CYP17A1 Antibody [G22K11] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat

Lane 1: Mouse testis, Lane 2: Rat testis

Usage Information

Dilution
WB1:1000 IP1:50 IF1:200

Application
WB, IP, IF

Reactivity
Human, Mouse, Rat

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
55 kDa

Datasheet & SDS

Biological Description

Specificity
CYP17A1 Antibody [G22K11] detects endogenous levels of total CYP17A1 protein.

Clone
G22K11

Synonym(s)
Steroid 17-alpha-hydroxylase/17,20 lyase; 17-alpha-hydroxyprogesterone aldolase; CYPXVII; Cytochrome P450 17A1; Cytochrome P450-C17 (Cytochrome P450c17); Steroid 17-alpha-monooxygenase; CYP17A1; CYP17; S17AH

Background
CYP17A1 (cytochrome P450 17A1, also known as CYP17 or P450c17) is a bifunctional steroidogenic cytochrome‑P450 enzyme expressed predominantly in the adrenal cortex and gonads, where it catalyzes both 17α‑hydroxylase and 17,20‑lyase reactions on C21 steroids such as pregnenolone and progesterone to generate key androgen precursors. In the adrenal zona reticularis and gonadal Leydig and theca cells, CYP17A1 first converts pregnenolone to 17α‑hydroxypregnenolone and then cleaves the C17–C20 bond to yield dehydroepiandrosterone (DHEA), the first committed step in the classical androgen‑synthesis pathway that leads to testosterone and downstream dihydrotestosterone. CYP17A1 also participates in the backdoor and C11‑oxy androgen‑production pathways by acting on 11‑oxygenated precursors, thereby providing alternative routes to potent androgenic steroids in pathological and developmental contexts. The enzyme is embedded in the mitochondrial membrane with its heme‑containing active site oriented toward the matrix, and its activity is tightly regulated by substrate availability, electron‑donor systems, and transcriptional control of steroid‑pathway genes. In castration‑resistant prostate cancer, CYP17A1 remains a major source of intratumoral and adrenal androgen production, and it is the primary target of abiraterone, which is converted in vivo to Δ4‑abiraterone (D4A); D4A inhibits CYP17A1 as well as other steroidogenic enzymes such as 3β‑hydroxysteroid dehydrogenase and 5α‑reductase and further antagonizes the androgen receptor, thereby suppressing synthesis and action of 5α‑dihydrotestosterone and blocking androgen‑driven growth of tumor cells.

Background

CYP17A1 (cytochrome P450 17A1, also known as CYP17 or P450c17) is a bifunctional steroidogenic cytochrome‑P450 enzyme expressed predominantly in the adrenal cortex and gonads, where it catalyzes both 17α‑hydroxylase and 17,20‑lyase reactions on C21 steroids such as pregnenolone and progesterone to generate key androgen precursors. In the adrenal zona reticularis and gonadal Leydig and theca cells, CYP17A1 first converts pregnenolone to 17α‑hydroxypregnenolone and then cleaves the C17–C20 bond to yield dehydroepiandrosterone (DHEA), the first committed step in the classical androgen‑synthesis pathway that leads to testosterone and downstream dihydrotestosterone. CYP17A1 also participates in the backdoor and C11‑oxy androgen‑production pathways by acting on 11‑oxygenated precursors, thereby providing alternative routes to potent androgenic steroids in pathological and developmental contexts. The enzyme is embedded in the mitochondrial membrane with its heme‑containing active site oriented toward the matrix, and its activity is tightly regulated by substrate availability, electron‑donor systems, and transcriptional control of steroid‑pathway genes. In castration‑resistant prostate cancer, CYP17A1 remains a major source of intratumoral and adrenal androgen production, and it is the primary target of abiraterone, which is converted in vivo to Δ4‑abiraterone (D4A); D4A inhibits CYP17A1 as well as other steroidogenic enzymes such as 3β‑hydroxysteroid dehydrogenase and 5α‑reductase and further antagonizes the androgen receptor, thereby suppressing synthesis and action of 5α‑dihydrotestosterone and blocking androgen‑driven growth of tumor cells.

References
https://pubmed.ncbi.nlm.nih.gov/26668369/ https://pubmed.ncbi.nlm.nih.gov/32007561/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%