ArticleMolecular and cellular biology2004
The Ku protein complex interacts with YY1, is up-regulated in human heart failure, and represses alpha myosin heavy-chain gene expression.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 43 citations in OpenAlex.
- Postprandial cardiac hypertrophy is sustained by mechanics, epigenetic, and metabolic reprogramming in pythons.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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- DDX5 mRNA-targeting antisense oligonucleotide as a new promising therapeutic in combating castration-resistant prostate cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
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- Biological roles of Yin Yang 2: Its implications in physiological and pathological events.Journal of cellular and molecular medicine · 2020Review
- The left ventricle undergoes biomechanical and gene expression changes in response to increased right ventricular pressure overload.Physiological reports · 2020Article
- Contribution of Increased Expression of Yin Yang 2 to Development of Cardiomyopathy.Frontiers in molecular biosciences · 2020Article
- Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-Based Regulation of Transcription.Cell · 2019Article
- Maternal obesity impairs fetal cardiomyocyte contractile function in sheep.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- YY1 Expression Is Sufficient for the Maintenance of Cardiac Progenitor Cell State.Stem cells (Dayton, Ohio) · 2017Article
- Chromatin association of XRCC5/6 in the absence of DNA damage depends on the XPE gene product DDB2.Molecular biology of the cell · 2017Article
- Transgenic over-expression of YY1 induces pathologic cardiac hypertrophy in a sex-specific manner.Biochemical and biophysical research communications · 2015Article
- Function of YY1 in Long-Distance DNA Interactions.Frontiers in immunology · 2014Review
- DNA ends alter the molecular composition and localization of Ku multicomponent complexes.Molecular & cellular proteomics : MCP · 2012Article
- YY1 controls immunoglobulin class switch recombination and nuclear activation-induced deaminase levels.Molecular and cellular biology · 2012Article
- Oxidative DNA damage in neurons: implication of ku in neuronal homeostasis and survival.International journal of cell biology · 2012Article
- Transcription factors in heart: promising therapeutic targets in cardiac hypertrophy.Current cardiology reviews · 2011Review
- The DNA repair complex Ku70/86 modulates Apaf1 expression upon DNA damage.Cell death and differentiation · 2011Article
- Reversible epigenetic modifications of the two cardiac myosin heavy chain genes during changes in expression.Gene expression · 2010Article
- Physical interaction between TBX5 and MEF2C is required for early heart development.Molecular and cellular biology · 2009Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Human heart failure is accompanied by repression of genes such as alpha myosin heavy chain (alphaMyHC) and SERCA2A and the induction of fetal genes such as betaMyHC and atrial natriuretic factor. It seems likely that changes in MyHC isoforms contribute to the poor contractility seen in heart failure, because small changes in isoform composition can have a major effect on the contractility of cardiac myocytes and the heart. Our laboratory has recently shown that YY1 protein levels are increased in human heart failure and that YY1 represses the activity of the human alphaMyHC promoter. We have now identified a region of the alphaMyHC promoter that binds a factor whose expression is increased sixfold in failing human hearts. Through peptide mass spectrometry, we identified this binding activity to be a heterodimer of Ku70 and Ku80. Expression of Ku represses the human alphaMyHC promoter in neonatal rat ventricular myocytes. Moreover, overexpression of Ku70/80 decreases alphaMyHC mRNA expression and increases skeletal alpha-actin. Interestingly, YY1 interacts with Ku70 and Ku80 in HeLa cells. Together, YY1, Ku70, and Ku80 repress the alphaMyHC promoter to an extent that is greater than that with YY1 or Ku70/80 alone. Our results suggest that Ku is an important factor in the repression of the human alphaMyHC promoter during heart failure.
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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 Socratic graph.