The analysis of OS-4 like gene and homeo protein like gene as a putative choriocarcinoma suppressor gene.

为了分离可能的绒毛膜癌抑制基因，我们使用了1)定位克隆和2)消减技术。最初被认为是7q11.22的缺失位点与新报道的序列草案中公布的7q11.21相比，被认为是7q11.21。OS-4基因最初被认为是一个更重要的候选基因，但并未包括在该序列草案中。我们优先选择草案序列中包含ARRAY的6-8个克隆，并对其进行分析。在绒毛膜癌7q11.21共同缺失区的10种基因中，有6-8个克隆以草稿序列的形式出现在阵列中。这是人畸胎癌指(HTF)12基因中具有KRAB结构域和锌指结构域的基因。将HTF12基因与全长载体连接，导入绒毛膜癌细胞株。诱导后细胞变大，细胞团培养质量变差。细胞合成能力变化不大。细胞融合…更多的是从诱导细胞开始的。伴随着细胞变得巨大而恶化。三种剪接变异体产生的启动子不同。在两种诱导条件下，细胞增殖均受到抑制。这次用于诱导的是HTF12-2。根据正常胎盘绒毛组织中HTF12-1锌指结构域数目的不同而各有不同。据此推测，Krav结构域在5‘端参与了细胞融合、增殖抑制。我们了解到在同源性分析中有很多相似的基因。特别是在19号染色体上的家族性葡萄胎的连锁分析中提供的关注区域与现有的ZF1基因具有较近的同源性和80%的同源性。ZF1基因在胎盘和绒毛膜癌中均有表达，两者的差异引起了人们的注意。我认为这与导致细胞恶化的基因有关，我认为我参与了绒毛滋养层细胞的合法化。当绒毛细胞滋养层细胞成为融合的合胞体细胞时，HPL、CSH等标记物表达，而类似的标记物表达是免疫组织化学方法，并得到证实，并估算了与合并化作用机制相同的产物。这个NECC1基因只在老鼠发病时所需的同源盒基因上理解，这与HOP相同。在胎盘取回不被认为是它。较少

For the isolation of the putative choriocarcinoma suppressor gene, we used 1) positional cloning and 2) subtraction technique. The delection site that it was regarded as 7q11.22 at first understood that it was 7q11.21 by comparison with bulletin of newly reported draft sequence. OS-4 gene regarded as a candidate important more at first was not included in this draft sequence. We gave priority to the 6-8 clone that draft sequence included array and analyzed it. Among ten kinds of gene which there is in common deletion region of 7q11.21 of choriocarcinoma, 6-8 clone is included in array given a presentation in draft sequence. This was gene having KRAB domain and Zn finger domain in human teratocarcinoma finger (HTF) 12 gene. HTF12 gene was conjugated by in full length vector plasmid and was introduced into choriocarcinoma cell strain. By induction, becoming gigantic of cell occurred, and cell mass culturing deteriorated. The syndesis ability of cell did not change very much. Cell fusion … More begins in induction cell. It was accompanied with deterioration with becoming gigantic of cell. Three kinds of splicing variants produced by a difference of promotor. By both induction, cell propagation was restrained. It was HTF12-2 that used for induction this time. It was each a thing on the basis of a difference of number of domain of Zn finger domain in HTF12-1 that appeared in normal placental villus. On this account it was estimated that the KRAV domain which there was in 5' site participated in cell fusion, propagation inhibition. We understood that there was a lot of similar gene in homology analysis. In particular concern area provided in linkage analysis of familial hydatidiform mole on the chromosome 19 has near by existing ZF1 gene and homology of 80%. The gene expression of ZF1 is recognized both in placenta and choriocarcinoma, and a difference of the work attracts attention.NECC1 provided by subtraction technique was gene provided than human gingival cDNA library. It was thought with the gene which contributed to deterioration of cell, and I thought that I participated in the legalization of villous trophoblast cell. When villous cytotrophoblast cell became the syncytium cell which fused, marker such as HPL, CSH expressed, but it was immunohistochmestrical that marker of similar expressed, and it was proved, and what I produced in mechanism same as syncitionization was estimated. This NECC1 understood gene only for homeobox needed in case of incidence of mouse, a thing same as HOP. Retrieval in placenta is not considered to be it. Less