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AB109831

Recombinant human AKR1C4 protein (His tag N-Terminus)

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Recombinant human AKR1C4 protein (His tag N-Terminus) is a Human Full Length protein, in the 1 to 343 aa range, expressed in Escherichia coli, with >90%, suitable for SDS-PAGE, Mass Spec, FuncS.

대체 명칭 보기

CHDR, AKR1C4, Aldo-keto reductase family 1 member C4, 3-alpha-hydroxysteroid 3-dehydrogenase type I, Chlordecone reductase, Dihydrodiol dehydrogenase 4, HAKRA, 3-alpha-HSD1, CDR, DD-4, DD4

1 이미지
SDS-PAGE - Recombinant human AKR1C4 protein (His tag N-Terminus) (AB109831)
  • SDS-PAGE

Unknown

SDS-PAGE - Recombinant human AKR1C4 protein (His tag N-Terminus) (AB109831)

15% SDS-PAGE image, using ab109831 at 3ug

주요 정보

Purity

>90% SDS-PAGE

ab109831 was purified using conventional chromatography.

발현 시스템

Escherichia coli

Tags

His tag N-Terminus

Applications

FuncS, SDS-PAGE, Mass Spec

applications

Biologically active

Yes

Biological activity

Specific activity is > 700 pmol/min/μg, and is defined as the amount of enzyme that catalyzes the reduction of 1.0 pmole 3-chlorobenzaldehyde in the presence of NADP per minute at pH 8.8 at 25°C.

Accession

Animal free

No

Carrier free

No

Species

Human

보관 버퍼

pH: 8 Constituents: 20% Glycerol (glycerin, glycerine), 0.58% Sodium chloride, 0.32% Tris HCl, 0.02% (R*,R*)-1,4-Dimercaptobutan-2,3-diol

storage-buffer

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보완 제품

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Recombinant Human AKR1A1 protein (Tag Free)

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AB85415

Recombinant Human AKR1B10 protein (Tag Free)

SDS-PAGE - Recombinant Human AKR1B10 protein (Tag Free) (AB85415)

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Reactivity 정보

{ "title": "Reactivity Data", "filters": { "stats": ["", "Reactivity", "Dilution Info", "Notes"] }, "values": { "SDS-PAGE": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" }, "Mass Spec": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" }, "FuncS": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" } } }
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제품 세부 정보

Previously labelled as HSD3a.
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서열 정보

[{"linker":null,"sequence":"MGSSHHHHHHSSGLVPRGSHMDPKYQRVELNDGHFMPVLGFGTYAPPEVPRNRAVEVTKLAIEAGFRHIDSAYLYNNEEQVGLAIRSKIADGSVKREDIFYTSKLWCTFFQPQMVQPALESSLKKLQLDYVDLYLLHFPMALKPGETPLPKDENGKVIFDTVDLSATWEVMEKCKDAGLAKSIGVSNFNCRQLEMILNKPGLKYKPVCNQVECHPYLNQSKLLDFCKSKDIVLVAHSALGTQRHKLWVDPNSPVLLEDPVLCALAKKHKRTPALIALRYQLQRGVVVLAKSYNEQRIRENIQVFEFQLTSEDMKVLDGLNRNYRYVVMDFLMDHPDYPFSDEY","proteinLength":"Full Length","predictedMolecularWeight":"39.2 kDa","actualMolecularWeight":null,"aminoAcidEnd":343,"aminoAcidStart":1,"nature":"Recombinant","expressionSystem":"Escherichia coli","accessionNumber":"P17516","tags":[{"tag":"His","terminus":"N-Terminus"}]}]
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특성 및 보관 정보

제형
Liquid
배송 시 보관 조건
Blue Ice
적절한 단기 보관 기간
1-2 weeks
적절한 단기 보관 조건
+4°C
적절한 장기 보관 조건
-20°C
분주 정보
Upon delivery aliquot
보관 정보
Avoid freeze / thaw cycle
True
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추가 정보

This supplementary information is collated from multiple sources and compiled automatically.

AKR1C4 also known as Aldo-keto reductase family 1 member C4 plays a role in the metabolism of steroid hormones. It acts mainly as a ketosteroid reductase involved in the conversion of aldo-keto forms. The protein has a molecular mass of approximately 37 kDa. AKR1C4 is expressed in several tissues with high levels found in the liver. In the liver it contributes to the oxidative inactivation of various steroid hormones thereby maintaining hormonal balance.
Biological function summary

AKR1C4 functions to reduce ketosteroids into their respective alcohol forms. This activity is important in steroid metabolism and detoxification processes. AKR1C4 is not part of any major enzyme complexes but its function is essential for processing steroids within cells. It impacts hormonal activity by converting potent steroids into their less active forms facilitating the regulation of physiological responses.

Pathways

AKR1C4 is part of the steroid hormone metabolic pathway and the bile acid biosynthesis pathway. In steroid hormone metabolism it interacts closely with proteins such as AKR1C3 which also acts on similar substrates. Its activity in bile acid biosynthesis ensures the proper conversion and excretion of bile acids essential for lipid digestion and absorption.

