The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
1/1000 - 1/10000. Detects a band of approximately 55 kDa (predicted molecular weight: 57 kDa).
1/10 - 1/100.
Use at an assay dependent concentration.
ab172730-Rabbit monoclonal IgG, is suitable for use as an isotype control with this antibody.
1/100 - 1/250.
Is unsuitable for IHC-P.
Conversion of pregnenolone and progesterone to their 17-alpha-hydroxylated products and subsequently to dehydroepiandrosterone (DHEA) and androstenedione. Catalyzes both the 17-alpha-hydroxylation and the 17,20-lyase reaction. Involved in sexual development during fetal life and at puberty.
Lipid metabolism; steroid biosynthesis.
Involvement in disease
Defects in CYP17A1 are the cause of adrenal hyperplasia type 5 (AH5) [MIM:202110]. AH5 is a form of congenital adrenal hyperplasia, a common recessive disease due to defective synthesis of cortisol. Congenital adrenal hyperplasia is characterized by androgen excess leading to ambiguous genitalia in affected females, rapid somatic growth during childhood in both sexes with premature closure of the epiphyses and short adult stature. Four clinical types: "salt wasting" (SW, the most severe type), "simple virilizing" (SV, less severely affected patients), with normal aldosterone biosynthesis, "non-classic form" or late onset (NC or LOAH), and "cryptic" (asymptomatic).
Belongs to the cytochrome P450 family.
Phosphorylation is necessary for 17,20-lyase, but not for 17-alpha-hydroxylase activity.
Flow Cytometry analysis of HeLa (human cervix adenocarcinoma) cells labeling Cytochrome P450 17A1 with purified ab125022 at 1/220 dilution (10ug/ml) (red). Cells were fixed with 4% paraformaldehyde and permeabilised with 90% methanol. A Goat anti rabbit IgG (Alexa Fluor® 488) (1/2000 dilution) was used as the secondary antibody. Rabbit monoclonal IgG (Black) was used as the isotype control, cells without incubation with primary antibody and secondary antibody (Blue) were used as the unlabeled control.
Wu S et al. Obesity-induced infertility and hyperandrogenism are corrected by deletion of the insulin receptor in the ovarian theca cell. Diabetes63:1270-82 (2014).
Read more (PubMed: 24379345) »
Dowling AR et al. Genetic factors modulate the impact of pubertal androgen excess on insulin sensitivity and fertility. PLoS One8:e79849 (2013).
Read more (PubMed: 24278193) »