Browse our anti-HDAC4 (HDAC4) Antibodies

Fruit Fly (Drosophila melanogaster) Histone Deacetylase 4 (HDAC4) interaction partners

1. SIK3-HDAC4 signaling in M cells regulates MSDR by regulating the molecular oscillation in DN1 neurons.

2. We also demonstrate that HDAC4 and Ubc9 interact genetically during memory formation, opening new avenues for investigating the mechanisms through which HDAC4 regulates memory formation and other neurological processes.

3. RNAi-mediated knockdown of HDAC4 in Drosophila dampens circadian function.

4. HDAC4 is not only a repressor of long-term memory, but also modulates normal memory formation

5. dHDAC4, is a novel, catalytically active class II Drosophila histone deacetylase and is involved in the segmentation regulatory pathway and suggested complex transcriptional regulation as a potential mechanism that controls its expression

Human Histone Deacetylase 4 (HDAC4) interaction partners

1. SMRT binding does not activate the cryptic deacetylase activity of HDAC4; class IIa HDACs and the SMRT-HDAC3 complex are coordinated during gene regulation

2. HDAC4 expression was reduced in ischemic stroke, which may contribute to the pathogenesis of ischemic stroke by promoting neuronal death and inhibiting angiogenesis and neurogenesis. [review]

3. Mutations in HDAC4 disrupt the deacetylation of FoxO1, subsequently decrease the beta-cell insulin secretion resulting in diabetes.

4. MicroRNA-145-3p suppresses proliferation and promotes apotosis and autophagy of osteosarcoma cell by targeting HDAC4

5. hsa-miR-20a-5p attenuates allergic inflammation in HMC-1 cells by targeting HDAC4.

6. Bioinformatics predicted the targeting of miR-520b on HDAC4. MiR-520b directly targeted the 3' untranslated region of HDAC4. MiR-520b decreases HDAC4 expression to control cell proliferation in lung cancer.

7. Study reports for the first time a genetic association between DNA variation in the HDAC4 gene and intra-individual response time variability which is proposed as a viable endophenotype for many psychiatric disorders.

8. Study demonstrated that HDAC4 was significantly upregulated in glioma, and promoted glioma cell proliferation and invasion mediated through, at least partially, the repression of p21, p27, E-cadherin and betacatenin, and by the potentiation of CDK1, CDK2 and vimentin.

9. we suggest that STAT1HDAC4 signaling induces malignant tumor features such as EMT and sphere formation in CUG2overexpressing cancer cells.

10. MiR-22 was up-regulated in CD4+ T cells in peripheral blood and intestinal mucosa tissues of inflammatory intestinal disease patients, which could promote Th17 cell differentiation via targeting HDAC4 to be involved in inflammatory intestinal disease progression

11. HO-1 plays a key role in protecting tumor cells from apoptosis, in a process that involves Smad7 and HDAC4/5 in apoptosis of B-ALL cells

12. Auithors found no significant association between the previously implicated CpG in HDAC4 and either AN or BN. We found that three CpGs were nominally associated with AN (P=0.02-0.03); the largest difference was a 9% hypermethylation in AN.

13. our results demonstrated that MIAT competitively binds to miR-29a-3p and consequently upregulates the expression of HDAC4, which is a downstream target of miR-29a-3p. In conclusion, the present study highlighted the involvement of the MIAT/miR-29a-3p/HDAC4 axis in the development of Gastric cancer (GC), which provided potential diagnostic and therapeutic targets for GC.

14. miR-29a regulated osteogenesis of the subchondral mesenchymal stem cells through modulation of HDAC4 and Wnt3a.

15. Results show that HDAC4 promoter methylation is inversely associated with arachidonic acid post-prandially in adult males.

16. The cytoplasmic location and function of HDAC4 is controlled by the activity of salt-inducible kinase (SIK). These results establish a cytoplasmic role for HDAC4 and identify HDAC4, SIK, and ENIGMA as mediators of vascular calcification.

17. Strong correlation has been proved between the expression levels of HDAC4 and SIRT6.

18. HDAC4 regulates thimerosal-induced cell death in neurons and that treatment with MC1568 prevents thimerosal-induced activation of caspase-3 in the rat prefrontal cortex.

19. HDAC4 promotes proliferation and G1/S cell cycle progression in esophageal carcinoma cells by inhibiting CDK inhibitors p21 and p27 and up-regulating CDK2/4 and CDK-dependent Rb phosphorylation. HDAC4 also enhances ESCC cell migration. Furthermore, HDAC4 positively regulates epithelial-mesenchymal transition (EMT) by increasing the expression of Vimentin and decreasing the expression of E-Cadherin/alpha-Catenin.

