ArticleThe Journal of biological chemistry2008
Expression of S100A6 in cardiac myocytes limits apoptosis induced by tumor necrosis factor-alpha.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- Toxoplasma gondii hijacks host S100A6 to enhance cell migration and brain cyst formation.Communications biology · 2026Article
- Overexpression of PRDM16 attenuates acute kidney injury progression: genetic and pharmacological approaches.MedComm · 2024Article
- S100A6 Regulates nucleus pulposus cell apoptosis via Wnt/β-catenin signaling pathway: an in vitro and in vivo study.Molecular medicine (Cambridge, Mass.) · 2024Article
- The Role of S100A6 in Human Diseases: Molecular Mechanisms and Therapeutic Potential.Biomolecules · 2023Review
- S100 proteins in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2023Review
- Apoptotic Cell Death in Bicuspid-Aortic-Valve-Associated Aortopathy.International journal of molecular sciences · 2023Article
- S100A6 Protein-Expression and Function in Norm and Pathology.International journal of molecular sciences · 2023Review
- S100 Proteins in Fatty Liver Disease and Hepatocellular Carcinoma.International journal of molecular sciences · 2022Review
- Glial S100A6 Degrades β-amyloid Aggregation through Targeting Competition with Zinc Ions.Aging and disease · 2019Article
- S100A6/miR193a regulates the proliferation, invasion, migration and angiogenesis of lung cancer cells through the P53 acetylation.American journal of translational research · 2019Article
- Sex differences in distribution of cannabinoid receptors (CB1 and CB2), S100A6 and CacyBP/SIP in human ageing hearts.Biology of sex differences · 2018Article
- Comparative evaluation of cannabinoid receptors, apelin and S100A6 protein in the heart of women of different age groups.BMC cardiovascular disorders · 2018Article
- The Apoptotic, Angiogenic and Cell Proliferation Genes CD63, S100A6 e GNB2L1 are Altered in Patients with Endometriosis.Revista brasileira de ginecologia e obstetricia : revista da Federacao Brasileira das Sociedades de Ginecologia e Obstetricia · 2018Article
- High Expression of S100A6 Predicts Unfavorable Prognosis of Lung Squamous Cell Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- S100A6 protein: functional roles.Cellular and molecular life sciences : CMLS · 2017Review
- Article
- Cardiac Overexpression of S100A6 Attenuates Cardiomyocyte Apoptosis and Reduces Infarct Size After Myocardial Ischemia-Reperfusion.Journal of the American Heart Association · 2017Article
- Influence of doxazosin on biosynthesis of S100A6 and atrial natriuretic factor peptides in the heart of spontaneously hypertensive rats.Experimental biology and medicine (Maywood, N.J.) · 2016Article
- Identification of potential therapeutic targets for papillary thyroid carcinoma by bioinformatics analysis.Oncology letters · 2016Article
- Molecular characterization of the porcine S100A6 gene and analysis of its expression in pigs infected with highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV).Journal of applied genetics · 2015Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
S100A6 is induced in myocardium post-infarction in vivo and in response to growth factors and inflammatory cytokines in vitro. Forced expression of S100A6 in cardiomyocytes inhibits regulation of cardiac specific gene expression in response to trophic stimulation. To define regulation and function of S100A6, we characterized the human S100A6 promoter and mapped upstream regulatory elements in rat neonatal cardiac myocytes, fibroblasts, and vascular smooth muscle cells and defined a functional role for S100A6 in tumor necrosis factor-alpha-induced myocyte apoptosis. The functional S100A6 promoter was localized to region -167/+134 containing 167 upstream base pairs. The S100A6 promoter is regulated by positive (-361/-167 and -588/-361) and negative (-1371/-1194) elements. Tumor necrosis factor-alpha induced the maximal S100A6 promoter and transcription factor NF-kappaB (p65 subunit). Electrophoretic mobility shift showed that tumor necrosis factor-alpha induced p65 binding to a potential NF-kappaB-binding site at -460/-451. Chromatin immunoprecipitation analysis revealed p65 is recruited to the S100A6 promoter upon tumor necrosis factor-alpha stimulation. The NF-kappaB inhibitor caffeic acid phenethyl ester and mutation of the NF-kappaB-binding site inhibited S100A6 promoter activation by tumor necrosis factor-alpha. Tumor necrosis factor-alpha induced cardiac myocyte apoptosis. Specific inhibition of S100A6 using a small interfering RNA directed against S100A6 potentiated tumor necrosis factor-alpha-induced myocyte apoptosis, whereas overexpression of S100A6 by gene transfer prevented tumor necrosis factor-alpha-induced myocyte apoptosis by interfering with p53 phosphorylation. These results demonstrate that S100A6 is induced by tumor necrosis factor-alpha via an NF-kappaB-dependent mechanism, serving a role in homeostasis to limit tumor necrosis factor-alpha-induced apoptosis by regulating p53 phosphorylation.
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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.