Cytochrome P450 17A1 Recombinant Rabbit mAb (一抗) - WB | Bioss

bsm-54306R

重组兔单抗

Cytochrome P450 17A1 Recombinant Rabbit mAb

细胞色素P450 17A1重组兔单抗

CYP17; CYPXVII; CPT7; P450C17; S17AH; CP17A_FELCA; CYP17A1; 17-alpha-hydroxyprogesterone aldolase; Cytochrome P450 17A1; Cytochrome P450-C17 (Cytochrome P450c17); Steroid 17-alpha-monooxygenase; 1.14.14.19; CP17A_PANTR; CP17A_MESAU; CP17A_HORSE; CP17A_HUMAN; cytochrome P450 family 17 subfamily A member 1; cytochrome P450, subfamily XVII (steroid 17-alpha-hydroxylase), adrenal hyperplasia; cytochrome P450, family 17, subfamily A, polypeptide 1

Rabbit

A synthesized peptide derived from human Cytochrome P450 17A1: 101-220

IgG

Liquid

affinity purified by Protein A

Recombinant

2F7

57 kDa

55 kDa

1mg/ml

0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.

Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.

This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

Cytochrome P450 17A1 (CYP17A1) belongs to the cytochrome P450 family; it plays a role in the conversion of pregnenolone and progesterone into their 17-alpha-hydroxylated products and subsequently to dehydroepiandrosterone (DHEA) and androstenedione. CYP17A1 also catalyzes both the 17-alpha-hydroxylation and the 17,20-lyase reaction. CYP17A1 is involved in sexual development during fetal life and at puberty. Defects in CYP17A1 are the cause of adrenal hyperplasia type 5 (AH5). AH5 is a form of congenital adrenal hyperplasia, a common recessive disease due to defective synthesis of cortisol.

CYP17A1

Steroid 17-alpha-hydroxylase/17, 20 lyase

Membrane.

Phosphorylation is necessary for 17,20-lyase, but not for 17-alpha-hydroxylase activity.

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.

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.