Jemtland R, Rian E, Gautvik K M
Institutt for medisinsk biokjemi Universitetet i Oslo.
Tidsskr Nor Laegeforen. 1991 May 30;111(14):1738-42.
Humoral hypercalcemia in malignant disease results from the production of humoral factors that act on bone to demineralize the skeleton, with subsequent release of calcium. It is characteristic of certain tumours without bony metastases. A recently discovered parathyroid hormone-related protein (PTHrP) has been implicated as a causative hypercalcemic agent. PTHrP exerts its calcium-mobilizing effects by interaction with parathyroid hormone (PTH) receptors in bone and kidney through its amino-terminal sequence, which is homologous with that of PTH. The human PTHrP gene could encode multiple isoforms of the protein due to alternative exon usage. Apart from its involvement in humoral hypercalcemia of malignancy, PTHrP has also been identified in normal tissues, such as keratinocytes and placenta, and is present in high concentration in milk. PTHrP may modulate the calcium homeostasis in some normal physiological conditions, probably acting in a paracrine fashion.
恶性疾病中的体液性高钙血症是由作用于骨骼使骨骼脱矿质并随后释放钙的体液因子产生所致。它是某些无骨转移肿瘤的特征。最近发现的甲状旁腺激素相关蛋白（PTHrP）被认为是导致高钙血症的因子。PTHrP通过其氨基末端序列与骨和肾中的甲状旁腺激素（PTH）受体相互作用发挥其钙动员作用，该序列与PTH的序列同源。由于外显子的选择性使用，人PTHrP基因可编码该蛋白的多种同工型。除了参与恶性肿瘤的体液性高钙血症外，PTHrP也已在正常组织如角质形成细胞和胎盘中被鉴定出来，并且在牛奶中含量很高。PTHrP可能在某些正常生理条件下调节钙稳态，可能以旁分泌方式起作用。
