ArticleMolecular biology of the cell2011
Ubiquitin-dependent degradation of HDAC4, a new regulator of random cell motility.
Article in Molecular biology of the cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 70 citations in OpenAlex.
- Class IIa HDACs forced degradation allows resensitization of oxaliplatin-resistant FBXW7-mutated colorectal cancer.Molecular oncology · 2026Article
- Class IIa HDACs Are Important Signal Transducers with Unclear Enzymatic Activities.Biomolecules · 2025Review
- The food dye Tartrazine disrupts vascular formation both in zebrafish larvae and in human primary endothelial cells.Scientific reports · 2024Article
- Roles of Histone Deacetylase 4 in the Inflammatory and Metabolic Processes.Diabetes & metabolism journal · 2024Review
- Acetylation and Phosphorylation in the Regulation of Hypoxia-Inducible Factor Activities: Additional Options to Modulate Adaptations to Changes in Oxygen Levels.Life (Basel, Switzerland) · 2023Review
- HDAC4 in cancer: A multitasking platform to drive not only epigenetic modifications.Frontiers in molecular biosciences · 2023Review
- Trichostatin D as a Novel KLF2 Activator Attenuates TNFα-Induced Endothelial Inflammation.International journal of molecular sciences · 2022Article
- Spatial and temporal dynamics of HDACs class IIa following mild traumatic brain injury in adult rats.Molecular psychiatry · 2022Article
- HDAC4 Inhibitors as Antivascular Senescence Therapeutics.Oxidative medicine and cellular longevity · 2022Review
- HDAC4 degradation during senescence unleashes an epigenetic program driven by AP-1/p300 at selected enhancers and super-enhancers.Genome biology · 2021Article
- Non-canonical role of wild-type SEC23B in the cellular stress response pathway.Cell death & disease · 2021Article
- Inhibition of HDAC4 by GSK3β leads to downregulation of KLF5 and ASK1 and prevents the progression of intravertebral disc degeneration.Clinical epigenetics · 2021Article
- Quis Custodiet Ipsos Custodes (Who Controls the Controllers)? Two Decades of Studies on HDAC9.Life (Basel, Switzerland) · 2021Review
- Regulation of histone deacetylase activities and functions by phosphorylation and its physiological relevance.Cellular and molecular life sciences : CMLS · 2021Review
- Repeated stress exposure in mid-adolescence attenuates behavioral, noradrenergic, and epigenetic effects of trauma-like stress in early adult male rats.Scientific reports · 2020Article
- Deletion of Glycogen Synthase Kinase-3β in DBiological psychiatry · 2020Article
- The role of histone deacetylase 4 during chondrocyte hypertrophy and endochondral bone development.Bone & joint research · 2020Review
- Histone Deacetylase 4 Downregulation Elicits Post-Traumatic Psychiatric Disorders through Impairment of Neurogenesis.Journal of neurotrauma · 2019Article
- HDAC7-mediated control of tumour microenvironment maintains proliferative and stemness competence of human mammary epithelial cells.Molecular oncology · 2019Article
- Histone Deacetylase 4 Promotes Osteosarcoma Cell Proliferation and Invasion by Regulating Expression of Proliferating Cell Nuclear Antigen.Frontiers in oncology · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HDAC4 (histone deacetylase 4) belongs to class IIa of histone deacetylases, which groups important regulators of gene expression, controlling pleiotropic cellular functions. Here we show that, in addition to the well-defined nuclear/cytoplasmic shuttling, HDAC4 activity is modulated by the ubiquitin-proteasome system. Serum starvation elicits the poly-ubiquitination and degradation of HDAC4 in nontransformed cells. Phosphorylation of serine 298 within the PEST1 sequence plays an important role in the control of HDAC4 stability. Serine 298 lies within a glycogen synthase kinase 3β consensus sequence, and removal of growth factors fails to trigger HDAC4 degradation in cells deficient in this kinase. GSK3β can phosphorylate HDAC4 in vitro, and phosphorylation of serine 302 seems to play the role of priming phosphate. We have also found that HDAC4 modulates random cell motility possibly through the regulation of KLF2 transcription. Apoptosis, autophagy, cell proliferation, and growth arrest were unaffected by HDAC4. Our data suggest a link between regulation of HDAC4 degradation and the control of cell motility as operated by growth factors.
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