Alkaline Phosphatase/ALPL 蛋白, Mouse (HEK293, Fc)

Alkaline Phosphatase/ALPL Protein is a preproprotein that is proteolytically cleaved to yield a signal peptide and a proproptein that is subsequently processed to generate the active mature peptide. ALPL is also a membrane-bound glycosylated enzyme that catalyzes the hydrolysis of phosphate esters at alkaline pH. Mice that lack ALPL show symptoms of osteomalacia, softening of the bones. Moreover, ALPL stimulates mineralization mainly through modulation of the balance between inorganic phosphate (Pi) and inorganic pyrophosphate (PPi) and also has a role in cardiovascular remodelling. Alkaline Phosphatase/ALPL Protein, Mouse (HEK293, Fc) is the recombinant mouse-derived Alkaline Phosphatase/ALPL protein, expressed by HEK293 , with C-hFc labeled tag. The total length of Alkaline Phosphatase/ALPL Protein, Mouse (HEK293, Fc) is 502 a.a., with molecular weight of ~80.3 kDa.

碱性磷酸酶 (ALPL) 是一种前蛋白原，经过蛋白水解裂解产生信号肽和原蛋白，随后经过加工生成活性成熟肽。ALPL 也是一种膜结合糖基化酶，可在碱性 pH 条件下催化磷酸酯的水解。成熟肽维持骨矿化所需的无机磷酸盐与无机焦磷酸盐的比例。缺乏 ALPL 的小鼠会出现骨软化、骨骼软化的症状。在人类中，该基因的突变与低磷酸酯酶症有关，低磷酸酯酶症是一种遗传性代谢性骨病，缺乏这种酶会抑制骨矿化，导致骨骼缺陷。ALPL 在矿化组织细胞中高度表达，在硬组织的形成中发挥关键作用。ALPL 会增加无机磷酸盐的局部比率，促进矿化，并降低细胞外焦磷酸盐浓度 (矿物质形成的抑制剂)。此外，ALPL 主要通过调节无机磷酸盐 (Pi) 和无机焦磷酸盐 (PPi) 之间的平衡来刺激矿化，并在心血管重塑中发挥作用^[1][2][3]。

Mouse

HEK293

C-hFc

BAH03518 (M1-S502)

11647  [NCBI]

Approximately 80.3 kDa

Greater than 90% as determined by reducing SDS-PAGE.

<1 EU/μg, determined by LAL method.