Reactive species
Human;Mouse
Applications
IHC;IF;ELISA
Antibody type
Polyclonal Antibody
Protein name
Chromodomain-helicase-DNA-binding protein 4
Immunogen
The antiserum was produced against synthesized peptide derived from human CHD4. AA range:571-620
Specificity
Mi2-β Polyclonal Antibody detects endogenous levels of Mi2-β protein.
Constitute
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Source
Polyclonal, Rabbit,IgG
Dilution rate
Immunohistochemistry: 1/100 - 1/300. Immunofluorescence: 1/200 - 1/1000. ELISA: 1/20000. Not yet tested in other applications.
Purification process
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Other name
CHD4; Chromodomain-helicase-DNA-binding protein 4; CHD-4; ATP-dependent helicase CHD4; Mi-2 autoantigen 218 kDa protein; Mi2-beta
Background
The product of this gene belongs to the SNF2/RAD54 helicase family. It represents the main component of the nucleosome remodeling and deacetylase complex and plays an important role in epigenetic transcriptional repression. Patients with dermatomyositis develop antibodies against this protein. Somatic mutations in this gene are associated with serous endometrial tumors. Alternative splicing results in multiple transcript variants encoding different isoforms. [provided by RefSeq, Jul 2014],
Function
disease:One of the main antigens reacting with anti-MI-2 positive sera of dermatomyositis.,function:Probable transcription regulator.,PTM:Phosphorylated upon DNA damage, probably by ATM or ATR.,similarity:Belongs to the SNF2/RAD54 helicase family.,similarity:Contains 1 helicase ATP-binding domain.,similarity:Contains 1 helicase C-terminal domain.,similarity:Contains 2 chromo domains.,similarity:Contains 2 PHD-type zinc fingers.,subunit:Central component of the nucleosome remodeling and histone deacetylase (NuRD) repressor complex. Interacts with TRIM27. Part of a complex containing ATR and HDAC2. Interacts with KLF1; the interaction depends on sumoylation of KLF1, and leads to its transcriptional repression.,
