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BET Bromodomains Mediate Transcriptional Pause Release in Heart Failure
Open accessAbstract
Heart failure (HF) is driven by the interplay between regulatory transcription factors and dynamic alterations in chromatin structure. Pathologic gene transactivation in HF is associated with recruitment of histone acetyl-transferases and local chromatin hyperacetylation. We therefore assessed the role of acetyl-lysine reader proteins, or bromodomains, in HF. Using a chemical genetic approach, we establish a central role for BET family bromodomain proteins in gene control during HF pathogenesis. BET inhibition potently suppresses cardiomyocyte hypertrophy in vitro and pathologic cardiac remodeling in vivo. Integrative transcriptional and epigenomic analyses reveal that BET proteins function mechanistically as pause-release factors critical to expression of genes that are central to HF pathogenesis and relevant to the pathobiology of failing human hearts. This study implicates epigenetic readers as essential effectors of transcriptional pause release during HF pathogenesis and identifies BET coactivator proteins as therapeutic targets in the heart.
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“BET inhibition exerted a strong protective effect on left ventricular ejection fraction (Fig. 1B)4,6-10.”
From Chromatin remodelling drives immune cell–fibroblast communication in heart failure (2024) · cites this paper as [6]
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“As BET proteins are transcriptional co-activators and their inhibition is associated with protection in heart failure models6-8”
From Chromatin remodelling drives immune cell–fibroblast communication in heart failure (2024) · cites this paper as [6]
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Ultrafast and memory-efficient alignment of short DNA sequences to the human genome.
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Selective inhibition of BET bromodomains
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“We and others have utilized this chemical genetic tool to probe BET function in a number of developmental and disease contexts, such as cancer (Delmore et al., 2011; Filippakopoulos et al., 2010), HIV infection (Banerjee et al.”
InfluentialSelf-citationSelective Inhibition of Tumor Oncogenes by Disruption of Super-Enhancers
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“Furthermore, the very recent discovery of asymmetrically loaded BRD4 on a critical subset of state-specific enhancers termed superenhancers (Lovén et al., 2013) raises the possibility that such superenhancers might also be active in the stressed myocardium and contribute to BET target specificity.”
Self-citationBET Bromodomain Inhibition as a Therapeutic Strategy to Target c-Myc
Delmore, J. E., Issa, G. C., Lemieux, M. E., Rahl, P. B., Shi, J., Jacobs, H. M., Kastritis, E., Gilpatrick, T., Paranal, R. M., Qi, J., et al. (2011) · Cell · doi:10.1016/j.cell.2011.08.017 · Cited by 2,888 · cited 4×
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InfluentialSelf-citationXie, X., Lu, J., Kulbokas, E. J., Golub, T. R., Mootha, V., Lindblad-Toh, K., Lander, E. S., & Kellis, M. (2005) · Nature · doi:10.1038/nature03441 · Cited by 1,872 · cited 1×
“Specifically, we studied the Broad Institute Molecular Signatures Database C3 motif gene sets (Xie et al., 2005), as well as three functional, in vivo signatures of CMspecific transcriptional effectors: Calcineurin-NFAT (Bousette et al.”
RNAi screen identifies Brd4 as a therapeutic target in acute myeloid leukaemia
Zuber, J., Shi, J., Wang, E., Rappaport, A. R., Herrmann, H., Sison, E. A., Magoon, D., Qi, J., Blatt, K., Wunderlich, M., et al. (2011) · Nature · doi:10.1038/nature10334 · Cited by 1,870 · cited 2×
“Prior studies from our laboratory and others have implicated BET bromodomains in neoplastic MYC transcription in hematopoietic tumors (Delmore et al., 2011; Zuber et al., 2011).”
Self-citationHistone Recognition and Large-Scale Structural Analysis of the Human Bromodomain Family
Filippakopoulos, P., Picaud, S., Mangos, M., Keates, T., Lambert, J., Baršytė-Lovejoy, D., Felletár, I., Volkmer, R., Müller, S., Pawson, T. J., et al. (2012) · Cell · doi:10.1016/j.cell.2012.02.013 · Cited by 1,759 · cited 1×
“Context-specific recognition of Kac at regions of actively transcribed euchromatin is mediated by epigenetic ‘‘reader’’ proteins possessing a Kac-recognition module or bromodomain (Filippakopoulos et al., 2012).”