20. level of myotubes MTM1 mutations do not dramatically affect calcium homeostasis and calcium release mediated through the ryanodine receptor 1, 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, a decrease in muscle-specific microRNAs and a considerable up-regulation of HDAC4.

Mouse (Murine) Histone Deacetylase 4 (HDAC4) interaction partners

1. This study identified new functions of HDAC4 in skeletal muscle in ALS, whose deletion is sufficient to induce an earlier onset of the disease, characterized by muscle denervation, decrease in NMJ size and functional deficit, accompanied by exacerbated muscle atrophy over time.

2. exercise enhanced HDAC4-NT levels, and mice with a cardiomyocyte-specific deletion of Hdac4 show reduced exercise capacity, which was characterized by cardiac fatigue and increased expression of Nr4a1

3. results identify HDAC4 as an epigenetic regulator of neuronal morphology that controls dendritic arborization via the expression of VEGFD

4. These findings are the first to define activated HDAC4 as a crucial regulator for myocardial ischemia and reperfusion injury.

5. intracellular trafficking of HDAC4 contributes to the vulnerability of cells expressing pathogenic alpha-synuclein mutants.

6. Exercise-induced GLUT4 transcription via inactivation of HDAC4/5 in mouse skeletal muscle in an AMPKalpha2-dependent manner.

7. HDAC4 stimulates MRTF-A expression and drives fibrogenesis in hepatic stellate cells by targeting miR-206

8. The cytoplasmic location and function of HDAC4 is controlled by the activity of salt-inducible kinase (SIK). These results establish a cytoplasmic role for HDAC4 and identify HDAC4, SIK, and ENIGMA as mediators of vascular calcification.

9. CaMKIV is a key regulator of neuronal intracellular HDAC4 trafficking during stroke

10. This study suggested that HDAC4-induced transcriptional inactivation of CREB is responsible for isoflurane-induced cognitive dysfunction in the brain.

11. the phenotype seen in the Hdac4(-/-) mice is partially derived from elevation in MMP-13 and may be due to a bone remodeling disorder caused by overexpression of this enzyme.

12. beige adipocyte renaissance was governed by liver kinase b1 and histone deacetylase 4 in white adipocytes.

13. class IIa HDAC function could be used to enhance metabolic health in chronic diseases driven by physical inactivity.

14. Results show that HDAC4 inhibits myogenic differentiation and promoted C2C12 cell proliferation. Its expression is under the regulation of mir-378a which targets its promotor region.

15. our results imply that under steady stage, HDAC4 is not required for the development and function of multiple T cell lineages

16. HDAC4-mediated SUMOylation of the corepressor DACH1 is decreased, which protects DACH1 from proteasomal degradation

17. The eating-disorder (ED) associated HDAC4(A778T) mutation alters feeding behaviors in female mice. The HDAC4(A778T) mouse line is a novel model of ED-related behaviors and identifies mitochondrial biogenesis as a potential molecular pathway contributing to behavioral deficits.

18. Nuclear HDAC4 binds to chromatin as well as to MEF2A transcription factor, leading to histone deacetylation and altered neuronal gene expression. By using a Cdkl5 knockout (Cdkl5 -/Y) mouse model, we found that hypophosphorylated HDAC4 translocates to the nucleus of neural precursor cells, thereby reducing histone 3 acetylation.

19. Data (including data from studies using knockout mice) suggest that S100A1 (S-100 calcium-binding protein A1, alpha chain) is involved in protein kinase A- (RIIalpha and RIIbeta)-dependent signaling resulting in nuclear redistribution/influx of HDAC4 (histone deacetylase 4) in skeletal muscle fibers.

20. results are the first to demonstrate that the protective effects of irisin in cardiomyoblasts exposed to hypoxia/reoxygenation might be associated with HDAC4 degradation.

Zebrafish Histone Deacetylase 4 (HDAC4) interaction partners

1. Results demonstrate that Hdac4 is a regulator of cranial neural crest-derived palatal skeletal precursors during early embryogenesis.

2. region between -698 and -302 might contain mild negative regulatory elements

Cow (Bovine) Histone Deacetylase 4 (HDAC4) interaction partners

1. our results revealed the mechanism in which miR-1 and miR-206 positively regulate bovine skeletal muscle satellite cell myogenic differentiation via Pax7 and HDAC4 downregulation.