ArticleJournal of cell science2013
A pathway involving HDAC5, cFLIP and caspases regulates expression of the splicing regulator polypyrimidine tract binding protein in the heart.
Article in Journal of cell science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Role of Histone Deacetylase and Inhibitors in Cardiovascular Diseases.Cell proliferation · 2025Review
- A ratiometric catalog of protein isoform shifts in the cardiac fetal gene program.JCI insight · 2025Article
- Alternative Splicing in the Heart: The Therapeutic Potential of Regulating the Regulators.International journal of molecular sciences · 2024Review
- PTBP1 as a potential regulator of disease.Molecular and cellular biochemistry · 2024Review
- The expression of long non-coding RNAs is associated with H3Ac and H3K4me2 changes regulated by the HDA6-LDL1/2 histone modification complex inNAR genomics and bioinformatics · 2020Article
- Modulation of hepatitis B virus pregenomic RNA stability and splicing by histone deacetylase 5 enhances viral biosynthesis.PLoS pathogens · 2020Article
- Review
- mRNA Metabolism in Cardiac Development and Disease: Life After Transcription.Physiological reviews · 2020Review
- Lysine acetyltransferases and lysine deacetylases as targets for cardiovascular disease.Nature reviews. Cardiology · 2020Review
- Genome Wide Meta-Analysis identifies common genetic signatures shared by heart function and Alzheimer's disease.Scientific reports · 2019Article
- A developmentally regulated spliced variant of PTBP1 is upregulated in type 1 diabetic hearts.Biochemical and biophysical research communications · 2019Article
- A posttranscriptional mechanism that controls Ptbp1 abundance in the Xenopus epidermis.Molecular and cellular biology · 2015Article
- Histone deacetylase inhibitors promote glioma cell death by G2 checkpoint abrogation leading to mitotic catastrophe.Cell death & disease · 2014Article
- Dysregulation of histone acetyltransferases and deacetylases in cardiovascular diseases.Oxidative medicine and cellular longevity · 2014Review
- How voltage-gated calcium channels gate forms of homeostatic synaptic plasticity.Frontiers in cellular neuroscience · 2014Review
- New insights into functional roles of the polypyrimidine tract-binding protein.International journal of molecular sciences · 2013Review
- Stat3 inhibits PTPN13 expression in squamous cell lung carcinoma through recruitment of HDAC5.BioMed research international · 2013Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
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Abstract
Polypyrimidine tract binding protein (PTB) regulates pre-mRNA splicing, having special relevance for determining gene expression in the differentiating muscle. We have previously shown that PTB protein abundance is progressively reduced during heart development without reduction of its own transcript. Simultaneous reduction of histone deacetylase (HDAC) expression prompted us to investigate the potential link between these events. HDAC5-deficient mice have reduced cardiac PTB protein abundance, and HDAC inhibition in myocytes causes a reduction in endogenous expression of cellular FLICE-like inhibitory protein (cFLIP) and caspase-dependent cleavage of PTB. In agreement with this, cardiac PTB expression is abnormally high in mice with cardiac-specific executioner caspase deficiency, and cFLIP overexpression prevents PTB cleavage in vitro. Caspase-dependent cleavage triggers further fragmentation of PTB, and these fragments accumulate in the presence of proteasome inhibitors. Experimental modification of the above processes in vivo and in vitro results in coherent changes in the alternative splicing of genes encoding tropomyosin-1 (TPM1), tropomyosin-2 (TPM2) and myocyte enhancer factor-2 (MEF2). Thus, we report a pathway connecting HDAC, cFLIP and caspases regulating the progressive disappearance of PTB, which enables the expression of the adult variants of proteins involved in the regulation of contraction and transcription during cardiac muscle development.
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