ArticleBiochimica et biophysica acta2014
Lysine methyltransferase Smyd2 suppresses p53-dependent cardiomyocyte apoptosis.
Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- Role of SMYD2 in gastrointestinal cancer progression (Review).Oncology letters · 2025Review
- Article
- Dissecting the Role of SMYD2 and Its Inhibitor (LLY-507) in the Treatment of Chemically Induced Non-Small Cell Lung Cancer (NSCLC) by Using FePharmaceuticals (Basel, Switzerland) · 2023Article
- Targeting Epigenetic Changes Mediated by Members of the SMYD Family of Lysine Methyltransferases.Molecules (Basel, Switzerland) · 2023Review
- SMYD2 targets RIPK1 and restricts TNF-induced apoptosis and necroptosis to support colon tumor growth.Cell death & disease · 2022Article
- Histone Lysine Methylation Modification and Its Role in Vascular Calcification.Frontiers in endocrinology · 2022Review
- SMYD2-mediated TRAF2 methylation promotes the NF-κB signaling pathways in inflammatory diseases.Clinical and translational medicine · 2021Article
- Article
- Histone methyltransferase SMYD2: ubiquitous regulator of disease.Clinical epigenetics · 2019Review
- SMYD2 promotes cervical cancer growth by stimulating cell proliferation.Cell & bioscience · 2019Article
- SMYD2-OE promotes oxaliplatin resistance in colon cancer through MDR1/P-glycoprotein via MEK/ERK/AP1 pathway.OncoTargets and therapy · 2019Article
- Inhibition of SMYD2 Sensitized Cisplatin to Resistant Cells in NSCLC Through Activating p53 Pathway.Frontiers in oncology · 2019Article
- Structure of a Novel Dimeric SET Domain Methyltransferase that Regulates Cell Motility.Journal of molecular biology · 2018Article
- Hydroxytyrosol and olive leaf extract exert cardioprotective effects by inhibiting GRP78 and CHOP expression.Journal of biomedical research · 2018Article
- Article
- Article
- The Histone Methyltransferase Mixed Lineage Leukemia (MLL) 3 May Play a Potential Role on Clinical Dilated Cardiomyopathy.Molecular medicine (Cambridge, Mass.) · 2017Article
- Inhibition of MiR-92a May Protect Endothelial Cells After Acute Myocardial Infarction in Rats: Role of KLF2/4.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Discovery and Characterization of a Highly Potent and Selective Aminopyrazoline-Based in Vivo Probe (BAY-598) for the Protein Lysine Methyltransferase SMYD2.Journal of medicinal chemistry · 2016Article
- Coordination of stress signals by the lysine methyltransferase SMYD2 promotes pancreatic cancer.Genes & development · 2016Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
Abstract
Apoptosis, or programmed cell death, is an essential physiological process for proper embryogenesis as well as for homeostasis during aging. In addition, apoptosis is one of the major mechanisms causing cell loss in pathophysiological conditions such as heart failure. Thus, inhibition of apoptosis is an important approach for preventive and therapeutic strategies. Here we show that the histone 3 lysine 4- and lysine 36-specific methyltransferase Smyd2 acts as an endogenous antagonistic player of p53-dependent cardiomyocyte apoptosis. Smyd2 protein levels were significantly decreased in cardiomyocytes upon cobalt chloride-induced apoptosis or myocardial infarction, while p53 expression was enhanced. siRNA-mediated knockdown of Smyd2 in cultured cardiomyocytes further enhanced cobalt chloride-induced cardiomyocyte apoptosis. In contrast, Smyd2 overexpression resulted in marked methylation of p53 and prevented its accumulation as well as apoptotic cell death in an Hsp90-independent manner. Moreover, overexpression, of Smyd2, but not Smyd2Y240F lacking a methyl transferase activity, significantly rescued CoCl2-induced apoptosis in H9c2 cardioblasts. Finally, Smyd2 cardiomyocyte-specific deletion in vivo promoted apoptotic cell death upon myocardial infarction, which correlated with enhanced expression of p53 and pro-apoptotic Bax. Collectively, our data indicate Smyd2 as a cardioprotective protein by methylating p53.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.