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Recombinant Mouse THOP1 Protein (His Tag)

Uniprot : A0A0R4IZY0
  • Cat.No.:PKSM040464

  • Expression host: Baculovirus-Insect Cells

To Purchase PKSM040464

Size:
  • 50μg
Price: $867
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Description

Synonyms AI131655;AI327041;EP24.15
Species Mouse
Expression_host Baculovirus-Insect Cells
Sequence Lys 2-Cys 687
Accession NP_073144.3
Mol_Mass 80.1 kDa
AP_Mol_Mass 75 kDa
Tag N-His
Bio_Activity Measured by its ability to cleave a fluorogenic peptide substrate, (7-methoxycoumarin-4-yl)acetyl-Pro-Leu-Gly-Pro-D-Lys(2, 4-dinitrophenyl)-OH or Mca-PLGPK(Dnp)-OH. The specific activity is > 100 pmoles/min/μg.

Properties

Purity > 90 % as determined by reducing SDS-PAGE.
Endotoxin level < 1.0 EU per μg of the protein as determined by the LAL method.
Storage Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months.
Shipping This product is provided as lyophilized powder which is shipped with ice packs.
Formulation Lyophilized from sterile 20mM Tris, 500mM NaCl, pH 7.4, 10% glycerol
Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization.
Please refer to the specific buffer information in the printed manual.
Reconstitution Please refer to the printed manual for detailed information.

Background

THOP1, also known as Thimet oligopeptidase 1, Thimet oligopeptidase, EC 3.4.24.15, or EP24.15, is a zinc(II) endopeptidase implicated in the processing of numerous physiological peptides. As an intracellular enzyme, highly expressed in the brain, kidneys and neuroendocrine tissue, THOP1 has been proposed to metabolize peptides within cells, thereby affecting antigen presentation and G protein-coupled receptor signal transduction. Its substrates is gonadotrophin-releasing hormone (GnRH), an important hypothalamic hormone that regulates the synthesis and release of oestradiol and facilitates female sexual behaviour. THOP1 against toxic effects of Abeta in the early stages of Alzheimer disease (AD) pathology, and suggest that the observed increase in THOP1 expression might be part of a compensatory defense mechanism of the brain against an increased Abeta load.

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