ELISA/assay

Rat Corticosterone (CORT) ELISA Kit

MBS269128

48-Strip-Wells

260 USD

ELISA Kit

Rat Corticosterone (CORT) ELISA Kit

[Corticosterone (CORT)]

[cytochrome P450 11B2, mitochondrial; Cytochrome P450 11B2, mitochondrial; cytochrome P450 11B2, mitochondrial; cytochrome P-450C18; aldosterone synthase; cytochrome P-450Aldo; steroid 11-beta-monooxygenase; steroid 11-beta/18-hydroxylase; aldosterone-synthesizing enzyme; steroid 18-hydroxylase, aldosterone synthase, P450C18, P450aldo; mitochondrial cytochrome P450, family 11, subfamily B, polypeptide 2; cytochrome P450, subfamily XIB (steroid 11-beta-hydroxylase), polypeptide 2; cytochrome P450, family 11, subfamily B, polypeptide 2; Aldosterone synthase (EC:1.14.15.4, EC:1.14.15.5); ALDOS; Aldosterone-synthesizing enzyme; CYPXIB2; Cytochrome P-450Aldo; Cytochrome P-450C18; Steroid 18-hydroxylase]

[CORT]

[CYP11B2; CYP11B2; CPN2; ALDOS; CYP11B; CYP11BL; CYPXIB2; P450C18; P-450C18; P450aldo; ALDOS]

C11B2_HUMAN

Rat

503

No cross-reaction with other factors.

Store all reagents at 2-8 degree C.

Typical Testing Data/Standard Curve (for reference only)

Samples: Rat Serum, Plasma Or Cell Culture Supernatant And Organizations In The Natural And Recombinant Col1 Concentration. Assay Type: Sandwich. Detection Range: 10 ng/ml-0.156ng/ml. Sensitivity: 0.05 ng/ml.

Intra-assay Precision: <= 8%. Inter-assay Precision: <= 12%

Principle of the Assay: This experiment use double-sandwich elisa technique and the ELISA Kit provided is typical. The pre-coated antibody is Rat COL1 monoclonal antibody and the detecting antibody is polyclonal antibody with biotin labeled. Samples and biotin labeling antibody are added into ELISA plate wells and washed out with PBS or TBS. Then Avidin-peroxidase conjugates are added to ELISA wells in order; Use TMB substrate for coloring after reactant thoroughly washed out by PBS or TBS. TMB turns into blue in peroxidase catalytic and finally turns into yellow under the action of acid. The color depth and the testing factors in samples are positively correlated.

119829183

NP_000489.3

NM_000498.3

57,560 Da

ACE Inhibitor Pathway (198763); Biological Oxidations Pathway (105698); C21-Steroid Hormone Biosynthesis, Progesterone = Corticosterone/aldosterone Pathway (413394); C21-Steroid Hormone Biosynthesis, Progesterone = Corticosterone/aldosterone Pathway (468295); C21-Steroid Hormone Biosynthesis, Progesterone = Cortisol/cortisone Pathway (413395); C21-Steroid Hormone Biosynthesis, Progesterone = Cortisol/cortisone Pathway (468370); Cytochrome P450 - Arranged By Substrate Type Pathway (105700); Endogenous Sterols Pathway (105701); Glucocorticoid Mineralcorticoid Metabolism Pathway (198902); Glucocorticoid Biosynthesis Pathway (106152)

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 mitochondrial inner membrane. The enzyme has steroid 18-hydroxylase activity to synthesize aldosterone and 18-oxocortisol as well as steroid 11 beta-hydroxylase activity. Mutations in this gene cause corticosterone methyl oxidase deficiency. [provided by RefSeq, Jul 2008]

CYP11B2: Preferentially catalyzes the conversion of 11- deoxycorticosterone to aldosterone via corticosterone and 18- hydroxycorticosterone. Defects in CYP11B2 are the cause of corticosterone methyloxidase type 1 deficiency (CMO-1 deficiency); also known as aldosterone deficiency due to defect in 18- hydroxylase or aldosterone deficiency I. CMO-1 deficiency is an autosomal recessive disorder of aldosterone biosynthesis. There are two biochemically different forms of selective aldosterone deficiency be termed corticosterone methyloxidase (CMO) deficiency type 1 and type 2. In CMO-1 deficiency, aldosterone is undetectable in plasma, while its immediate precursor, 18- hydroxycorticosterone, is low or normal. Defects in CYP11B2 are the cause of corticosterone methyloxidase type 2 deficiency (CMO-2 deficiency). CMO-2 is an autosomal recessive disorder of aldosterone biosynthesis. In CMO-2 deficiency, aldosterone can be low or normal, but at the expense of increased secretion of 18- hydroxycorticosterone. Consequently, patients have a greatly increased ratio of 18-hydroxycorticosterone to aldosterone and a low ratio of corticosterone to 18-hydroxycorticosterone in serum. Defects in CYP11B2 are a cause of familial hyperaldosteronism type 1 (FH1). It is a disorder characterized by hypertension, variable hyperaldosteronism, and abnormal adrenal steroid production, including 18-oxocortisol and 18-hydroxycortisol. There is significant phenotypic heterogeneity, and some individuals never develop hypertension. The molecular defect causing hyperaldosteronism familial type 1 is an anti-Lepore-type fusion of the CYP11B1 and CYP11B2 genes. The hybrid gene has the promoting part of CYP11B1, ACTH-sensitive, and the coding part of CYP11B2. Belongs to the cytochrome P450 family. Protein type: EC 1.14.15.5; Oxidoreductase; Lipid Metabolism - C21-steroid hormone; EC 1.14.15.4; Lipid Metabolism - androgen and estrogen; Mitochondrial. Chromosomal Location of Human Ortholog: 8q21-q22. Cellular Component: mitochondrion; mitochondrial inner membrane. Molecular Function: corticosterone 18-monooxygenase activity; steroid 11-beta-monooxygenase activity; iron ion binding; heme binding. Biological Process: steroid metabolic process; xenobiotic metabolic process; mineralocorticoid biosynthetic process; renal water homeostasis; C21-steroid hormone biosynthetic process; aldosterone mediated regulation of blood volume; sodium ion homeostasis; aldosterone biosynthetic process; potassium ion homeostasis; sterol metabolic process; cellular response to hormone stimulus. Disease: Corticosterone Methyloxidase Type Ii Deficiency; Corticosterone Methyloxidase Type I Deficiency

48-Strip-Wells

260 USD

96-Strip-Wells

405

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1615

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2880