Transcriptional Regulation and Its Misregulation in Disease
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“As alterations in higher-order chromatin structure modulate the net output of multiple, simultaneously activated transcriptional networks (Lee and Young, 2013; Schreiber and Bernstein, 2002), manipulation of cardiac gene control via targeting of chromatin-dependent signal transduction represents a potentially powerful…”
InfluentialSuppression of inflammation by a synthetic histone mimic
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“5 hr and increased over time (Figures 2B and 2C), consistent with the emerging role of BETs as coactivators of inducible gene expression programs (Nicodeme et al., 2010).”
Transcriptional Amplification in Tumor Cells with Elevated c-Myc
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“Traveling ratio is a validated measure of transcriptional pause release that compares promoter and elongating gene body occupancy levels of Pol II to quantify the ratio of paused to elongating Pol II (Lin et al., 2012; Wade and Struhl, 2008).”
Self-citationWriting Group Members, Roger, V. L., Go, A. S., Lloyd-Jones, D. M., Benjamin, E. J., Berry, J. D., Borden, W. B., Bravata, D. M., Dai, S., Ford, E. S., et al. (2012) · Circulation · doi:10.1161/cir.0b013e3182456d46 · Cited by 1,512
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c-Myc Regulates Transcriptional Pause Release
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“(E and F) Empirical cumulative distribution plots of Pol II traveling ratios (TR) (Rahl et al., 2010) for genes that are transcriptionally active in either sham or TAC-treated hearts (E) and genes that are TAC induced and reversed by JQ1 (F).”
Self-citationControlling the elongation phase of transcription with P-TEFb
Peterlin, B. M., & Price, D. H. (2006) · Molecular Cell · doi:10.1016/j.molcel.2006.06.014 · Cited by 1,144 · cited 2×
“Interestingly, we also observed significant upregulation of the P-TEFb inhibitory protein HEXIM1 (Espinoza-Derout et al., 2009; Peterlin and Price, 2006; Yoshikawa et al., 2012) during JQ1 treatment, suggesting an additional mechanism by which BET bromodomain inhibition may inhibit transcriptional elongation (Figures…”
Recruitment of P-TEFb for Stimulation of Transcriptional Elongation by the Bromodomain Protein Brd4
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Class II Histone Deacetylases Act as Signal-Responsive Repressors of Cardiac Hypertrophy
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“(Figure 4D) typically seen after 4 weeks of TAC (Sano et al., 2007; Song et al., 2010).”
Histone deacetylases 1 and 2 redundantly regulate cardiac morphogenesis, growth, and contractilityPreprint
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“Previous studies in NIH 3T3 cells and macrophages have demonstrated that BRD4 interacts with P-TEFb and facilitates stimulus-coupled recruitment of P-TEFb to target promoters (Hargreaves et al., 2009; Patel et al., 2013).”
Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3β activity
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Signaling effectors underlying pathologic growth and remodeling of the heart
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Small-Molecule Inhibition of BRDT for Male Contraception
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“First, using a chemical biology approach, we leveraged the validated small-molecule probe of BET bromodomain function, JQ1 (Figure 1A), in the established NRVM model in vitro (Simpson et al., 1982).”
Targeting Epigenetic Readers in Cancer
Dawson, M. A., Kouzarides, T., & Huntly, B. J. P. (2012) · New England Journal of Medicine · doi:10.1056/nejmra1112635 · Cited by 405 · cited 1×
“Molecular recognition of Kac by bromodomain-containing proteins serves to increase the effective molarity of transcriptional complexes promoting chromatin remodeling, transcriptional initiation, and elongation (Dawson et al., 2012).”
Signaling Network Model of Chromatin
Schreiber, S. L., & Bernstein, B. (2002) · Cell · doi:10.1016/s0092-8674(02)01196-0 · Cited by 399 · cited 2×
“Transcriptional activation is associated with local N-ε-acetylation of lysine sidechains on the unstructured amino-terminal tail of histone proteins (Schreiber and Bernstein, 2002).”
Conserved P-TEFb-interacting domain of BRD4 inhibits HIV transcription
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“Defining the extent to which BETs alter transcriptional elongation through direct interactions with components of the P-TEFb complex (Bisgrove et al., 2007) or regulation of HEXIM-1 expression represent important avenues of future investigation.”
BET bromodomain inhibition targets both c-Myc and IL7R in high-risk acute lymphoblastic leukemia
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Self-citationThe Transcription Factors GATA4 and GATA6 Regulate Cardiomyocyte Hypertrophy in Vitro and in Vivo
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Toward transcriptional therapies for the failing heart: chemical screens to modulate genes
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“Notably, stress pathways activated in HF are associated with dynamic remodeling of chromatin (McKinsey and Olson, 2005; Sayed et al., 2013), including global changes in histone acetylation and DNA methylation.”
