysis of histones associated with HSV-1 revealed covalent amino tail modifications similar to those associated with active host mammalian genes, which suggest that productive infection may be accompanied by acquisition of a permissive chromatin state.
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LKB1 is recruited to the p21/WAF1 promoter by p53 to mediate transcriptional activation.

TL;DR: It is found that, consistent with previous studies, LKB1 stabilizes p53 in vivo, correlating with activation of p21/WAF1 and directly or indirectly phosphorylates p53 Ser15 (previously shown to be phosphorylated by AMP-dependent kinase) and p53Ser392, required for L KB1-dependent cell cycle G(1) arrest.
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Trimethylation of Histone H3 Lysine 4 by Set1 in the Lytic Infection of Human Herpes Simplex Virus 1

TL;DR: The results indicate that H3K4me3 mediated by Set1 is required for optimal gene expression and replication of HSV-1 during lytic infection and suggest that this pathway could be a potential point of pharmacological intervention during HSv-1 infection.