表单
buffered aqueous solution
质量水平
比活
≥5 units/mg protein
UniProt登记号
运输
dry ice
储存温度
−20°C
基因信息
human ... KLK1(3816)
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一般描述
Kallikrein肽酶属于15个高度保守的胰蛋白酶或胰凝乳蛋白酶家庭的成员。血浆激肽释放酶（PK）是一种来源于血浆前激肽释放酶的丝氨酸蛋白酶，也是一种在血液循环中含量较高的酶原。KLKB1基因位于人染色体4q35.2上。
应用
从人血浆中提取的激肽释放酶已用于：
- 培养人肝癌细胞系
- 研究其对来自脑膜炎奈瑟氏菌的奈瑟球菌肝素结合抗原（NHBA）的裂解作用
- 肽酶抑制分析
生化/生理作用
血浆激肽释放酶（PK）参与缓激肽的合成，可维持血液代谢物水平和高血压。它还参与凝血因子XII的激活，促进炎症和内源性凝血途径。PK控制心血管系统中的蛋白水解级联反应，如激肽酶激肽系统、肾素血管紧张素系统、纤维蛋白溶解系统和补体旁路等。它参与胰高血糖素样肽-1（GLP-1）和神经肽Y（NPY） 的裂解，这表明血浆激肽释放酶可能会影响代谢和糖尿病。
外形
溶于20 mM Tris-HCl (pH 7.8)和100 mM NaCl的溶液中。
其他说明
一个酶活性单位是指在pH 8.7、25°C条件下，每分钟将1.0 μMNα-苯甲酰基-L-精氨酸乙酯（BAEE）水解为Nα-苯甲酰基-L-精氨酸和乙醇所需的酶量。
储存分类代码
12 - Non Combustible Liquids
WGK
WGK 1
闪点(°F)
Not applicable
闪点(°C)
Not applicable
个人防护装备
Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)
法规信息
高风险级别生物产品--人源产品
常规特殊物品
历史批次信息供参考:
分析证书(COA)
Lot/Batch Number
Ekaterina Zubareva et al.
Pharmaceuticals (Basel, Switzerland), 14(11) (2021-11-28)
The disfunction or deficiency of the C1 esterase inhibitor (C1INH) is associated with hereditary or acquired angioedema (HAE/AAE), a rare life-threatening condition characterized by swelling in the skin, respiratory and gastrointestinal tracts. The current treatment options may carry the risks
Georgia Sotiropoulou et al.
The Journal of biological chemistry, 284(48), 32989-32994 (2009-10-13)
Kallikrein-related peptidases constitute a single family of 15 (chymo)trypsin-like proteases (KLK1-15) with pleiotropic physiological roles. Aberrant regulation of KLKs has been associated with diverse diseases such as hypertension, renal dysfunction, skin disorders, inflammation, neurodegeneration, and cancer. Recent studies suggested that
A new case of homozygous C1-inhibitor deficiency suggests a role for Arg378 in the control of kinin pathway activation.
Alberto López-Lera et al.
The Journal of allergy and clinical immunology, 126(6), 1307-1310 (2010-09-25)
L E Stolz et al.
Drugs of today (Barcelona, Spain : 1998), 46(8), 547-555 (2010-09-11)
Hereditary angioedema (HAE) is a debilitating, potentially fatal disease characterized by variable and unpredictable acute attacks of swelling affecting the subcutaneous tissue and mucosa. It is an autosomal dominant disorder resulting from a genetic deficiency of functional C1-esterase inhibitor. Available
A Allart Stoop et al.
Biological chemistry, 391(4), 425-433 (2010-02-26)
Engineering of protein-protein interactions is used to enhance the affinity or specificity of proteins, such as antibodies or protease inhibitors, for their targets. However, fully diversifying all residues in a protein-protein interface is often unfeasible. Therefore, we limited our phage
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