Transcriptional and Epigenomic Regulation of Adipogenesis DOI Open Access
Ji‐Eun Lee, Hannah Schmidt, Binbin Lai

и другие.

Molecular and Cellular Biology, Год журнала: 2019, Номер 39(11)

Опубликована: Март 29, 2019

Understanding adipogenesis, the process of adipocyte development, may provide new ways to treat obesity and related metabolic diseases. Adipogenesis is controlled by coordinated actions lineage-determining transcription factors epigenomic regulators. Peroxisome proliferator-activated receptor gamma (PPARγ) C/EBPα are master "adipogenic" factors. In recent years, a growing number studies have reported identification novel transcriptional regulators adipogenesis. However, many these not been validated in development vivo their working mechanisms often far from clear. this minireview, we discuss advances regulation with focus on shared both white adipogenesis brown Studies highlight importance investigating differentiation rather than drawing conclusions based knockdown experiments cell culture. Advances understanding revealed critical roles histone methylation/demethylation, acetylation/deacetylation, chromatin remodeling, DNA methylation, microRNAs differentiation. We also future research directions that help identify regulating

Язык: Английский

The molecular hallmarks of epigenetic control DOI
C. David Allis, Thomas Jenuwein

Nature Reviews Genetics, Год журнала: 2016, Номер 17(8), С. 487 - 500

Опубликована: Июнь 27, 2016

Язык: Английский

Процитировано

2313

Epigenetic Determinants of Cancer DOI Open Access
Stephen B. Baylin, Peter A. Jones

Cold Spring Harbor Perspectives in Biology, Год журнала: 2016, Номер 8(9), С. a019505 - a019505

Опубликована: Май 18, 2016

Stephen B. Baylin1 and Peter A. Jones2 1Cancer Biology Program, Johns Hopkins University, School of Medicine, Baltimore, Maryland 21287 2Van Andel Research Institute, Grand Rapids, Michigan 49503 Correspondence: sbaylin{at}jhmi.edu

Язык: Английский

Процитировано

1078

HDACs and HDAC Inhibitors in Cancer Development and Therapy DOI Open Access
Yixuan Li, Edward Seto

Cold Spring Harbor Perspectives in Medicine, Год журнала: 2016, Номер 6(10), С. a026831 - a026831

Опубликована: Сен. 6, 2016

Yixuan Li and Edward Seto George Washington University Cancer Center, Department of Biochemistry Molecular Medicine, University, Washington, DC 20037 Correspondence: seto{at}gwu.edu

Язык: Английский

Процитировано

1043

Targeting epigenetic regulators for cancer therapy: mechanisms and advances in clinical trials DOI Creative Commons
Yuan Cheng, He Cai, Manni Wang

и другие.

Signal Transduction and Targeted Therapy, Год журнала: 2019, Номер 4(1)

Опубликована: Дек. 17, 2019

Epigenetic alternations concern heritable yet reversible changes in histone or DNA modifications that regulate gene activity beyond the underlying sequence. dysregulation is often linked to human disease, notably cancer. With development of various drugs targeting epigenetic regulators, epigenetic-targeted therapy has been applied treatment hematological malignancies and exhibited viable therapeutic potential for solid tumors preclinical clinical trials. In this review, we summarize aberrant functions enzymes methylation, acetylation methylation during tumor progression highlight inhibitors targeted at enzymes.

Язык: Английский

Процитировано

891

Histone Modifications and Cancer DOI Open Access
James E. Audia, Robert M. Campbell

Cold Spring Harbor Perspectives in Biology, Год журнала: 2016, Номер 8(4), С. a019521 - a019521

Опубликована: Апрель 1, 2016

Histone posttranslational modifications represent a versatile set of epigenetic marks involved not only in dynamic cellular processes, such as transcription and DNA repair, but also the stable maintenance repressive chromatin. In this article, we review many key newly identified histone known to be deregulated cancer how impacts function. The latter part article addresses challenges current status drug development process it applies therapeutics.

Язык: Английский

Процитировано

829

Cardiac fibrosis DOI Open Access
Nikolaos G. Frangogiannis

Cardiovascular Research, Год журнала: 2020, Номер 117(6), С. 1450 - 1488

Опубликована: Окт. 26, 2020

Abstract Myocardial fibrosis, the expansion of cardiac interstitium through deposition extracellular matrix proteins, is a common pathophysiologic companion many different myocardial conditions. Fibrosis may reflect activation reparative or maladaptive processes. Activated fibroblasts and myofibroblasts are central cellular effectors in serving as main source proteins. Immune cells, vascular cells cardiomyocytes also acquire fibrogenic phenotype under conditions stress, activating fibroblast populations. Fibrogenic growth factors (such transforming factor-β platelet-derived factors), cytokines [including tumour necrosis factor-α, interleukin (IL)-1, IL-6, IL-10, IL-4], neurohumoral pathways trigger signalling cascades binding to surface receptors, downstream cascades. In addition, matricellular macromolecules deposited remodelling myocardium regulate assembly, while modulating signal transduction protease factor activity. Cardiac can sense mechanical stress mechanosensitive ion channels integrins, intracellular that contribute fibrosis response pressure overload. Although subpopulations fibroblast-like exert important protective actions both interstitial/perivascular ultimately fibrotic changes perturb systolic diastolic function, play an role pathogenesis arrhythmias. This review article discusses molecular mechanisms involved various diseases, including infarction, heart failure with reduced preserved ejection fraction, genetic cardiomyopathies, diabetic disease. Development fibrosis-targeting therapies for patients diseases will require not only understanding functional pluralism dissection basis remodelling, but appreciation heterogeneity fibrosis-associated

Язык: Английский

Процитировано

724

Cardiac fibrosis: Cell biological mechanisms, molecular pathways and therapeutic opportunities DOI Creative Commons
Nikolaos G. Frangogiannis

Molecular Aspects of Medicine, Год журнала: 2018, Номер 65, С. 70 - 99

Опубликована: Авг. 2, 2018

Язык: Английский

Процитировано

678

Off-target toxicity is a common mechanism of action of cancer drugs undergoing clinical trials DOI Open Access
Ann Lin, Christopher J. Giuliano, Ann Palladino

и другие.

Science Translational Medicine, Год журнала: 2019, Номер 11(509)

Опубликована: Сен. 11, 2019

CRISPR reveals that many cancer drug targets are dispensable for cell proliferation and identifies CDK11 as the target of one mischaracterized agent.

Язык: Английский

Процитировано

596

Writers and Readers of Histone Acetylation: Structure, Mechanism, and Inhibition DOI Open Access
Ronen Marmorstein, Ming Zhou

Cold Spring Harbor Perspectives in Biology, Год журнала: 2014, Номер 6(7), С. a018762 - a018762

Опубликована: Июль 1, 2014

Ronen Marmorstein1 and Ming-Ming Zhou2 1Program in Gene Expression Regulation, Wistar Institute, Department of Chemistry, University Pennsylvania, Philadelphia, 19104 2Department Structural Chemical Biology, Icahn School Medicine at Mount Sinai, New York, York 10065 Correspondence: marmor{at}wistar.org

Язык: Английский

Процитировано

540

Modulation of cellular processes by histone and non-histone protein acetylation DOI
Maria Shvedunova, Asifa Akhtar

Nature Reviews Molecular Cell Biology, Год журнала: 2022, Номер 23(5), С. 329 - 349

Опубликована: Янв. 18, 2022

Язык: Английский

Процитировано

519