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Rabbit Anti-AKR1C3 Recombinant Antibody (V2-639398) (CBMAB-EN134-LY)


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Summary

Host Animal
Rabbit
Specificity
Human
Clone
V2-639398
Antibody Isotype
IgG
Application
WB, FC, ICC/IF, IP

Basic Information

Immunogen
A synthesized peptide derived from human Aldo-keto Reductase 1C3/AKR1C3.
Host Species
Rabbit
Specificity
Human
Antibody Isotype
IgG
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
IF(ICC)1:50-1:200
IP1:30
WB1:500-1:1,000
FC1:50

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

Format
Liquid
Buffer
PBS, pH 7.4, 150mM NaCl, 50% glycerol
Preservative
0.02% sodium azide
Concentration
Batch dependent
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Introduction
This gene encodes 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 cofactors. The enzymes display overlapping but distinct substrate specificity. This enzyme catalyzes the reduction of prostaglandin (PG) D2, PGH2 and phenanthrenequinone (PQ), and the oxidation of 9alpha,11beta-PGF2 to PGD2. It may play an important role in the pathogenesis of allergic diseases such as asthma, and may also have a role in controlling cell growth and/or differentiation. This gene shares high sequence identity with three other gene members and is clustered with those three genes at chromosome 10p15-p14. Three transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Dec 2011]
Entrez Gene ID
8644
UniProt ID
P42330
Alternative Names
Aldo-Keto Reductase Family 1 Member C3; Prostaglandin F Synthase; Trans-1,2-Dihydrobenzene-1,2-Diol Dehydrogenase; 3-Alpha Hydroxysteroid Dehydrogenase, Type II; Testosterone 17-Beta-Dehydrogenase 5; Chlordecone Reductase Homolog HAKRb; Dihydrodiol Dehydrogenase 3; Dihydrodiol Dehydrogenase X; 3-Alpha-HSD Type II, Brain; Indanol Dehydrogenase; HSD17B5; HA1753; PGFS; DD3; Aldo-Keto Reductase Family 1, Member C3 (3-Alpha Hydroxysteroid Dehydrogenase, Type II); Type IIb 3-Alpha Hydroxysteroid Dehydrogenase; 17-Beta-Hydroxysteroid Dehydrogenase Type 5; 3-Alpha-Hydroxysteroid Dehydrogenase Type 2; Hydroxysteroid (17-Beta) Dehydrogenase 5;
Function
Cytosolic aldo-keto reductase that catalyzes the NADH and NADPH-dependent reduction of ketosteroids to hydroxysteroids. Acts as a NAD(P)(H)-dependent 3-, 17- and 20-ketosteroid reductase on the steroid nucleus and side chain and regulates the metabolism of androgens, estrogens and progesterone (PubMed:10622721, PubMed:11165022, PubMed:7650035, PubMed:9415401, PubMed:9927279). 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, PubMed:11165022). Acts preferentially as a 17-ketosteroid reductase and has the highest catalytic efficiency of the AKR1C enzyme for the reduction of delta4-androstenedione to form testosterone (PubMed:20036328). Reduces prostaglandin (PG) D2 to 11beta-prostaglandin F2, progesterone to 20alpha-hydroxyprogesterone and estrone to 17beta-estradiol (PubMed:15047184, PubMed:20036328, PubMed:10622721, PubMed:11165022, PubMed:10998348, PubMed:19010934). Catalyzes the transformation of the potent androgen dihydrotestosterone (DHT) into the less active form, 5-alpha-androstan-3-alpha,17-beta-diol (3-alpha-diol) (PubMed:10998348, PubMed:14672942, PubMed:11165022, PubMed:7650035, PubMed:9415401, PubMed:10557352). Displays also retinaldehyde reductase activity toward 9-cis-retinal (PubMed:21851338).
Biological Process
Cellular response to cadmium ion Source: UniProtKB
Cellular response to calcium ion Source: UniProtKB
Cellular response to corticosteroid stimulus Source: UniProtKB
Cellular response to jasmonic acid stimulus Source: UniProtKB
Cellular response to prostaglandin D stimulus Source: UniProtKB
Cellular response to prostaglandin stimulus Source: UniProtKB
Cellular response to reactive oxygen species Source: UniProtKB
Cellular response to starvation Source: UniProtKB
Cyclooxygenase pathway Source: Reactome
Daunorubicin metabolic process Source: UniProtKB
Doxorubicin metabolic process Source: UniProtKB
Farnesol catabolic process Source: UniProtKB
G protein-coupled receptor signaling pathway Source: UniProtKB
Keratinocyte differentiation Source: UniProtKB
Macromolecule metabolic process Source: UniProtKB
Male gonad development Source: UniProtKB
Negative regulation of retinoic acid biosynthetic process Source: UniProtKB
Positive regulation of cell death Source: UniProtKB
Positive regulation of cell population proliferation Source: UniProtKB
Positive regulation of endothelial cell apoptotic process Source: UniProtKB
Positive regulation of protein kinase B signaling Source: UniProtKB
Positive regulation of reactive oxygen species metabolic process Source: UniProtKB
Progesterone metabolic process Source: UniProtKB
Prostaglandin metabolic process Source: UniProtKB
Regulation of retinoic acid receptor signaling pathway Source: UniProtKB
Regulation of testosterone biosynthetic process Source: UniProtKB
Renal absorption Source: UniProtKB
Response to nutrient Source: UniProtKB
Retinal metabolic process Source: UniProtKB
Retinoid metabolic process Source: Reactome
Retinol metabolic process Source: GOC
Steroid metabolic process Source: UniProtKB
Testosterone biosynthetic process Source: UniProtKB
Cellular Location
Cytoplasm
More Infomation

