ELISA/assay

Mouse CYTOCHROME P-45017 ALPHA GENE ELISA KIT (CYP17)

MBS733824

48-Strip-Wells

470 USD

ELISA Kit

Mouse CYTOCHROME P-45017 ALPHA GENE ELISA KIT (CYP17)

CYTOCHROME P-45017 ALPHA GENE ELISA KIT (CYP17)

cytochrome P450c17; Steroid 17-alpha-hydroxylase/17,20 lyase; steroid 17-alpha-hydroxylase/17,20 lyase; CYPXVII; OTTHUMP00000020382; cytochrome P450c17; cytochrome P450-C17; cytochrome P450 17A1; cytochrome p450 XVIIA1; steroid 17-alpha-monooxygenase; cytochrome P450, subfamily XVII (steroid 17-alpha-hydroxylase), adrenal hyperplasia; cytochrome P450, family 17, subfamily A, polypeptide 1; CYPXVII; Cytochrome P450 17A1; Cytochrome P450-C17; Cytochrome P450c17; Steroid 17-alpha-monooxygenase

CYP17

CYP17A1; CYP17A1; CPT7; CYP17; S17AH; P450C17; CYP17; S17AH

CP17A_HUMAN

Mouse

508

This assay has high sensitivity and excellent specificity for detection of CYP-17alpha. No significant cross-reactivity or interference between CYP-17alpha and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between CYP-17alpha and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Competitive. Sensitivity: 1.0 pg/mL.

Intended Uses: This CYP-17alpha ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Mouse CYP-17alpha. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Mouse ELISA Kit

Principle of the assay: CYP-17alpha ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-CYP-17alpha antibody and an CYP-17alpha-HRP conjugate. The assay sample and buffer are incubated together with CYP-17alpha-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the CYP-17alpha concentration since CYP-17alpha from samples and CYP-17alpha-HRP conjugate compete for the anti-CYP-17alpha antibody binding site. Since the number of sites is limited, as more sites are occupied by CYP-17alpha from the sample, fewer sites are left to bind CYP-17alpha-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The CYP-17alpha concentration in each sample is interpolated from this standard curve.

386992

AAA36405.1

P05093

57,371 Da

Androgen Biosynthesis Pathway (106154); Biological Oxidations Pathway (105698); Cytochrome P450 - Arranged By Substrate Type Pathway (105700); Endogenous Sterols Pathway (105701); Glucocorticoid Mineralcorticoid Metabolism Pathway (198902); Glucocorticoid Biosynthesis Pathway (106152); Metabolic Pathways (132956); Metabolism Of Lipids And Lipoproteins Pathway (160976); Metabolism Of Steroid Hormones And Vitamins A And D Pathway (106150); Phase 1 - Functionalization Of Compounds Pathway (105699)

This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This protein localizes to the endoplasmic reticulum. It has both 17alpha-hydroxylase and 17,20-lyase activities and is a key enzyme in the steroidogenic pathway that produces progestins, mineralocorticoids, glucocorticoids, androgens, and estrogens. Mutations in this gene are associated with isolated steroid-17 alpha-hydroxylase deficiency, 17-alpha-hydroxylase/17,20-lyase deficiency, pseudohermaphroditism, and adrenal hyperplasia. [provided by RefSeq, Jul 2008]

CYP17A1: 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. 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. 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. Protein type: Lipid Metabolism - C21-steroid hormone; EC 4.1.2.30; EC 1.14.99.9; Oxidoreductase. Chromosomal Location of Human Ortholog: 10q24.3. Cellular Component: endoplasmic reticulum membrane; cell soma; mitochondrion; endoplasmic reticulum; axon. Molecular Function: 17-alpha-hydroxyprogesterone aldolase activity; steroid 17-alpha-monooxygenase activity; iron ion binding; heme binding; oxygen binding. Biological Process: steroid metabolic process; response to cAMP; dibenzo-p-dioxin metabolic process; androgen biosynthetic process; progesterone metabolic process; response to insecticide; Leydig cell differentiation; biphenyl metabolic process; response to methylmercury; hormone biosynthetic process; response to nutrient levels; response to drug; response to retinoic acid; adrenal gland development; hippocampus development; phthalate metabolic process; response to herbicide; ovulation; response to acetate; response to steroid hormone stimulus; response to cytokine stimulus; xenobiotic metabolic process; response to ionizing radiation; glucocorticoid biosynthetic process; steroid biosynthetic process; sex differentiation; sterol metabolic process; phenol metabolic process. Disease: Adrenal Hyperplasia, Congenital, Due To 17-alpha-hydroxylase Deficiency

48-Strip-Wells

470 USD

96-Strip-Wells

675