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We also demonstrate that HDAC4 and Ubc9 (show UBE2I ELISA Kits) interact genetically during memory formation, opening new avenues for investigating the mechanisms through which HDAC4 regulates memory formation and other neurological processes.
RNAi-mediated knockdown of HDAC4 in Drosophila dampens circadian function.
HDAC4 is not only a repressor of long-term memory, but also modulates normal memory formation
dHDAC4, is a novel, catalytically active class II Drosophila histone deacetylase (show HDAC1 ELISA Kits) and is involved in the segmentation regulatory pathway and suggested complex transcriptional regulation as a potential mechanism that controls its expression
HDAC4 promotes proliferation and G1/S cell cycle progression in esophageal carcinoma cells by inhibiting CDK (show CDK4 ELISA Kits) inhibitors p21 (show CDKN1A ELISA Kits) and p27 (show PAK2 ELISA Kits) and up-regulating CDK2 (show CDK2 ELISA Kits)/4 and CDK (show CDK4 ELISA Kits)-dependent Rb phosphorylation. HDAC4 also enhances ESCC cell migration. Furthermore, HDAC4 positively regulates epithelial-mesenchymal transition (EMT (show ITK ELISA Kits)) by increasing the expression of Vimentin (show VIM ELISA Kits) and decreasing the expression of E-Cadherin (show CDH1 ELISA Kits)/alpha-Catenin (show CTNNA1 ELISA Kits).
level of myotubes MTM1 (show MTM1 ELISA Kits) mutations do not dramatically affect calcium homeostasis and calcium release mediated through the ryanodine receptor 1 (show RYR1 ELISA Kits), though they do affect myotube size and nuclear content..mature muscles such as those obtained from patient muscle biopsies exhibit a significant decrease in expression of the ryanodine receptor 1 (show RYR1 ELISA Kits), a decrease in muscle-specific (show EIF3K ELISA Kits) microRNAs and a considerable up-regulation of HDAC4.
7-amino-4-methylcoumarin did not affect acetyllysine preference in a multiply acetylated substrate. In contrast, AMC significantly enhanced KDAC6 substrate affinity, greatly reduced Sirt1 (show SIRT1 ELISA Kits) activity, eliminated the substrate sequence specificity of KDAC4, and had no consistent effect with KDAC8 substrates.
Suggest that HDAC4 and HDAC6 (show HDAC6 ELISA Kits) are guardians of irradiation-induced DNA damage and stemness, thus promoting radioresistance in glioblastoma cells.
TGF-beta1 (show TGFB1 ELISA Kits) increases NADPH oxidase 4 (NOX4 (show NOX4 ELISA Kits)) mRNA and protein expression in normal human lung fibroblasts (NHLFs) and causes nuclear export of HDAC4.
elevated HO-1 (show HMOX1 ELISA Kits) produced less reactive oxygen species, resulting in nuclear localization of HDAC4 and miR (show MLXIP ELISA Kits)-206 repression.
Results show that HDAC4 is a direct target of miR (show MLXIP ELISA Kits)-29b in multiple myeloma cells and its high mRNA expression inversely correlates with miR (show MLXIP ELISA Kits)-29b levels in multiple myeloma samples.
in leiomyosarcomas (LMS), this two-faced trait of MEF2 (show MEF2A ELISA Kits) is relevant for tumor aggressiveness. Class IIa HDACs are overexpressed in 22% of LMS, where high levels of MEF2 (show MEF2A ELISA Kits), HDAC4 and HDAC9 (show HDAC9 ELISA Kits) inversely correlate with overall survival. The knock out of HDAC9 (show HDAC9 ELISA Kits) suppresses the transformed phenotype of LMS cells, by restoring the transcriptional proficiency of some MEF2 (show MEF2A ELISA Kits)-target loci
Collectively, we suggest that VSV treatment will be a useful therapeutic strategy for HCV-infected hepatocellular carcinoma cells because HCV core protein suppresses the anti-viral threshold by down-regulation of the STAT1 (show STAT1 ELISA Kits)-HDAC4 signaling axis.
