research use only
Cat.No.: F4981
| Dilution |
|---|
|
| Application |
|---|
| WB, IHC, ELISA |
| Reactivity |
|---|
| Human |
| Source |
|---|
| Mouse Monoclonal Antibody |
| Storage Buffer |
|---|
| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
|---|
| -20°C (avoid freeze-thaw cycles), 2 years |
| Predicted MW Observed MW |
|---|
| 39 kDa 39 kDa |
| *Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization. |
| Specificity |
|---|
| HDAC11 Antibody [H19H1] detects endogenous levels of total HDAC11 protein. |
| Clone |
|---|
| H19H1 |
| Synonym(s) |
|---|
| Histone deacetylase 11; EC:3.5.1.98; HD11; HDAC11 |
| Background |
|---|
| HDAC11 is the only member of the class IV histone deacetylase family, characterized by a compact catalytic domain and limited substrate specificity. It modulates gene expression and immune function in the brain, heart, and immune cells by deacetylating both histone and non-histone proteins. HDAC11 forms repressive complexes with transcription factors such as Egr1 and HEY1, deacetylating them to reduce p53 promoter activity and suppress apoptosis in tumor cells. In antigen-presenting cells, HDAC11 is recruited to IL-10 promoters, silencing this anti-inflammatory cytokine and facilitating T cell priming. Upon innate immune stimulation, HDAC11 integrates into MAPK-NF-κB signaling pathways, directly deacetylating RelA/p65 to sustain inflammatory gene transcription (e.g., TNF-α, IL-6) and coordinating neutrophil maturation via FoxO-dependent granulopoiesis. HDAC11 tempers immune responses by stabilizing FOXP3 in regulatory T cells through indirect deacetylation. This bidirectional control places HDAC11 at the intersection of immune tolerance and activation. Selective inhibitors of HDAC11 can enhance IL-10 expression and restore p53-mediated apoptosis. HDAC11 also regulates emergency myelopoiesis during infection and fine-tunes microglial activity in the CNS. Dysregulation of HDAC11 leads to immune suppression in lymphomas and hepatocellular carcinoma (via p53 silencing) or to hyperinflammation in autoimmune diseases. |
| References |
|---|
|
Tel: +1-832-582-8158 Ext:3
If you have any other enquiries, please leave a message.