【摘要】：人程序性細(xì)胞死亡分子10(Homo sapiens programmed cell death 10,PDCD10),最初被稱為TFAR15(TF-1 cell apoptosis related gene 15),是由撤除粒細(xì)胞-巨噬細(xì)胞集落刺激因子誘導(dǎo)凋亡的人紅白血病細(xì)胞系TF-1中克隆得到的1個(gè)凋亡相關(guān)基因.后來發(fā)現(xiàn)它的突變可引起散發(fā)性或家族性顱內(nèi)海綿狀血管瘤(cerebral cavernous malformations,CCMs)的發(fā)生,為CCMs的第3個(gè)致病基因,所以又被叫做CCM3.近年來研究發(fā)現(xiàn),PDCD10能夠和GCKⅢ蛋白、γ-PCDH、CCM2、VEGFR2、ERM等眾多蛋白相互作用,并能調(diào)控ERK-MAPK通路,增加MST4/VEGFR2的穩(wěn)定性,增強(qiáng)相應(yīng)的信號(hào)轉(zhuǎn)導(dǎo),促進(jìn)細(xì)胞的增殖、分化和中樞神經(jīng)系統(tǒng)的發(fā)育,與癌癥的發(fā)生相關(guān),還能調(diào)節(jié)細(xì)胞的凋亡.以上研究證明了PDCD10的多種生物學(xué)效應(yīng),并提示其在血管生成、氧化應(yīng)激、腫瘤中發(fā)揮重要作用.
[Abstract]:Human programmed cell death molecule (10 (Homo sapiens programmed cell death 10 / PDCD10), originally known as TFAR15 (TF-1 cell apoptosis related gene 15), is a apoptosis-related gene cloned from a human erythroleukemia cell line TF-1, which was induced by the removal of granulocyte-macrophage colony stimulating factor. It was later found that the mutation could cause sporadic or familial intracranial cavernous hemangioma (cerebral cavernous malformations,CCMs), which is the third pathogenic gene of CCMs, and therefore is also called CCM3.. In recent years, it has been found that PDCD10 can interact with many proteins such as GCK 鈪，

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