PDCD10，一个新的多功能信号转导调节分子

人程序性细胞死亡分子10(Homo sapiens programmed cell death 10, PDCD10)，最初被称为TFAR15(TF-1 cell apoptosis related gene 15)，是由撤除粒细胞 巨噬细胞集落刺激因子诱导凋亡的人红白血病细胞系TF-1中克隆得到的1个凋亡相关基因. 后来发现它的突变可引起散发性或家族性颅内海绵状血管瘤(cerebral cavernous malformations，CCMs)的发生，为CCMs的第3个致病基因，所以又被叫做CCM3.近年来研究发现,PDCD10能够和GCKⅢ蛋白、γ-PCDH、CCM2、VEGFR2、ERM等众多蛋白相互作用，并能调控ERK/MAPK通路，增加MST4/VEGFR2的稳定性，增强相应的信号转导，促进细胞的增殖、分化和中枢神经系统的发育，与癌症的发生相关，还能调节细胞的凋亡.以上研究证明了PDCD10 的多种生物学效应，并提示其在血管生成、氧化应激、肿瘤中发挥重要作用.

PDCD10，a Novel Signal Transduction Regulating Moleculewith Multiple Functions

Homo sapiens programmed cell death 10 (PDCD10), also termed as TF-1 cell apoptosis related gene 15 (TFAR15), was a apoptosis-related gene initially. It was originally identified in a premyeloid cell line TF-1, which was induced by removing granulocyte-macrophage colony stimulating factor (GM-CSF). Since the mutation of PDCD10 can give rise to sporadic or familial cerebral cavernous malformations, PDCD10 could also be referred as CCM3, the third disease gene of CCMs. It has been verified that PDCD10 can interact with a wide range of proteins including GCKⅢ,γ-PCDH,CCM2,VEGFR2 and ERM. It can also stimulate the ERK-MAPK pathway by stabilizing MST4/ VEGFR2, and thus enhance the signal transduction, promote proliferation and differentiation of cells. Recent studies revealed multiple biological effects from PDCD10. The results suggest that PDCD10 play important roles in angiogenesis, oxidative stress and oncogenesis.