ArticleBiochemical and biophysical research communications2007
Induction of high STAT1 expression in transgenic mice with LQTS and heart failure.
Article in Biochemical and biophysical research communications, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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
9 citing papers in PubMed, 21 citations in OpenAlex.
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- Study on Potential Differentially Expressed Genes in Idiopathic Pulmonary Fibrosis by Bioinformatics and Next-Generation Sequencing Data Analysis.Biomedicines · 2023Article
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- Identification of potentially relevant genes for myocardial infarction using RNA sequencing data analysis.Experimental and therapeutic medicine · 2018Article
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- Coherent functional modules improve transcription factor target identification, cooperativity prediction, and disease association.PLoS genetics · 2014Article
- LQTS mutation N1325S in cardiac sodium channel gene SCN5A causes cardiomyocyte apoptosis, cardiac fibrosis and contractile dysfunction in mice.International journal of cardiology · 2011Article
- Identification of biomarkers, pathways, and potential therapeutic targets for heart failure using next-generation sequencing data and bioinformatics analysis.Therapeutic advances in cardiovascular diseaseArticle
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Cardiac-specific expression of the N1325S mutation of SCN5A in transgenic mouse hearts (TG-NS) resulted in long QT syndrome (LQTS), ventricular arrhythmias (VT), and heart failure. In this study we carried out oligonucleotide mircoarray analysis to identify genes that are differentially expressed in the TG-NS mouse hearts. We identified 33 genes in five different functional groups that showed differential expression. None of the 33 genes are ion channel genes. STAT1, which encodes a transcription factor involved in apoptosis and interferon response, showed the most significant difference of expression between TG-NS and control mice (a nearly 10-fold increase in expression, P=4x10(-6)). The results were further confirmed by quantitative real-time PCR and Western blot analyses. Accordingly, many interferon response genes also showed differential expression in TG-NS hearts. This study represents the first microarray analysis for LQTS and implicates STAT1 in the pathogenesis and progression of LQTS and heart failure.
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