Datasheet

生物学的記述

Specificity	HDAC11 Antibody [H19H1] detects endogenous levels of total HDAC11 protein.
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.

Specificity

HDAC11 Antibody [H19H1] detects endogenous levels of total HDAC11 protein.

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.

使用情報

Application

WB, IHC, ELISA

Dilution

WB	IHC
1:1000-1:6000	1:500-1:2000

Reactivity

Human

Source

Mouse Monoclonal Antibody

MW

39 kDa

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

プロトコール

References

https://pubmed.ncbi.nlm.nih.gov/30899397/
https://ashpublications.org/blood/article/110/11/1330/74078/A-Novel-Role-of-Histone-Deacetylase-11-HDAC11-in

Application Data

WB

Validated by Selleck

Lane 1: SK-OV-3, Lane 2: T47D