Abnormality of ubiquitin ligase controlling a TGF -βsignal and a study about the mechanism of the carcinoma

转化生长因子-β被认为是一种肿瘤抑制因子，一方面是由于角质层细胞的增殖控制作用，另一方面是细胞外基质的蓄积作用和血管形成的促进作用，对免疫的抑制，荷瘤细胞系具有多种生理活性，并认为我的工作对于控制细胞的增加/分化具有重要意义。泛素连接酶是一种受体和信号传递分子，泛素连接酶对Smad的表达有调控作用，但关于这种β的调控机制还不清楚。本研究认为，它是一种新的指标，可以作为一种新的指标来评价p…通过分析转化生长因子-β信号在多种肿瘤细胞中的异常，在未来的癌症研究中进行更多的基因组分析。迄今为止，在不同的肿瘤组织中，关于转化生长因子-6受体和参与转化生长因子-β信号的Smad基因群的表达分析已经完成了许多报道。我们关注了转化生长因子-β信号通路中产生Smad泛素的Hect型E3连接酶S-MURF1和S-MURF1，并通过寻找其在肿瘤中的表达来检验其与临床病理背景因素的相关性。SMurf2能分解Hect型E3泛素连接酶SMurf1和活性形式转化生长因子-β特异性模型Smad2，参与BM的分解？特殊的模型Smadl/5在原子核中移动，并与Smad7相连。两者的复合体由于CRM1依赖而移至胞外，并已了解到我与转化生长因子-βI型受体连接，抑制信号传递。基于到目前为止提供的分析结果，我制定了一个等于或小于它的计划，因为我能够得到一个恒定的分析结果，所以我研究了一个实验，而不是仍然搜索到这些SMurf1和SMurf2中的癌症组织中的表达，因为我能够得到持续的分析结果。较少

TGF - β is known as a tumor suppressor factor because of a cuticle cell does the proliferation control On the other hand, a cumulative action and the vascularization promotion action of the matrix out of cell, restraint for the immunity, charge cell line have various physiology activity, and that I work important for control of an increase / the differentiation of the cell is clarified. And it develops in the cancer of much Homo sapiens excessively and promotes a vascularization, and it is suggested as the factor which promotes permeation and the fibrosis of the cancer cell by letting you aggravate the destruction of the basement membrane, cell outside matrix accumulation, control and migration ability of the cell adhesion.Expression control of ubiquitin ligase dismantling Smad which is a receptor and a signal transmission molecule is suggested, but, about control adjustment of this TGF-β, the mechanism is not clarified.In this study, it is thought that it is it to a new index of the p … More roteome analysis in the future cancer research by analyzing the TGF-β signal abnormality in various cancer cells.In various cancer organizations, many reports are accomplished about expression analysis of the TGF-6 receptor and Smad gene group participating in a TGF-β signal till now. We paid our attention to Smurf1 and Smurf1 which were the HECT type E3 ligase which made Smad ubiquitin this time in TGF-β signal courses and examined correlation with the background factor of the clinical pathology by searching the expression in the cancer. Smurf2 to resolve HECT type E3 ubiquitin ligase Smurfl and active form TGF-β peculiar model Smad2 participating in the resolution of BM? peculiar model Smadl/5 into shifts in a nucleus and is connected with Smad7. The complex of both shifts to the nucleus outside for CRM1 dependence and has already understood that I am connected with a TGF-βI type acceptor and restrain signal transmission. I make a plan to be equal to or less than it based on the analysis result that was provided so far how expression in the cancer organization contributes to cancer biologically and study an experiment without it being still searched about the expression in the cancer organization in these Smurfl and Smurf2 enough and report it because I was able to get a constant analysis result. Less