Kisspeptin-10,humanTFA是一种有效的血管收缩剂和血管生成抑制剂。Kisspeptin-10,humanTFA通过其受体GPR54来抑制肿瘤转移作用。Kisspeptin-10-GPR54系统在胚胎肾脏发育中起重要作用。Kisspeptin-10/GPR54信号通过NFATc4介导的BMP2表达来诱导成骨细胞分化。
货号:ajcx30874
CAS:N/A
分子式:C63H83N17O14.C2HF3O2
分子量：1416.46
溶解度:H2O: 4 mg/mL (2.82 mM)
纯度：98%
存储：Store at -20°C
库存：现货

Background:

Kisspeptin-10, human TFA is a potent vasoconstrictor and inhibitor of angiogenesis. Kisspeptin-10, human TFA acts as a tumor metastasis suppressor via its receptor GPR54. Kisspeptin-10-GPR54 system plays an important role in embryonic kidney development. Kisspeptin-10/GPR54 signaling induces osteoblast differentiation via NFATc4-mediated BMP2 expression[1].

Kisspeptin-10 (KP-10) and its receptor GPR54 are key components in the regulation of GnRH secretion in humans and other mammals. Kisspeptin-10 protein binds to GPR54. Activation of Kisspeptin-10 suppresses pulmonary human melanoma and Kisspeptin-10 is a metastasis suppressor in breast cancer cells[1].

Intravenous infusion of kisspeptin-10 (7.5, 35, and 100 nM) induces a dose-dependent increase in LH secretion. The stimulatory effect of kisspeptin-10 (100 n nM) on LH secretion is blocked by the GnRH antagonist cetrorelix, precluding a singular action on gonadotropes[4]. Kisspeptin-10 inhibits angiogenesis in vivo. Kp-10 inhibits tumor growth in SCID mice xenografted with human prostate cancer cells (PC-3) through inhibiting tumor angiogenesis[5].

[1]. Son HE, et al. Kisspeptin-10 (KP-10) stimulates osteoblast differentiation through GPR54-mediated regulation of BMP2 expression and activation. Sci Rep. 2018 Feb 1;8(1):2134.