English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Differential positioning of the histone variant H2A.Z in a p53 dependent manner was shown to regulate  p21  transcription. Whether H2A.Z is involved in  p21  activity in the absence of p53 is not known. The  p21  gene is repressed in estrogen receptor (ER) negative cell lines that are p53−/− and hormone independent for their growth. Here we demonstrate that class I and II pan Histone deacetylase inhibitors (HDACi) induce  p21  transcription and reduce cell proliferation of MDA-MB231, an ERα-negative mammary tumor cell line, in a H2A.Z dependent manner. H2A.Z is associated with the transcription start site (TSS) of the repressed  p21  gene. Depleting H2A.Z did not lead to transcription of  p21  but annihilated the stimulating effect of HDACi on this gene. Acetylation of H2A.Z but not of H3K9 at the  p21  promoter correlated with  p21  activation. We further show that HDACi treatment reduced the presence of the p400 chromatin remodeler at the  p21  TSS. We propose a model in which association of p400 negatively affects  p21  transcription by interfering with acetylation of H2A.Z.

Activation of p21 by HDAC Inhibitors Requires Acetylation of H2A.Z