Recombinant Full Length Naumovozyma Castellii Palmitoyltransferase Akr1(Akr1) Protein, His-Tagged
Cat.No. : | RFL11568NF |
Product Overview : | Recombinant Full Length Naumovozyma castellii Palmitoyltransferase AKR1(AKR1) Protein (Q876A6) (1-757aa), fused to N-terminal His tag, was expressed in E. coli. |
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Source : | E.coli expression system |
Species : | Naumovozyma castellii (strain ATCC 76901 / CBS 4309 / NBRC 1992 / NRRL Y-12630) (Yeast) (Saccharomyces castellii) |
Tag : | His |
Form : | Lyophilized powder |
Protein Length : | Full Length (1-757) |
AA Sequence : | MSDINTESGESTSLPNSTDPPLSDV NIDVEDDDTAESISSLQPIVSNTTN PPEEPINPVL GQYHQACQKGDLATVKQLLDSGVLD LNTDLTGDITGLHWASINNRLSVVK YLISQGIDVN AKAGDLEATPLHWAARYGYVHIVDC LLNKGADPTMCDMQGFNLLHLAVNS SNVMLVAYVL FFVVAKGIIDIDCQDPKGRTPLLWA AYQGDSLSVMLLLKFGASTKIVDEG GFTPLHWATV KGQPYVLTHLIRDGADFFLKTNDGK DCFTIAQEMNTSHSFKDALSICGFN QDGYPKRKLF KKSDHAKVITFFVPLVALSIIFILF THLHPLFALLISLIFGLAVNKALKE LILPSYSNYG LHSTSLLKSPFLSGTFFGSLLLLTI VWIFKIAPFTIFKSRLLTNFFMFLI LMQIYYLFIK LIFSDPGCVPIETDHENVRGTIKEL LDTGKFDIKNFCLETWIRKPLRSHF STLNTHNVAR FDHFCPWIYNDIGLKNHKNFMWFIL LTEVGIWFFISLTMKYFDILEDTNE DVACFLLGDD ELCAGFVYDRFTFLIALWALIQSVW VGFLIVVQVFQTFTGVTNKEFNKYV KEKKNQHAFD PIFFNDTFNTTPEELRNDDDDTAAS RTGNNPNHSNGTTIPSEGSRINTRK PRTCFNLCFA ITGLDQVRTIVRETLGIGGANEMSR MQLLSSIPTNYGWKRNLADFWLTSD VMAPIWRRLF YSPVESRALLNGVEVDYFKLYDFPE KTYPEPTGPESV |
Purity : | Greater than 90% as determined by SDS-PAGE. |
Notes : | Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week. |
Storage : | Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles. |
Storage Buffer : | Tris/PBS-based buffer, 6% Trehalose, pH 8.0 |
Reconstitution : | We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference. |
Gene Name : | AKR1 |
Synonyms : | AKR1; NCAS_0C05280; Palmitoyltransferase AKR1; Ankyrin repeat-containing protein AKR1 |
UniProt ID : | Q876A6 |
Gene Name : | AKR1 |
Synonyms : | AKR1; NCAS_0C05280; Palmitoyltransferase AKR1; Ankyrin repeat-containing protein AKR1 |
UniProt ID : | Q876A6 |
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For Research Use Only. Not intended for any clinical use. No products from Creative BioMart may be resold, modified for resale or used to manufacture commercial products without prior written approval from Creative BioMart.
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Q&As (12)
Ask a questionHuman AKR1 enzymes catalyze the conversion of either weak ligands to form potent ligands for nuclear receptors or they are involved in the elimination of these ligands. In this manner AKR1 enzymes control the levels of potent ligands that can occupy and trans-activate nuclear receptors within endocrine target tissues.
AKR1 enzymes control concentrations of active androgens and regulate the occupancy and trans-activation of androgen receptor (AR) in the prostate. AKR1C3 catalyzes the reduction of D4 -androstene-3,17-dione to form the potent androgen estosterone (Kd = 109 M for AR) and the reduction of 5a-androstane-3,17-dione to yield the most potent androgen 5a-DHT (Kd = 1010 Mfor the AR).
Many synthetic steroids contain the D4 or 3-keto, 20-keto-steroid structural motif and are anticipated to be substrates for the AKR1 enzymes. In support of this contention AKR1 enzymes are involved in the metabolism of tibolone and the rogestins, norethynodrel and dydrogesterone as well as the synthetic glucocorticoids budesonide and flunisolide.
Inherited mutations in AKR1D1 have been studied in patients with bile-acid deficiency that develops in infants and is characterized by reduced formation of bile acids and accumulation of D4-3-keto steroids and 5a-reduced (allo-bile acids) which are hepatotoxic.
Tibolone is a prodrug used for the treatment of post-menopausal symptoms. Its tissue specific effects which make it a "selective tissue estrogen activity regulator" is likely mediated by AKR metabolism.
Altered regulation of AKR1 gene transcription, including epigenetic modifications, transcriptional regulation (induction, repression, alternative splicing) should be further investigated. For example, AKR1C genes are up-regulated by androgen deprivation in prostate cancer but it is not known how AKR1C genes are regulated by hormone deprivation and whether this would be seen in other malignancies.
Among all AKR1 SNPs included in the SNP database there are currently only 5 SNPs with a minor allelic frequency (MAF) greater than 0.05. These correspond to Phe46Tyr in AKR1C2 with a MAF = 0.051; His5Gln and Lys104Asn in AKR1C3 with MAF of 0.428 and 0.132, respectfully; and Ser145Cys and Leu311Val in AKR1C4, both with MAF of 0.104. So far SNPs in AKR1C1, AKR1C2 and AKR1C4 have been studied at the protein level and Phe46Tyr has been associated with disease.
AKR1 enzymes control concentrations of estrogens and regulate occupancy and trans-activation of estrogen receptors a and b (ERa and ERb). AKR1C3 catalyzes reduction of estrone (Kd = 0.3 nM and 0.4 nM for ERa and ERb, respectively) to yield the more potent estrogen 17b-estradiol, (Kd = 0.1 nM for ERa and ERb) and thus controls activation of ERa and ERb.
The main function of AKR1 is to regulate the differentiation, growth and damage repair of cardiomyocytes and skeletal muscle cells.
Steroid preferences of AKR1 enzymes are characterized by determination of their kinetic properties in vitro, where catalytic efficiencies (kcat/KM values) are compared, and products of the reactions are identified, preferably by liquid hromatography mass spectrometry.
A functional genomics approach would contribute enormously. After studying enzymatic activities of recombinant AKR1 enzymes (substrate specificity, catalytic efficiency, product profiling), their activities in model or transfected cell lines, and their ability to alter transactivation of uclear receptors should be examined. Proof-of-principle experiments in human cell lines using siRNA or sh-RNA approaches are needed to clarify the athophysiological roles of AKR1 enzymes.
Under normal circumstances, AKR1 expression is regulated, but in some diseases such as myocardial infarction, muscle disease, diabetes, and other cell and tissue damage, AKR1 expression is significantly increased. This suggests that AKR1 plays a key role in cell growth and damage repair.
Customer Reviews (4)
Write a reviewHigh solubility makes it easy to prepare the desired concentration.
Had good crystallinity, which was beneficial for crystallographic study.
Good antigenicity and could induce target immune responses.
High catalytic efficiency.
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