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Thimet Oligopeptidase/THOP1 Protein, Mouse, Recombinant (His)

产品编号 TMPY-02393

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.

Thimet Oligopeptidase/THOP1 Protein, Mouse, Recombinant (His)

产品编号 TMPY-02393

规格	价格	库存	数量
50 μg	¥ 3,820	5日内发货

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产品信息

生物活性	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.
产品描述	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.
种属	Mouse
表达系统	Baculovirus Insect Cells
标签	N-His
蛋白编号	Q8C1A5
别名	thimet oligopeptidase 1,EP24.15,AI327041,AI131655
蛋白构建	A DNA sequence encoding the mouse THOP1 (NP_073144.3) (Lys 2-Cys 687) was fused with a polyhistidine tag at the N-terminus. Predicted N terminal: Met
蛋白纯度	> 90 % as determined by SDS-PAGE
分子量	80.1 kDa (predicted); 75 kDa (reducing conditions)
内毒素	< 1.0 EU/μg of the protein as determined by the LAL method.
缓冲液	Lyophilized from a solution filtered through a 0.22 μm filter, containing 20 mM Tris, 500 mM NaCl, pH 7.4, 10% gly. Typically, a mixture containing 5% to 8% trehalose, mannitol, and 0.01% Tween 80 is incorporated as a protective agent before lyophilization.
复溶方法	A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information.
存储	It is recommended to store recombinant proteins at -20°C to -80°C for future use. Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.
运输方式	In general, Lyophilized powders are shipping with blue ice.
研究背景	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.