| Project/Area Number |
17390488
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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 |
Morphological basic dentistry
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| Research Institution | Nihon University |
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Principal Investigator |
HANAZAWA Shigemasa Nihon University, College of Bioresource Science, Professor, 生物資源科学部, 教授 (60060258)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAGUCHI Noboru Kyushu University, Faculty of Dental Science, Assiistant, 大学院・歯学研究院, 助手 (00230368)
MASUHIRO Yoshikazu Nihon University, Advanced Research Institute for Sciences and Humanities (ARISH), Lecture, 大学院・総合科学研究科, 講師 (00336083)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥15,100,000 (Direct Cost: ¥15,100,000)
Fiscal Year 2006: ¥7,300,000 (Direct Cost: ¥7,300,000)
Fiscal Year 2005: ¥7,800,000 (Direct Cost: ¥7,800,000)
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| Keywords | TLR / SOCS / Regulatory molecule / Interacting protein / Regulatory mechanisms |
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| Research Abstract |
We screened proteins that interact with human suppressor of cytokine signalin-3(hSOCS-3) from a human testis cDNA library, using yeast-two hybrid system. And we found that DP-1, an important regulatory factor during cell cycling, is detected as a its interacting protein with high ratio. A recent study has suggested that Toll-like receptor (TLR) 4 signaling is able to stimulate cell proliferation of human fibroblasts. This study proposed to us a possible mechanism that DP-1 acts as a regulatory factor of TLR -mediated stimulation of the cell proliferation. Thus, in this study, we investigated with detail a molecular mechanism between hSOCS-3 and DP-1 and also explored a novel regulatory action of SOCS-3 in TLR 4 signaling system. And we observed N terminal 156-172 region of hSOCS-3 is a domain that is able to interact with DP-1. This defected mutant of hSOCS-3 was not able to inhibit cycline E-dependent transcriptional activity in HEK 293 cells. Our cytoflow analysis exhibited that wild hSOCS-3 significantly retarded DP-1-mediated cell cycle and proliferation of HEK 292 cells. However, such retardation was not observed in the cells transfected with defected mutant of hSOCS-3. These results demonstrated that hSOCS-3 is an important regulatory molecule in DP-1-dependent cell cycling system and also proposed to us a possibility that h-SOCS-3 may act as a potent regulator of TLR-mediated cell proliferation via DP-1.
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