Zhu, P., Feng, R., Lu, X., Liao, Y., Du, Z., Zhai, W., & Chen, K. (2021). Diagnostic and prognostic values of AKR1C3 and AKR1D1 in hepatocellular carcinoma. Aging (Albany NY), 13(3), 4138.

Zhou, C., Wang, Z., Li, J., Wu, X., Fan, N., Li, D., ... & Zhao, Y. (2021). Aldo-Keto Reductase 1C3 Mediates Chemotherapy Resistance in Esophageal Adenocarcinoma via ROS Detoxification. Cancers, 13(10), 2403.

Arafah, K., Kriegsmann, M., Renner, M., Lasitschka, F., Fresnais, M., Kriegsmann, K., ... & Longuespée, R. (2020). Microproteomics and Immunohistochemistry Reveal Differences in Aldo‐Keto Reductase Family 1 Member C3 in Tissue Specimens of Ulcerative Colitis and Crohn's Disease. PROTEOMICS–Clinical Applications, 14(4), 1900110.

Hertzog, J. R., Zhang, Z., Bignan, G., Connolly, P. J., Heindl, J. E., Janetopoulos, C. J., ... & McDevitt, T. M. (2020). AKR1C3 mediates pan‐AR antagonist resistance in castration‐resistant prostate cancer. The Prostate, 80(14), 1223-1232.

Zhao, J., Zhang, M., Liu, J., Liu, Z., Shen, P., Nie, L., ... & Zeng, H. (2019). AKR1C3 expression in primary lesion rebiopsy at the time of metastatic castration‐resistant prostate cancer is strongly associated with poor efficacy of abiraterone as a first‐line therapy. The Prostate, 79(13), 1553-1562.

Miyazaki, Y., Teramoto, Y., Shibuya, S., Goto, T., Okasho, K., Mizuno, K., ... & Inoue, T. (2019). Consecutive Prostate Cancer Specimens Revealed Increased Aldo–Keto Reductase Family 1 Member C3 Expression with Progression to Castration-Resistant Prostate Cancer. Journal of clinical medicine, 8(5), 601.

Liu, J., He, P., Lin, L., Zhao, Y., Deng, W., Ding, H., ... & Wang, Z. (2019). Characterization of a highly specific monoclonal antibody against human aldo-keto reductase AKR1C3. Steroids, 143, 73-79.

Hashimoto, Y., Imai, A., Yamamoto, H., Hatakeyama, S., Yoneyama, T., & Ohyama, C. (2018). Aldo-keto-reductase 1C3 expression in prostate cancer. Annals of Oncology, 29, ix71-ix72.

Penning, T. M. (2017). Aldo-Keto Reductase (AKR) 1C3 inhibitors: a patent review. Expert opinion on therapeutic patents, 27(12), 1329-1340.

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For research use only. Not intended for any clinical use.

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