BET bromodomain inhibition as a novel strategy for reactivation of HIV-1
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Self-citationTranscriptional Genomics Associates FOX Transcription Factors With Human Heart Failure
Hannenhalli, S. S., Putt, M., Gilmore, J. M., Wang, J., Parmacek, M. S., Epstein, J. A., Morrisey, E. E., Margulies, K. B., & Cappola, T. P. (2006) · Circulation · doi:10.1161/circulationaha.106.632430 · Cited by 257 · cited 4×
“Gene expression profiles from left ventricles obtained from nonfailing versus failing human hearts were curated from a published data set (Hannenhalli et al., 2006).”
InfluentialSelf-citationPFI-1, a Highly Selective Protein Interaction Inhibitor, Targeting BET Bromodomains
Picaud, S., Costa, D. D., Thanasopoulou, A., Filippakopoulos, P., Fish, P. V., Philpott, M., Fedorov, O., Brennan, P. E., Bunnage, M. E., Owen, D. R., et al. (2013) · Cancer Research · doi:10.1158/0008-5472.can-12-3292 · Cited by 257
Self-citationHu, P., Zhang, D., Swenson, L., Chakrabarti, G., Abel, E. D., & Litwin, S. E. (2003) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00108.2003 · Cited by 245
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“Hyperactivation of P-TEFb and consequent increases in global transcription are considered a hallmark of pathologic cardiac hypertrophy in multiple systems (Espinoza-Derout et al., 2009; Sano et al., 2002; Yoshikawa et al., 2012).”
InfluentialCardiomyocyte GATA4 functions as a stress-responsive regulator of angiogenesis in the murine heart
Heineke, J., Auger‐Messier, M., Xu, J., Oka, T., Sargent, M. A., York, A. J., Klevitsky, R., Vaikunth, S. S., Duncan, S. A., Aronow, B. J., et al. (2007) · Journal of Clinical Investigation · doi:10.1172/jci32573 · Cited by 234 · cited 2×
“, 2012), and GATA4 (Heineke et al., 2007).”
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“Recently, BET bromodomains have also been shown to bind to enhancer elements in the eukaryotic genome (Lovén et al., 2013; Zhang et al., 2012).”
Patel, M. C., Debrosse, M., Smith, M. D., Dey, A., Huynh, W., Sarai, N., Heightman, T. D., Tamura, T., & Ozato, K. (2013) · Molecular and Cellular Biology · doi:10.1128/mcb.01180-12 · Cited by 182 · cited 1×
“Previous studies in NIH 3T3 cells and macrophages have demonstrated that BRD4 interacts with P-TEFb and facilitates stimulus-coupled recruitment of P-TEFb to target promoters (Hargreaves et al., 2009; Patel et al., 2013).”
Margulies, K. B., Matiwala, S., Cornejo, C., Olsen, H. S., Craven, W. A., & Bednarik, D. P. (2005) · Circulation Research · doi:10.1161/01.res.0000159390.03503.c3 · Cited by 178 · cited 1×
“Human Samples LV samples from healthy human hearts were obtained as described (Hannenhalli et al., 2006; Margulies et al., 2005) in accordance with the Investigation Review Committee at the Hospital of the University of Pennsylvania, Philadelphia, PA.”
Self-citationGene Expression Dynamics Inspector (GEDI): for integrative analysis of expression profiles
Eichler, G. S., Huang, S., & Ingber, D. E. (2003) · Bioinformatics · doi:10.1093/bioinformatics/btg307 · Cited by 176 · cited 1×
“To visualize the global transcriptional effects of TAC and BET bromodomain inhibition in the model over time, we performed gene expression dynamics inspector (GEDI) analysis (Eichler et al., 2003).”
Interaction Between NFκB and NFAT Coordinates Cardiac Hypertrophy and Pathological Remodeling
Liu, Q., Chen, Y., Auger‐Messier, M., & Molkentin, J. D. (2012) · Circulation Research · doi:10.1161/circresaha.111.260729 · Cited by 176
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Quantitative Control of Adaptive Cardiac Hypertrophy by Acetyltransferase p300
Wei, J. Q., Shehadeh, L. A., Mitrani, J. M., Pessanha, M. G., Slepak, T. I., Webster, K. A., & Bishopric, N. H. (2008) · Circulation · doi:10.1161/circulationaha.107.760488 · Cited by 138 · cited 3×
“, 2011), as well as histone modifying enzymes such as EP300 and HDAC2 (Trivedi et al., 2007; Wei et al., 2008; Zhang et al., 2002) activate a CM gene expression program that results in cellular dysfunction.”
