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Article

HDAC6 deficiency or inhibition blocks FGFR3 accumulation and improves bone growth in a model of achondroplasia.

Human molecular genetics - 1 Oct 2016

Ota Sara, Zhou Zi-Qiang, Romero Megan P, Yang Guang, Hurlin Peter J

Abstract excerpt

Mutations that cause increased and/or inappropriate activation of FGFR3 are responsible for a collection of short-limbed chondrodysplasias. These mutations can alter receptor trafficking and enhance receptor stability, leading to increased receptor accumulation and activity. Here, we show that wildtype and mutant activated forms of FGFR3 increase expression of the cytoplasmic deacetylase HDAC6 (Histone...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 27506979
DOI: 10.1093/hmg/ddw255

Genes

FGFR3
HDAC6

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

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