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Article

A short N-terminal domain of HDAC4 preserves photoreceptors and restores visual function in retinitis pigmentosa.

Nature communications - 14 Aug 2015

Guo Xinzheng, Wang Shao-Bin, Xu Hongping, Ribic Adema, Mohns Ethan J, Zhou Yu, Zhu Xianjun, Biederer Thomas, Crair Michael C, Chen Bo

Abstract excerpt

Retinitis pigmentosa is a leading cause of inherited blindness, with no effective treatment currently available. Mutations primarily in genes expressed in rod photoreceptors lead to early rod death, followed by a slower phase of cone photoreceptor death. Rd1 mice provide an invaluable animal model to evaluate therapies for the disease. We previously reported that overexpression of histone deacetylase 4 (HDAC4)...

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Share to Electroretinography
Share to Gene Deletion

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Histone Deacetylases

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Share to Retinitis Pigmentosa

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Source

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Identifiers

PMID: 26272629
DOI: 10.1038/ncomms9005
PMCID: PMC4538705

Genes

HDAC4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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A short N-terminal domain of HDAC4 preserves photoreceptors and restores visual function in retinitis pigmentosa.PMID 26272629Read ↗

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