AKR1C4 involvement has been noted in liver diseases and hormone-related disorders. Dysregulation or altered expression of AKR1C4 can contribute to conditions such as hepatic steatosis and endocrine disorders like polycystic ovary syndrome (PCOS). Its interaction with proteins like the androgen receptor is also significant as it modulates androgen availability and activity potentially impacting androgen-sensitive conditions.
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일반 정보

기능

Cytosolic aldo-keto reductase that catalyzes NADPH-dependent reduction of ketosteroids to hydroxysteroids. Displays broad substrate specificity with distinct positional and stereochemistry, primarily generating 3alpha/beta-, 17beta- and 20alpha-hydroxysteroids (PubMed : 10634139, PubMed : 10998348, PubMed : 11158055, PubMed : 14672942, PubMed : 1530633, PubMed : 12604236, PubMed : 19218247, PubMed : 21802064, PubMed : 7650035). Required for male sex determination as a component of the 'backdoor' androgen biosynthesis pathway that generates 5alpha-dihydrotestosterone (5alpha-DHT) via pregnanes. Acts together with AKR1C2 to convert 5alpha-dihydroprogesterone (5alpha-DHP) to 3alpha-hydroxy-5alpha-pregnan-20-one (3alpha,5alpha-THP/allopregnanolone), leading to 5alpha-DHT secretion necessary for embryonic gonad differentiation into testis (PubMed : 21802064). May regulate the concentrations of circulating neurosteroids. Reduces 5alpha-dihydroprogesterone (5-alpha-DHP) and 5alpha-dihydrodeoxycorticosterone (5-alpha-DHDOC) precursors to 3alpha-hydroxy-5alpha-pregnan-20-one (3alpha,5alpha-THP/allopregnanolone) and 3alpha,21-dihydroxy-5alpha-pregnane-20-one (3alpha,5alpha-THDOC) neuroactive steroids known to alter neural excitability via allosteric activation of gamma-aminobutyric acid type A receptors (GABAAR) (PubMed : 12604236). Regulates ligand availability for steroid hormone receptors. Catalyzes the inactivation of 5alpha-DHT and progesterone converting them into 3alpha/beta-androstanediols and (20S)-hydroxypregn-4-en-3-one, respectively (PubMed : 10998348, PubMed : 11158055, PubMed : 14672942). May contribute to the metabolism of adrenal-derived androgens via reduction of 11-keto-5alpha-androstane-3,17-dione (11K-Adione) into 11-ketoandrosterone (11KAST) and of 11-ketodihydrotestosterone (11KDHT) into 11-keto-5alpha-androstane-3alpha/beta,17beta-diol (11K-A3diol) (PubMed : 31926269). Catalyzes the reduction of estrone into 17beta-estradiol but with low efficiency (PubMed : 14672942). In androgen catabolism, may predominantly act as a phase I enzyme by introducing a hydroxyl group prior to conjugation. It can nevertheless participate in the alternative phase II pathway by directly reducing sulfate- or glucuronide-conjugated androgens (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). In vitro can efficiently catalyze bidirectional conversion between ketosteroids and hydroxysteroids using NADPH/NADP(+) or NADH/NAD(+) as cofactors. In vivo however, the reductase activity prevails since the major reducing cofactor NADPH inhibits NAD(+)-dependent oxidase activity (PubMed : 14672942).

서열 유사성

Belongs to the aldo/keto reductase family.

Post-translational modifications

The N-terminus is blocked.

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제품 프로토콜

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타겟 정보

Cytosolic aldo-keto reductase that catalyzes NADPH-dependent reduction of ketosteroids to hydroxysteroids. Displays broad substrate specificity with distinct positional and stereochemistry, primarily generating 3alpha/beta-, 17beta- and 20alpha-hydroxysteroids (PubMed : 10634139, PubMed : 10998348, PubMed : 11158055, PubMed : 14672942, PubMed : 1530633, PubMed : 12604236, PubMed : 19218247, PubMed : 21802064, PubMed : 7650035). Required for male sex determination as a component of the 'backdoor' androgen biosynthesis pathway that generates 5alpha-dihydrotestosterone (5alpha-DHT) via pregnanes. Acts together with AKR1C2 to convert 5alpha-dihydroprogesterone (5alpha-DHP) to 3alpha-hydroxy-5alpha-pregnan-20-one (3alpha,5alpha-THP/allopregnanolone), leading to 5alpha-DHT secretion necessary for embryonic gonad differentiation into testis (PubMed : 21802064). May regulate the concentrations of circulating neurosteroids. Reduces 5alpha-dihydroprogesterone (5-alpha-DHP) and 5alpha-dihydrodeoxycorticosterone (5-alpha-DHDOC) precursors to 3alpha-hydroxy-5alpha-pregnan-20-one (3alpha,5alpha-THP/allopregnanolone) and 3alpha,21-dihydroxy-5alpha-pregnane-20-one (3alpha,5alpha-THDOC) neuroactive steroids known to alter neural excitability via allosteric activation of gamma-aminobutyric acid type A receptors (GABAAR) (PubMed : 12604236). Regulates ligand availability for steroid hormone receptors. Catalyzes the inactivation of 5alpha-DHT and progesterone converting them into 3alpha/beta-androstanediols and (20S)-hydroxypregn-4-en-3-one, respectively (PubMed : 10998348, PubMed : 11158055, PubMed : 14672942). May contribute to the metabolism of adrenal-derived androgens via reduction of 11-keto-5alpha-androstane-3,17-dione (11K-Adione) into 11-ketoandrosterone (11KAST) and of 11-ketodihydrotestosterone (11KDHT) into 11-keto-5alpha-androstane-3alpha/beta,17beta-diol (11K-A3diol) (PubMed : 31926269). Catalyzes the reduction of estrone into 17beta-estradiol but with low efficiency (PubMed : 14672942). In androgen catabolism, may predominantly act as a phase I enzyme by introducing a hydroxyl group prior to conjugation. It can nevertheless participate in the alternative phase II pathway by directly reducing sulfate- or glucuronide-conjugated androgens (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). In vitro can efficiently catalyze bidirectional conversion between ketosteroids and hydroxysteroids using NADPH/NADP(+) or NADH/NAD(+) as cofactors. In vivo however, the reductase activity prevails since the major reducing cofactor NADPH inhibits NAD(+)-dependent oxidase activity (PubMed : 14672942).
See full target information AKR1C4
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Product promise

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