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. Alterations in methylation of CpG sites of specific genes (HDAC4, RAX2, APOA5 and CES1 loci) may contribute to childhood obesity.

2. Nuclear resident HDAC4 induces senescence in human fibroblasts (BJ-TERT). HDAC4-induced senescence depends on TP53 activation.

3. HDAC4 over-expression is important for the development of advanced hepatocellular carcinoma.

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

5. 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]

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

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

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

9. 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.

10. 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.

11. 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.

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

13. 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

14. 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

15. 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.

16. 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.

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

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

19. 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.

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

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

1. Hdac4 influences cortical bone mass and thickness and knockout of Hdac4 prevents the catabolic effect of parathyroid hormone in cortical bone.

2. this study identified P21 and Sharp1 as HDAC4 target genes.

3. Overexpression of an HDAC4 cytoplasm-concentrated mutant (S266E) increased cocaine reward behavior in the cocaine conditioned place preference assay, suggesting that cocaine-induced nuclear export of HDAC4 might function to facilitate the development of cocaine reward behaviors through a role in the cell cytoplasm.

4. Under cold stimulation, adipocyte HDAC4 activation could promote beige adipocyte renaissance non-cell autonomously.

5. HDAC4-mediated FoxO3a acetylation regulates Ang II-induced autophagy activation, which in turn plays an essential role in causing vascular inflammation.

6. 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.

7. 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

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

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

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

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

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

13. 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.

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

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

16. 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.

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

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

19. 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.

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

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.