Song, X., Kusakari, Y., Xiao, C., Kinsella, S., Rosenberg, M. A., Scherrer‐Crosbie, M., Hara, K., Rosenzweig, A., & Matsui, T. (2010) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00338.2010 · Cited by 131 · cited 1×
“(Figure 4D) typically seen after 4 weeks of TAC (Sano et al., 2007; Song et al., 2010).”
Kruppel-like factor 15 regulates skeletal muscle lipid flux and exercise adaptation
Haldar, S. M., Jeyaraj, D., Anand, P., Zhu, H., Lu, Y., Prosdocimo, D. A., Eapen, B. L., Kawanami, D., Okutsu, M., Brotto, L. S., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1121060109 · Cited by 118
Self-citationThe transition from transcriptional initiation to elongation
Wade, J. T., & Struhl, K. (2008) · Current Opinion in Genetics & Development · doi:10.1016/j.gde.2007.12.008 · Cited by 117 · cited 1×
“Traveling ratio is a validated measure of transcriptional pause release that compares promoter and elongating gene body occupancy levels of Pol II to quantify the ratio of paused to elongating Pol II (Lin et al., 2012; Wade and Struhl, 2008).”
Hypertrophic growth in cardiac myocytes is mediated by Myc through a Cyclin D2‐dependent pathway
Zhong, W., Mao, S., Tobis, S., Angelis, E., Jordan, M. C., Roos, K. P., Fishbein, M. C., de Alborán, I. M., & MacLellan, W. R. (2006) · The EMBO Journal · doi:10.1038/sj.emboj.7601252 · Cited by 115 · cited 3×
“These three time points capture induction of early response genes such as c-Myc (Zhong et al., 2006), as well as the late hypertrophic expression program.”
InfluentialKlf15 Deficiency Is a Molecular Link Between Heart Failure and Aortic Aneurysm Formation
Haldar, S. M., Lu, Y., Jeyaraj, D., Kawanami, D., Cui, Y., Eapen, S. J., Hao, C., Li, Y., Doughman, Y., Watanabe, M., et al. (2010) · Science Translational Medicine · doi:10.1126/scitranslmed.3000502 · Cited by 111
Self-citationvan Berlo, J. H., Elrod, J. W., Aronow, B. J., Pu, W. T., & Molkentin, J. D. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1104499108 · Cited by 101
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“Functional pathway analysis of TAC-inducible transcripts that were suppressed by JQ1 showed enrichment for key biological processes involved in pathologic myocardial remodeling and HF progression in vivo (Figure 5F) (Song et al., 2012; Zhao et al., 2004).”
Microarray analysis of gene expression after transverse aortic constriction in mice
Zhao, M., Chow, A., Powers, J. C., Fajardo, G., & Bernstein, D. (2004) · Physiological Genomics · doi:10.1152/physiolgenomics.00040.2004 · Cited by 82 · cited 1×
“Functional pathway analysis of TAC-inducible transcripts that were suppressed by JQ1 showed enrichment for key biological processes involved in pathologic myocardial remodeling and HF progression in vivo (Figure 5F) (Song et al., 2012; Zhao et al., 2004).”
Bousette, N., Chugh, S., Fong, V., Isserlin, R., Kim, K.-H., Volchuk, A., Backx, P. H., Liu, P., Kislinger, T., MacLennan, D. H., et al. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1013555107 · Cited by 61 · cited 2×
“, 2005), as well as three functional, in vivo signatures of CMspecific transcriptional effectors: Calcineurin-NFAT (Bousette et al., 2010), NFkB (Maier et al.”
