ArticleCirculation research2009
Positive transcription elongation factor b activity in compensatory myocardial hypertrophy is regulated by cardiac lineage protein-1.
Article in Circulation research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 30 citations in OpenAlex.
- The role of complement C3 in the outcome of regional myocardial infarction.Biochemistry and biophysics reports · 2023Article
- Identify Tcea3 as a novel anti-cardiomyocyte hypertrophy gene involved in fatty acid oxidation and oxidative stress.Frontiers in cardiovascular medicine · 2023Article
- P-TEFb as A Promising Therapeutic Target.Molecules (Basel, Switzerland) · 2020Review
- Hepatic DNA Damage Induced by Electronic Cigarette Exposure Is Associated With the Modulation of NAD+/PARP1/SIRT1 Axis.Frontiers in endocrinology · 2019Article
- HMBA is a putative HSP70 activator stimulating HEXIM1 expression that is down-regulated by estrogen.The Journal of steroid biochemistry and molecular biology · 2017Article
- Hexim1, a Novel Regulator of Leptin Function, Modulates Obesity and Glucose Disposal.Molecular endocrinology (Baltimore, Md.) · 2016Article
- BET-ting on chromatin-based therapeutics for heart failure.Journal of molecular and cellular cardiology · 2014Review
- Negative elongation factor controls energy homeostasis in cardiomyocytes.Cell reports · 2014Article
- Lead optimization of HMBA to develop potent HEXIM1 inducers.Bioorganic & medicinal chemistry letters · 2014Article
- BET acetyl-lysine binding proteins control pathological cardiac hypertrophy.Journal of molecular and cellular cardiology · 2013Article
- Article
- Inducible re-expression of HEXIM1 causes physiological cardiac hypertrophy in the adult mouse.Cardiovascular research · 2013Article
- Cardiac lineage protein-1 (CLP-1) regulates cardiac remodeling via transcriptional modulation of diverse hypertrophic and fibrotic responses and angiotensin II-transforming growth factor β (TGF-β1) signaling axis.The Journal of biological chemistry · 2012Article
- Review
- Article
- HIV-1 replication and latency are regulated by translational control of cyclin T1.Journal of molecular biology · 2011Article
- A Network of Regulations by Small Non-Coding RNAs: The P-TEFb Kinase in Development and Pathology.Frontiers in genetics · 2011Article
- CLP-1 associates with MyoD and HDAC to restore skeletal muscle cell regeneration.Journal of cell science · 2010Article
- Dysregulation of positive transcription elongation factor B and myocardial hypertrophy.Circulation research · 2009Article
- The Bin3 RNA methyltransferase targets 7SK RNA to control transcription and translation.Wiley interdisciplinary reviews. RNAReview
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Emerging evidence illustrates the importance of the positive transcription elongation factor (P-TEF)b in control of global RNA synthesis, which constitutes a major feature of the compensatory response to diverse hypertrophic stimuli in cardiomyocytes. P-TEFb complex, composed of cyclin T and cdk9, is critical for elongation of nascent RNA chains via phosphorylation of the carboxyl-terminal domain of RNA polymerase (Pol) II. We and others have shown that the activity of P-TEFb is inhibited by its association with cardiac lineage protein (CLP)-1, the mouse homolog of human HEXIM1, in various physiological and pathological conditions. To investigate the mechanism of control of P-TEFb activity by CLP-1 in cardiac hypertrophy, we used a transgenic mouse model of hypertrophy caused by overexpression of calcineurin in the heart. We observed that the level of CLP-1 associated with P-TEFb was reduced markedly in hypertrophic hearts. We also generated bigenic mice (MHC-cyclin T1/CLP-1(+/-)) by crossing MHC-cyclin T1 transgenic mice with CLP-1 heterozygote. The bigenic mice exhibit enhanced susceptibility to hypertrophy that is accompanied with an increase in cdk9 activity via an increase in serine 2 phosphorylation of carboxyl-terminal domain and an increase in GLUT1/GLUT4 ratio. These mice have compensated systolic function without evidence of fibrosis and reduced lifespan. These data suggest that the reduced level of CLP-1 introduced in the background of elevated levels of cyclin T1 elevates derepression of P-TEFb activity and emphasizes the importance of the role of CLP-1 in the mechanism governing compensatory hypertrophy in cardiomyocytes.
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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.