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Mouse Anti-AKR1C4 Recombinant Antibody (V2-180482) (CBMAB-A1996-YC)

Provided herein is a Mouse monoclonal antibody against Human Aldo-Keto Reductase Family 1 Member C4. The antibody can be used for immunoassay techniques, such as ELISA, ICC, IF, IHC-P, WB.
See all AKR1C4 antibodies
Published Data
Mouse Anti-AKR1C4 Recombinant Antibody (2C11) in WB
Western blot illustrating a 2.3-fold increase in AKR1C4 protein expression in response to T1317 treatment for 48h. ...View More
Stayrook, K. R., Rogers, P. M., Savkur, R. S., Wang, Y., Su, C., Varga, G., ... & Burris, T. P. (2008). Regulation of human 3α-hydroxysteroid dehydrogenase (AKR1C4) expression by the liver X receptor α. Molecular pharmacology, 73(2), 607-612.

Summary

Host Animal
Mouse
Specificity
Human
Clone
V2-180482
Antibody Isotype
IgG1
Application
ELISA, ICC, IF, IHC-P, WB

Basic Information

Immunogen
AKR1C4 (AAH20744, 1 a.a. ~ 323 a.a) full-length recombinant protein with GST tag.
Host Species
Mouse
Specificity
Human
Antibody Isotype
IgG1
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
IF(ICC)15 μg/ml
IHC-P3 μg/ml

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, pH 7.4
Preservative
None
Concentration
Batch dependent
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
aldo-keto reductase family 1, member C4 (chlordecone reductase; 3-alpha hydroxysteroid dehydrogenase, type I; dihydrodiol dehydrogenase 4)
Introduction
AKR1C4 is a member of the aldo/keto reductase superfamily, which consists of more than 40 known enzymes and proteins. These enzymes catalyze the conversion of aldehydes and ketones to their corresponding alcohols by utilizing NADH and/or NADPH as cofactor
Entrez Gene ID
1109
UniProt ID
P17516
Alternative Names
Aldo-Keto Reductase Family 1 Member C4; Chlordecone Reductase; 3-Alpha Hydroxysteroid Dehydrogenase, Type I; Dihydrodiol Dehydrogenase 4; 3-Alpha-HSD1; HAKRA; CHDR; DD-4; CDR; DD4; Aldo-Keto Reductase Family 1, Member C4 (Chlordecone Reductase; 3-Alpha Hy
Function
Cytosolic aldo-keto reductase that catalyzes the NADH and NADPH-dependent reduction of ketosteroids to hydroxysteroids. Liver specific enzyme that acts as NAD(P)(H)-dependent 3-, 17- and 20-ketosteroid reductase on the steroid nucleus and side chain (PubMed:14672942, PubMed:10998348, PubMed:7650035, PubMed:1530633, PubMed:11158055, PubMed:10634139, PubMed:19218247). Displays the ability to catalyze both oxidation and reduction in vitro, but most probably acts as a reductase in vivo since the oxidase activity measured in vitro is inhibited by physiological concentration of NADPH (PubMed:14672942). Acts preferentially as a 3-alpha-hydroxysteroid dehydrogenase (HSD) with a subsidiary 3-beta-HSD activity (PubMed:14672942). Catalyzes efficiently the transformation of the potent androgen 5-alpha-dihydrotestosterone (5alpha-DHT or 17beta-hydroxy-5alpha-androstan-3-one) into the less active form, 5-alpha-androstan-3-alpha,17-beta-diol (3-alpha-diol) (PubMed:11158055, PubMed:10998348, PubMed:14672942). Catalyzes the reduction of estrone into 17beta-estradiol but with low efficiency (PubMed:14672942). Metabolizes a broad spectrum of natural and synthetic therapeutic steroid and plays an important role in metabolism of androgens, estrogens, progestereone and conjugated steroids (PubMed:10998348, PubMed:14672942, PubMed:19218247). Catalyzes the biotransformation of the pesticide chlordecone (kepone) to its corresponding alcohol leading to increased biliary excretion of the pesticide and concomitant reduction of its neurotoxicity since bile is the major excretory route (PubMed:2427522).
Biological Process
Androgen metabolic process Source: ProtInc
Bile acid and bile salt transport Source: ProtInc
Bile acid biosynthetic process Source: Reactome
Cellular response to jasmonic acid stimulus Source: UniProtKB
Daunorubicin metabolic process Source: UniProtKB
Doxorubicin metabolic process Source: UniProtKB
Progesterone metabolic process Source: GO_Central
Prostaglandin metabolic process Source: GO_Central
Retinoid metabolic process Source: Reactome
Steroid metabolic process
Cellular Location
Cytosol
Involvement in disease
46,XY sex reversal 8 (SRXY8): The gene represented in this entry may act as a disease modifier. A splicing mutation resulting in loss of AKR1C4 exon 2 has been found in affected individuals carrying a causative mutation in AKR1C2 (PubMed:21802064). These patients manifest a more severe disease phenotype than individuals only carrying mutations in AKR1C2. A disorder of sex development. Affected individuals have a 46,XY karyotype but present as phenotypically normal females.
PTM
The N-terminus is blocked.
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For research use only. Not intended for any clinical use.

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