2007 Fiscal Year Final Research Report Summary
Abnormality of ubiquitin ligase controlling a TGF -βsignal and a study about the mechanism of the carcinoma
| Project/Area Number |
17390354
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
TAKENOSHITA Seiichi Fukushima Medical University, Medicine, Department of surgeryII, Professor (10167489)
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| Co-Investigator(Kenkyū-buntansha) |
MANABU Iwadate Fukushima Medical University, Medicine, Department of surgeryII, Post doctoral fellow (00381393)
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| Project Period (FY) |
2005 – 2007
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| Keywords | TGF-β / ubigitin ligase / VEGF / Smurf1 / Smurf2 |
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| Research Abstract |
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
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