Results 61 to 70 of about 2,934,766 (329)

HDAC and HDAC Inhibitor: From Cancer to Cardiovascular Diseases [PDF]

open access: yesChonnam Medical Journal, 2016
Histone deacetylases (HDACs) are epigenetic regulators that regulate the histone tail, chromatin conformation, protein-DNA interaction, and even transcription. HDACs are also post-transcriptional modifiers that regulate the protein acetylation implicated in several pathophysiologic states.
Yoon, Somy, Eom, Gwang Hyeon
openaire   +2 more sources

Histone deacetylase inhibitors induce invasion of human melanoma cells in vitro via differential regulation of N-cadherin expression and RhoA activity [PDF]

open access: yes, 2016
Background: Histone deacetylase inhibitors (HDACi) exert multiple cytotoxic actions on cancer cells. Currently, different synthetic HDACi are in clinical use or clinical trials; nevertheless, since both pro-invasive and anti-invasive activities have been
Andrade, Ricardo   +6 more
core   +4 more sources

From molecular promise to preclinical results: HDAC inhibitors in the race for healthy aging drugs

open access: yesEMBO Molecular Medicine, 2019
Reversing or slowing the aging process brings great promise to treat or prevent age‐related disease, and targeting the hallmarks of aging is a strategy to achieve this.
Rebecca L. McIntyre   +4 more
semanticscholar   +1 more source

HDAC inhibitors as antifibrotic drugs in cardiac and pulmonary fibrosis

open access: yesTherapeutic Advances in Chronic Disease, 2019
Fibrosis usually results from dysregulated wound repair and is characterized by excessive scar tissue. It is a complex process with unclear mechanisms.
X. Lyu   +4 more
semanticscholar   +1 more source

Decreased DHRS2 expression is associated with HDACi resistance and poor prognosis in ovarian cancer

open access: yesEpigenetics, 2020
Histone deacetylases (HDACs) have been linked to a variety of cancers, and HDAC inhibitors (HDACi) are a promising class of drugs that have demonstrated anti-cancer effects.
Yingyan Han   +10 more
doaj   +1 more source

AKT activation controls cell survival in response to HDAC6 inhibition. [PDF]

open access: yes, 2016
HDAC6 is emerging as an important therapeutic target for cancer. We investigated mechanisms responsible for survival of tumor cells treated with a HDAC6 inhibitor.
Aboagye, EO   +3 more
core   +1 more source

Interplay between circadian and other transcription factors—Implications for cycling transcriptome reprogramming

open access: yesFEBS Letters, EarlyView.
This perspective highlights emerging insights into how the circadian transcription factor CLOCK:BMAL1 regulates chromatin architecture, cooperates with other transcription factors, and coordinates enhancer dynamics. We propose an updated framework for how circadian transcription factors operate within dynamic and multifactorial chromatin landscapes ...
Xinyu Y. Nie, Jerome S. Menet
wiley   +1 more source

HDAC1 inhibition by MS-275 in mesothelial cells limits cellular invasion and promotes MMT reversal [PDF]

open access: yes, 2018
Peritoneal fibrosis is a pathological alteration of the peritoneal membrane occurring in a variety of conditions including peritoneal dialysis (PD), post-surgery adhesions and peritoneal metastases.
Battistelli, Cecilia   +14 more
core   +1 more source

HDAC Inhibitors: Therapeutic Potential in Fibrosis-Associated Human Diseases

open access: yesInternational Journal of Molecular Sciences, 2019
Fibrosis is characterized by excessive deposition of the extracellular matrix and develops because of fibroblast differentiation during the process of inflammation. Various cytokines stimulate resident fibroblasts, which differentiate into myofibroblasts.
Somy Yoon, Gaeun Kang, G. Eom
semanticscholar   +1 more source

The role of histone modifications in transcription regulation upon DNA damage

open access: yesFEBS Letters, EarlyView.
This review discusses the critical role of histone modifications in regulating gene expression during the DNA damage response (DDR). By modulating chromatin structure and recruiting repair factors, these post‐translational modifications fine‐tune transcriptional programmes to maintain genomic stability.
Angelina Job Kolady, Siyao Wang
wiley   +1 more source

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