Browse our anti-Histone Deacetylase 5 (HDAC5) Antibodies

Human Histone Deacetylase 5 (HDAC5) interaction partners

1. HDAC5 overexpression in urothelial carcinoma cell lines decreases cell proliferation but can promote epithelial-to-mesenchymal transition.

2. It identified BMAL1 as a cAMP-responsive coactivator of HDAC5 to regulate hepatic gluconeogenesis

3. in hISMC from resected Crohn's strictures, we observed a significantly reduced contractile phenotype compared with patient-matched intrinsic controls that was associated with increased patient-specific expression of DNA methyltransferase 1, HDAC2, and HDAC5.

4. Latent autoimmune diabetes of adults (LADA) patients showed stronger binding of p-STAT3, HDAC5 and DNMT1 than controls.

5. HDAC5 expression was positively correlated with miR-2861 in lung cancer stem cells (LCSCs), and knockdown of miR-2861 decreased the expression of HDAC5, which implied that HDAC5 may be involved in the differentiation of LCSCs mediated by miR-2861.

6. These results demonstrate a previously unknown negative epigenetic regulation of hematopoietic stem cells (HSC) homing and engraftment by HDAC5, and allow for a new and simple translational strategy to enhance HSC transplantation.

7. Collectively, these data indicate that vIRF3 alters global gene expression and induces a hypersprouting formation in an HDAC5-binding-dependent and lymphatic endothelial cell-specific manner, ultimately contributing to Kaposi's sarcoma-associated herpesvirus-associated pathogenesis.

8. High HDAC5 expression is associated with invasion of lung cancer.

9. 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

10. Hdac5 and Hdac6 expression are required for the adequate expression of Icer and adipocyte function. Altered adipose expression of the two Hdacs in obesity by hypoxia may contribute to the development of metabolic abnormalities.

11. These findings demonstrate a novel mechanism for deregulation of HDAC5 in non-small cell lung cancer (NSCLC)and suggest that miR5895p/HDAC5 pathway may represent a new prognostic biomarker and therapeutic target against NSCLC.

12. HDAC5 was extensively expressed in human BC tissues, and high HDAC5 expression was associated with an inferior prognosis.

13. HDAC5 is a negative predictor of disease-free and overall survival in pancreatic neuroendocrine tumor patients.

14. Interference with both glucose and glutamine supply in HDAC5-inhibited cancer cells significantly increases apoptotic cell death.

15. these results suggest that HDAC5 is critical in regulating LSD1 protein stability through post-translational modification, and the HDAC5-LSD1 axis has an important role in promoting breast cancer development and progression.

16. The expression of HDAC5 was significantly increased in endothelial cells (ECs) from patients with systemic sclerosis (SSc) compared to healthy control endothelial cells. Silencing of HDAC5 in SSc ECs restored normal angiogenesis. HDAC5 knockdown followed by ATAC-seq assay in SSc ECs identified key HDAC5-regulated genes involved in angiogenesis and fibrosis, such as CYR61, PVRL2, and FSTL1.

17. the migration and invasion of hepatocellular carcinoma cells were impaired by knockdown of histone deacetylase 5 or hypoxia-inducible factor-1alpha but rescued when eliminating homeodomain-interacting protein kinase-2 in hepatocellular carcinoma cells, which suggested the critical role of histone deacetylase 5-homeodomain-interacting protein kinase-2-hypoxia-inducible factor-1alpha pathway in hypoxia-induced metastasis.

18. HDAC5 inhibits hepatic lipogenic genes expression by attenuating the transcriptional activity of liver X receptor.

19. HDAC5 promotes cellular proliferation through the upregulation of cMet, and may provide a novel therapeutic target for the treatment of patients with Wilms' tumor.

20. HDAC5 and HDAC6 were highly expressed in melanoma cells but exhibited low expression levels in normal skin cells.

Mouse (Murine) Histone Deacetylase 5 (HDAC5) interaction partners

1. It identified HDAC5 as a novel mediator of hepatic fatty acid oxidation by fasting and ER stress signals, and strategies to promote HDAC5 dephosphorylation could serve as new tools for the treatment of obesity-associated hepatic steatosis.

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

3. Hdac5 and Hdac6 expression are required for the adequate expression of Icer and adipocyte function. Altered adipose expression of the two Hdacs in obesity by hypoxia may contribute to the development of metabolic abnormalities.

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

5. HDAC5 emerges as a cellular conductor of MEF2C and M6a activity and is regulated by miR-124 and miR-9 to control neurite development.

6. This paper presents data for the first time directly supporting the role of HDAC5 as a scaffold recruiting a chromatin modifying co-repressor complex to specific transcription factors on unique gene promoters. These data for HDAC5 may reflect one of the functions of class IIa HDACs in transcriptional regulation distinct from its catalytic activity.

7. This study demonstrated that decreased HDAC5 function is able to exacerbate the long-term behavioral effects of adverse rearing environment in mice

8. As HDAC5 expression may help nullify AIS and identify progenitor cells, the precise delivery of miD2861 may serve as a vehicle for monitoring network remodeling with target specificity and signal sensitivity after drug exposure that identifies brain repair processes in adult animals.

9. HDAC5 inhibits hepatic lipogenic genes expression by attenuating the transcriptional activity of liver X receptor.

10. This study demonstrated that mice with learned helplessness protocol-induced behavioral despair exhibited higher levels of HDAC5 and HDAC5 binding to the promoter region of BDNF exon IV resulting in the decreased expression of BDNF.

11. inhibition of HDAC5 differentially regulates ghrelin and NUCB2/ nesfatin-1 expression by enhancing the acetylation and phosphorylation of Raptor, which subsequently suppress mTORC1 signaling

12. Results suggest a role for Hdac5 and Sirt2 in neuronal adaptations induced by chronic stress and antidepressant treatment and highlight the therapeutic potential of these targets in the treatment of depression

13. loss of HDAC5 weakens Treg suppressive function and iTreg formation, as well as IFN-gamma production in CD8+ T cells. Mice lacking HDAC5 do not develop spontaneous illness and do not have enhanced anti-tumor immunity.

14. These results suggest a strong regulatory function of HDAC5 in the pro-inflammatory response of macrophages.

15. increased sclerostin production achieved by HDAC5 shRNA is abrogated by simultaneous knockdown of MEF2C, indicating that MEF2C is a major target of HDAC5 in osteocytes

16. findings suggest a model in which filamin A local translation following axon injury controls localized HDAC5 activity to promote axon regeneration.

17. Data indicate that 4-phenylbutyric acid (4-PBA) increases glucose transporter type 4 (GLUT4) expression through a mechanism that involves suppression of the histonedeacetylase 5 (HDAC5) pathway, but without involving endoplasmic reticulum stress.

18. Data reveal a novel role of HDAC5 in modulating the KLF2 transcriptional activation and eNOS expression.

19. HDAC5 influences BMAL1 acetylation; interfering with normal expression levels of HDAC5 disrupts circadian rhythms.

20. In mouse muscle compensatory regulation of HDAC5 transcriptional repressor maintains metabolic integrity.

Cow (Bovine) Histone Deacetylase 5 (HDAC5) interaction partners

1. Protein kinase D-HDAC5 pathway plays an important role in VEGF regulation of gene transcription and angiogenesis

Arabidopsis thaliana Histone Deacetylase 5 (HDAC5) interaction partners

1. Regulation of flowering time by the histone deacetylase HDA5

Zebrafish Histone Deacetylase 5 (HDAC5) interaction partners

1. Proper heart valve formation in zebrafish critically depends on protein kinase D2-histone deacetylase 5-Kruppel-like factor signaling.