Results 41 to 50 of about 14,188 (207)

HDAC4 Regulates Muscle Fiber Type-Specific Gene Expression Programs [PDF]

open access: yes, 2015
Fiber type-specific programs controlled by the transcription factor MEF2 dictate muscle functionality. Here, we show that HDAC4, a potent MEF2 inhibitor, is predominantly localized to the nuclei in fast/glycolytic fibers in contrast to the sarco-plasm in
Meghan Kapur   +11 more
core   +1 more source

Myocyte-specific overexpressing HDAC4 promotes myocardial ischemia/reperfusion injury

open access: yesMolecular Medicine, 2018
Background Histone deacetylases (HDACs) play a critical role in modulating myocardial protection and cardiomyocyte survivals. However, Specific HDAC isoforms in mediating myocardial ischemia/reperfusion injury remain currently unknown.
Ling Zhang   +9 more
doaj   +1 more source

Knockdown of HDAC4 impairs LTM.

open access: yes, 2013
HDAC4-RNAi expression was restricted to the adult brain with the TARGET system. A. Expression of HDAC4-RNAi in the fly brain repressed HDAC4 expression to ~50% of that of control brains.
Silvia Schwartz (162929)   +3 more
core   +1 more source

Promotion of microRNA-146a by histone deacetylase 4 silencing contributes to radiosensitization of esophageal carcinoma

open access: yesJournal of Translational Medicine, 2022
Background Histone deacetylases (HDACs) have been identified to be implicated in the carcinogenesis and cancer progression. The present study was performed to probe into the effect of HDAC4 on radioresistance of esophageal carcinoma (EC).
Zhonghua Lu   +4 more
doaj   +1 more source

Neuronal activity‐dependent nucleocytoplasmic shuttling of HDAC4 and HDAC5 [PDF]

open access: yesJournal of Neurochemistry, 2003
AbstractThe class II histone deacetylases, HDAC4 and HDAC5, directly bind to and repress myogenic transcription factors of the myocyte enhancer factor‐2 (MEF‐2) family thereby inhibiting skeletal myogenesis. During muscle differentiation, repression of gene transcription by MEF‐2/HDAC complexes is relieved due to calcium/calmodulin‐dependent (CaM ...
Chawla, Sangeeta   +4 more
openaire   +2 more sources

Deacetylation of Glutaminase by HDAC4 contributes to Lung Cancer Tumorigenesis

open access: yesInternational Journal of Biological Sciences, 2022
Inhibiting cancer metabolism via glutaminase (GAC) is a promising strategy to disrupt tumor progression. However, mechanism regarding GAC acetylation remains mostly unknown. In this study, we demonstrate that lysine acetylation is a vital post-translational modification that inhibits GAC activity in non-small cell lung cancer (NSCLC).
Wang, Tao   +5 more
openaire   +2 more sources

Overexpression of HDAC4 impairs LTM.

open access: yes, 2013
In all cases, HDAC4 expression was restricted to the adult brain with the TARGET system. A, B. Courtship activity of naïve males was not altered by OK107-GAL4 mediated overexpression of HDAC4 (ANOVA, p=0.377) (A), but LTM was significantly impaired ...
Silvia Schwartz (162929)   +3 more
core   +1 more source

CTS-induced HDAC4 nuclear relocation in chondrocytes.

open access: yes, 2016
(A) Fluorescence microscope showed that GFP-HDAC4 was mainly located in the cytoplasm of cells in non-stretched control group (a-c), while GFP-HDAC4 was relocated to nucleus of cells subjected to CTS (d-f).
Zhi Lv (321968)   +9 more
core   +1 more source

Multifunctional hyaluronic acid hydrogel integrating exosome‐encapsulating gelatin microspheres accelerates skeletal muscle regeneration via TGF‐β1 activation and enhanced myogenic cell viability

open access: yesBMEMat, EarlyView.
Schematic illustration of preparation of injectable H/G@Co@miR‐206 hydrogel for efficient skeletal muscle regeneration in cardiotoxin‐induced skeletal muscle injury SD rat model. Abstract The effective treatment of acute skeletal muscle injuries remains challenging, necessitating therapeutic strategies that concurrently reestablish vascular perfusion ...
Zhengzhe Han   +9 more
wiley   +1 more source

Enhanced peripheral blood mononuclear cell lipid metabolism drives poor immunotherapy response via ferroptotic stress‐induced T cell exhaustion in hepatocellular carcinoma

open access: yesInterdisciplinary Medicine, EarlyView.
Integrated multi‐omics reveals that CD36‐mediated lipid overload in PBMCs drives T cell exhaustion via sub‐lethal ferroptotic stress and AKT suppression. This systemic metabolic signature serves as a robust predictor of immunotherapy response in HCC, suggesting that modulating lipid metabolism can rescue immune fitness.
Ying Zhu   +6 more
wiley   +1 more source

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