ArticleMolecular biology reports2025
Hdac11 inhibits apoptosis in zebrafish cells under cold stress via downregulating pdcd6 through its downstream enhancer.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundIt is widely recognized that histone deacetylase 11 (HDAC11) plays vital roles in a variety of biological processes including apoptosis, immunity and lipid metabolism in mammals, however, its role in zebrafish remains poorly elucidated. Here, we demonstrated that hdac11 knockout increases pdcd6 expression via pdcd6 + 310k enhancer, then promotes apoptosis in zebrafish cells under cold stress. METHODS AND
resultsThe current work reported that inhibition of Hdac11 promoted apoptosis and up-regulated programmed cell death protein 6 (pdcd6) in ZF4 cells under cold stress. ChIP-qPCR showed the enrichment of H3K27ac and Hdac11 at the + 310k region downstream of pdcd6. Dual-luciferase assay confirmed the enhancer activity of pdcd6 + 310k region. Chromatin conformation capture (3C) assay showed that pdcd6 promoter interacted with + 310k region, and that interaction frequency was enhanced after hdac11 knockout. Furthermore, siRNA knockdown of pdcd6 rescued the apoptosis induced by Hdac11 inhibition or cold stress in ZF4 cells.
conclusionsIn summary, Hdac11 targets pdcd6 + 310k enhancer to repress pdcd6 expression, which then inhibits apoptosis in zebrafish cells.
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