Key features and details
- Rabbit polyclonal to Chd7
- Suitable for: IP, WB
- Reacts with: Human
- Isotype: IgG
Product nameAnti-Chd7 antibody
See all Chd7 primary antibodies
DescriptionRabbit polyclonal to Chd7
Tested applicationsSuitable for: IP, WBmore details
Species reactivityReacts with: Human
Predicted to work with: Horse, Cow, Pig, Chimpanzee, Cynomolgus monkey, Rhesus monkey, Gorilla, Orangutan
- HeLa whole cell lysate (ab150035).
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 6.8
Preservative: 0.09% Sodium azide
Constituents: 0.1% BSA, 99% Tris buffered saline
Concentration information loading...
PurityImmunogen affinity purified
Purification notesab176807 was affinity purified using an epitope specific to Chd7 immobilized on solid support.
Our Abpromise guarantee covers the use of ab176807 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IP||Use at 2-5 µg/mg of lysate.|
|WB||1/2000 - 1/10000. Predicted molecular weight: 336 kDa.|
FunctionProbable transcription regulator.
Tissue specificityWidely expressed in fetal and adult tissues.
Involvement in diseaseDefects in CHD7 are a cause of CHARGE syndrome (CHARGES) [MIM:214800]. This syndrome, which is a common cause of congenital anomalies, is characterized by a non-random pattern of congenital anomalies including choanal atresia and malformations of the heart, inner ear, and retina.
Genetic variations in CHD7 are associated with susceptibility to idiopathic scoliosis type 3 (IS3) [MIM:608765]. Idiopathic scoliosis (IS) is the most common spinal deformity in children.
Defects in CHD7 are the cause of Kallmann syndrome type 5 (KAL5) [MIM:612370]. Kallmann syndrome is a disorder that associates hypogonadotropic hypogonadism and anosmia. Anosmia or hyposmia is related to the absence or hypoplasia of the olfactory bulbs and tracts. Hypogonadism is due to deficiency in gonadotropin-releasing hormone and probably results from a failure of embryonic migration of gonadotropin-releasing hormone-synthesizing neurons. In some patients other developmental anomalies can be present, which include renal agenesis, cleft lip and/or palate, selective tooth agenesis, and bimanual synkinesis. In some cases anosmia may be absent or inconspicuous.
Defects in CHD7 are a cause of idiopathic hypogonadotropic hypogonadism (IHH) [MIM:146110]. IHH is defined as a deficiency of the pituitary secretion of follicle-stimulating hormone and luteinizing hormone, which results in the impairment of pubertal maturation and of reproductive function.
Sequence similaritiesBelongs to the SNF2/RAD54 helicase family.
Contains 2 chromo domains.
Contains 1 helicase ATP-binding domain.
Contains 1 helicase C-terminal domain.
modificationsPhosphorylated upon DNA damage, probably by ATM or ATR.
- Information by UniProt
- ATP-dependent helicase CHD7 antibody
- ATP-dependent helicase chromodomain helicase DNA binding protein 7 antibody
- CHD-7 antibody
All lanes : Anti-Chd7 antibody (ab176807) at 0.04 µg/ml
Lane 1 : HeLa whole cell lysate at 50 µg
Lane 2 : HeLa whole cell lysate at 15 µg
Lane 3 : HeLa whole cell lysate at 5 µg
Developed using the ECL technique.
Predicted band size: 336 kDa
Exposure time: 10 seconds
Detection of Chd7 in immunoprecipitates of HeLa whole cell lysate (1 mg for IP, 20% of IP loaded) using ab176807 at 3 µg/mg lysate for IP (Lane 1) and at 1 µg/ml for subsequent Western blot detection. Lane 2 represents control IgG IP.
Detection: Chemiluminescence with an exposure time of 30 seconds.
ab176807 has been referenced in 3 publications.
- Su W et al. miR-30 disrupts senescence and promotes cancer by targeting both p16INK4A and DNA damage pathways. Oncogene N/A:N/A (2018). PubMed: 29907771
- Zhang X et al. G-quadruplex structures at the promoter of HOXC10 regulate its expression. Biochim Biophys Acta Gene Regul Mech 1861:1018-1028 (2018). PubMed: 30343692
- Doi T et al. Chd7 Collaborates with Sox2 to Regulate Activation of Oligodendrocyte Precursor Cells after Spinal Cord Injury. J Neurosci 37:10290-10309 (2017). PubMed: 28931573