Sayed, D. H., He, M., Yang, Z., Lin, L., & Abdellatif, M. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m112.429449 · Cited by 56 · cited 2×
“Consistent with our findings, other work has previously identified that Pol II pause release is a dominant mechanism for gene induction in both the developing heart and in the adult mouse heart during pressure overload, with de novo Pol II recruitment occurring at only 5% of induced genes in the TAC model (Sayed et al…”
Froese, N., Kattih, B., Breitbart, A., Grund, A., Geffers, R., Molkentin, J. D., Kispert, A., Wollert, K. C., Drexler, H., & Heineke, J. (2010) · Journal of Biological Chemistry · doi:10.1074/jbc.m110.176925 · Cited by 51
Espinoza‐Derout, J., Wagner, M., Salciccioli, L. F., Lazar, J., Bhaduri, S., Mascareno, E. J., Chaqour, B., & Siddiqui, M. A. Q. (2009) · Circulation Research · doi:10.1161/circresaha.108.191726 · Cited by 30 · cited 3×
“Interestingly, we also observed significant upregulation of the P-TEFb inhibitory protein HEXIM1 (Espinoza-Derout et al., 2009; Peterlin and Price, 2006; Yoshikawa et al., 2012) during JQ1 treatment, suggesting an additional mechanism by which BET bromodomain inhibition may inhibit transcriptional elongation (Figures…”
Yoshikawa, N., Shimizu, N., Maruyama, T., Sano, M., Matsuhashi, T., Fukuda, K., Kataoka, M., Satoh, T., Ojima, H., Sawai, T., et al. (2012) · PLoS ONE · doi:10.1371/journal.pone.0052522 · Cited by 17
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Phthalimide conjugation as a strategy for in vivo target protein degradation
Winter, G. E., Buckley, D. L., Paulk, J., Roberts, J. M., Souza, A., Dhe-Paganon, S., & Bradner, J. E. (2015) · Science · doi:10.1126/science.aab1433 · Cited by 1,760
Self-citationTargeting bromodomains: epigenetic readers of lysine acetylation
Filippakopoulos, P., & Knapp, S. (2014) · Nature Reviews Drug Discovery · doi:10.1038/nrd4286 · Cited by 1,298
The dTAG system for immediate and target-specific protein degradation
Nabet, B., Roberts, J. M., Buckley, D. L., Paulk, J., Dastjerdi, S., Yang, A., Leggett, A. L., Erb, M. A., Lawlor, M. A., Souza, A., et al. (2018) · Nature Chemical Biology · doi:10.1038/s41589-018-0021-8 · Cited by 1,118
Self-citationThe Mechanisms behind the Therapeutic Activity of BET Bromodomain Inhibition
Shi, J., & Vakoc, C. R. (2014) · Molecular Cell · doi:10.1016/j.molcel.2014.05.016 · Cited by 888
“Gene expression analysis of JQ1-treated cardiomyocytes identified systematic downregulation of NFkB target genes, further suggesting that BET inhibitors can attenuate NFkB function (Anand et al., 2013).”
BackgroundInfluentialNF-κB Directs Dynamic Super Enhancer Formation in Inflammation and Atherogenesis
Brown, J. D., Lin, C. Y., Duan, Q., Griffin, G., Federation, A. J., Paranal, R. M., Bair, S., Newton, G., Lichtman, A. H., Kung, A. L., et al. (2014) · Molecular Cell · doi:10.1016/j.molcel.2014.08.024 · Cited by 614
Self-citation
Metadata
- Authors
- Anand, P., Brown, J. D., Lin, C. Y., Qi, J., Zhang, R., Artero, P. C., Alaiti, M. A., Bullard, J., Alazem, K., Margulies, K. B., Cappola, T. P., Lemieux, M., Plutzky, J., Bradner, J. E., & Haldar, S. M.
- Affiliations
- University Hospitals of Cleveland (US)
- Brigham and Women's Hospital (US)
- Dana-Farber Cancer Institute (US)
- University of Pennsylvania (US)
- Harvard University (US)
- Corresponding author
- Bradner, James E.
- Haldar, Saptarsi M.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2013-08
- Volume
- 154
- Issue
- 3
- Pages
- 569-582
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4090947
- OpenAlex
- W2154924534
- Cited by
- 406
- References
- 63
- Citations by year
- 2026: 21 · 2025: 26 · 2024: 18 · 2023: 25 · 2022: 25 · 2021: 36 · 2020: 49 · 2019: 33 · 2018: 28 · 2017: 29 · 2016: 36 · 2015: 42 · 2014: 30 · 2013: 6
- FWCI
- 17.01
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Wellcome Trust
- National Heart, Lung, and Blood Institute (T32HL105338, K08HL105678, K08HL086614, R01HL105993, P01HL048743)
- National Cancer Institute (K08CA128972)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK093821)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Degradation and Inhibitors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- heart failure, BET proteins, chromatin acetylation, histone acetyltransferase, cardiac remodeling, cardiomyocyte hypertrophy, epigenetic reader protein, BET inhibition, gene expression regulation, chemical genetics
- MeSH terms
- Animals, Chromatin, Disease Models, Animal, Heart, Cardiomegaly, Heart Failure, Humans, Mice, Inbred C57BL, Transcription Factors, Transcription, Genetic, Protein Structure, Tertiary, Myocytes, Cardiac, Epigenesis, Genetic, Mice, Rats, Transcriptome
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