HDACs Antibodies

Histone deacetylase (HDAC) plays an important role in γ-aminobutyric acid (GABA) neurotransmission, synapse formation, synaptic plasticity, and memory formation. It is implicated in the pathogenesis of many central nervous system (CNS) disorders, including Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Huntington's disease (HD).

HDACs are now divided into four categories. Class I HDACs (1, 2, 3, and 8) are mainly located in the nucleus. Class II HDACs are further subdivided into two groups: Class IIa (4, 5, 7, and 9) and Class IIb (6 and 10). Class IIa HDACs have limited deacetylase activity and can move between the cytoplasm and nucleus, whereas class IIb HDACs are primarily found in the cytoplasm and act on non-histone targets. Silent information regulator 1 to Silent information regulator 7 are classified as Class III HDACs. HDAC11 is a class IV HDAC.

HDACs Overview

• HDACs influence neuronal survival and synaptic plasticity.

A number of HDACs have neuroprotective or toxic effects. The class I HDAC inhibitor valproic acid (VPA) may exert neuroprotective effects by reducing inflammatory responses and apoptosis and by activating the brain-derived neurotrophic factor (BDNF)/tyrosine kinase receptor B (TrkB) signaling pathway. Overexpression of HDAC2 and HDAC3 in the brain impairs memory and synapse formation. The positive feedback loop centered on HDAC2 and BDNF can mediate histone acetylation and programmed gene expression, which is the basis of synaptic plasticity and memory.

• Abnormal accumulation of misfolded proteins and autophagy are associated with HDACs.

The major pathological change in most neurodegenerative diseases is the abnormal accumulation of misfolded proteins in neurons, which have toxic effects on neurons. In HD patients, the formation and aggregation of mutant huntingtin protein (mHTT) damages the central nervous system, leading to chorea, cognitive impairment, and dementia. Several histone deacetylases in the cytoplasm are involved in regulating the degradation of abnormally accumulated proteins.

• HDACs affect the function of mitochondria and oxidative stress.

The pathogenesis of neurodegenerative diseases involves mitochondrial dysfunction caused by multiple factors, ultimately leading to neuronal degeneration, apoptosis or necrosis. SIRT1 can delay the progression of AD by regulating PGC-1α deacetylation. SIRT3 can activate several antioxidant factors such as FOXO3, manganese superoxide dismutase (MnSOD) and catalase (CAT) to prevent or delay damage caused by oxidative stress. SIRT3 may also protect neurons by scavenging free radicals in the mitochondria. Overexpression of SIRT3 promotes the antioxidant effect of mHTT cells, improves mitochondrial function, and plays a neuroprotective role in HD.

HDACs Antibodies Selection Guide

Choose the HDAC antibody that best suits your research from Creative Biolabs' library of HDAC antibodies, which are suitable for a variety of applications. If you can't find the antibody you need, contact us today to develop custom antibodies for specific targets, species, and applications.

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