In osteoarthritis (OA) chondrocytes, hydrostatic pressure (HP) restores the expression levels of some miRNAs, downregulates MMP-13 (show MMP13 ELISA Kits), ADAMTS-5 (show ADAMTS5 ELISA Kits), and HDAC-4, and modulates the Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) pathway activation.
the phenotype seen in the Hdac4 (show HDAC5 ELISA Kits)(-/-) mice is partially derived from elevation in MMP-13 (show MMP13 ELISA Kits) and may be due to a bone remodeling disorder caused by overexpression of this enzyme.
beige (show LYST ELISA Kits) adipocyte renaissance was governed by liver kinase b1 (show STK11 ELISA Kits) and histone deacetylase 4 (show HDAC5 ELISA Kits) in white adipocytes.
class IIa HDAC (show HDAC3 ELISA Kits) function could be used to enhance metabolic health in chronic diseases driven by physical inactivity.
Results show that HDAC4 (show HDAC5 ELISA Kits) inhibits myogenic differentiation and promoted C2C12 cell proliferation. Its expression is under the regulation of mir (show MLXIP ELISA Kits)-378a which targets its promotor region.
our results imply that under steady stage, HDAC4 (show HDAC5 ELISA Kits) is not required for the development and function of multiple T cell lineages
HDAC4 (show HDAC5 ELISA Kits)-mediated SUMOylation of the corepressor DACH1 (show DACH1 ELISA Kits) is decreased, which protects DACH1 (show DACH1 ELISA Kits) from proteasomal degradation
The eating-disorder (ED) associated HDAC4 (show HDAC5 ELISA Kits)(A778T) mutation alters feeding behaviors in female mice. The HDAC4 (show HDAC5 ELISA Kits)(A778T) mouse line is a novel model of ED-related behaviors and identifies mitochondrial biogenesis as a potential molecular pathway contributing to behavioral deficits.
Nuclear HDAC4 (show HDAC5 ELISA Kits) binds to chromatin as well as to MEF2A (show MEF2A ELISA Kits) transcription factor, leading to histone deacetylation and altered neuronal gene expression. By using a Cdkl5 (show CDKL5 ELISA Kits) knockout (Cdkl5 (show CDKL5 ELISA Kits) -/Y) mouse model, we found that hypophosphorylated HDAC4 (show HDAC5 ELISA Kits) translocates to the nucleus of neural precursor cells, thereby reducing histone 3 acetylation.
Data (including data from studies using knockout mice) suggest that S100A1 (show S100A1 ELISA Kits) (S-100 calcium-binding protein (show GUCA1B ELISA Kits) A1 (show BCL2A1 ELISA Kits), alpha chain (show FCGRT ELISA Kits)) is involved in protein kinase A- (RIIalpha and RIIbeta (show PRKAR2B ELISA Kits))-dependent signaling resulting in nuclear redistribution/influx of HDAC4 (histone deacetylase 4 (show HDAC5 ELISA Kits)) in skeletal muscle fibers.
results are the first to demonstrate that the protective effects of irisin (show FNDC5 ELISA Kits) in cardiomyoblasts exposed to hypoxia/reoxygenation might be associated with HDAC4 (show HDAC5 ELISA Kits) degradation.
Results demonstrate that Hdac4 is a regulator of cranial neural crest-derived palatal skeletal precursors during early embryogenesis.
our results revealed the mechanism in which miR-1 and miR (show MYLIP ELISA Kits)-206 positively regulate bovine skeletal muscle satellite cell myogenic differentiation via Pax7 (show PAX7 ELISA Kits) and HDAC4 downregulation.
Histones play a critical role in transcriptional regulation, cell cycle progression, and developmental events. Histone acetylation/deacetylation alters chromosome structure and affects transcription factor access to DNA. The protein encoded by this gene belongs to class II of the histone deacetylase/acuc/apha family. It possesses histone deacetylase activity and represses transcription when tethered to a promoter. This protein does not bind DNA directly, but through transcription factors MEF2C and MEF2D. It seems to interact in a multiprotein complex with RbAp48 and HDAC3.
histone deacetylase 4
, histone deacetylase A