Ohta Satoshi 太田聡

… Alternative Names

太田聡オオタサトシ

OHTA Satoshi 太田聡

Less

Researcher Number	40528428
Other IDs
External Links
Affiliation (Current)	2025: 自治医科大学, 医学部, 講師
Affiliation (based on the past Project Information) *help	2022 – 2023: 自治医科大学, 医学部, 講師 2016 – 2019: 自治医科大学, 医学部, 講師 2014 – 2015: 自治医科大学, 医学部, 助教 2009: 自治医科大学, 医学部, 助教
Review Section/Research Field	Principal Investigator Basic Section 48040:Medical biochemistry-related / General medical chemistry Except Principal Investigator General medical chemistry / Pathological medical chemistry
Keywords	Principal Investigator がん / がんの悪性化 / IL-33 / Ras / ARHGAP18 / がん悪性化 / 細胞遊走 / STK38 / MerTK / シグナル伝達 / Merチロシンキナーゼ / 発がんシグナル / Mer … More Except Principal Investigator … More シグナル伝達 / CD14 / IL-33 / MD2 / TLR4 / 炎症反応 / 細胞形質転換 / LPS受容体 / 細胞がん化 / LPS / ST2 / 免疫学 / 糖鎖 / タンパク質 / アレルギー・ぜんそく / 抗炎症作用 / 糖鎖修飾 / ST2遺伝子 Less

Ras変異体が誘導する新規細胞遊走シグナルの分子基盤とがん悪性化への影響の解明Principal Investigator
- Principal Investigator
  
  太田聡
- Project Period (FY)
  2022 – 2024
- Research Category
  
  Grant-in-Aid for Scientific Research (C)
- Review Section
  
  Basic Section 48040:Medical biochemistry-related
- Research Institution
  Jichi Medical University
The novel oncogenic signal with tyrosine phosphorylation induced by RasPrincipal Investigator
- Principal Investigator
  
  Ohta Satoshi
- Project Period (FY)
  2017 – 2019
- Research Category
  
  Grant-in-Aid for Scientific Research (C)
- Research Field
  
  General medical chemistry
- Research Institution
  Jichi Medical University
Investigation on inhibitory mechanism of soluble ST2 protein (secreted IL-33 receptor) against LPS signal
- Principal Investigator
  
  Yanagisawa Ken
- Project Period (FY)
  2014 – 2016
- Research Category
  
  Grant-in-Aid for Scientific Research (C)
- Research Field
  
  General medical chemistry
- Research Institution
  Jichi Medical University
Identification of functional regions the soluble ST2 protein against inflammation, and its possible application for novel drugs.
- Principal Investigator
  
  TOMINAGA Shinichi
- Project Period (FY)
  2007 – 2009
- Research Category
  
  Grant-in-Aid for Scientific Research (C)
- Research Field
  
  Pathological medical chemistry
- Research Institution
  Jichi Medical University

All 2023 2022 2019 2018 2017 2016 2015 2009 Other

All Journal Article Presentation Other

[Journal Article] Oncogenic Ras mutant causes thehyper-activation of NF-kB via acceleration of its transcriptional activation.2019
- Author(s)
  (10)Tago K, Funakoshi-Tago M, Ohta S, Kawata H, Saitoh H, Horie H, Aoki-Ohmura C, Yamauchi J, Tanaka A, Matsugi J, Yanagisawa K.
- Journal Title
  
  Mol Oncol.
  
  Volume: 13(11) Pages: 2493-2510
- Peer Reviewed / Open Access
- Data Source
  KAKENHI-PROJECT-17K08641
[Journal Article] STAT3 and ERK pathways are involved in cell growth stimulation of the ST2/IL1RL1 promoter2017
- Author(s)
  Tago K, Ohta S, Funakoshi-Tago M, Aoki-Ohmura C, Matsugi J, Tominaga SI, Yanagisawa K
- Journal Title
  
  FEBS Open Bio
  
  Volume: 7(2) Issue: 2 Pages: 293-302
- DOI
  10.1002/2211-5463.12192
- Peer Reviewed / Acknowledgement Compliant / Open Access / Int'l Joint Research
- Data Source
  KAKENHI-PROJECT-26440062, KAKENHI-PROJECT-26460376, KAKENHI-PROJECT-17K07343, KAKENHI-PROJECT-17K08286
[Journal Article] ST2 gene products critically contribute to cellular transformation caused by an oncogenic Ras mutant2017
- Author(s)
  Tago Kenji、Ohta Satoshi、Kashiwada Masaki、Funakoshi-Tago Megumi、Matsugi Jitsuhiro、Tominaga Shin-ichi、Yanagisawa Ken
- Journal Title
  
  Heliyon
  
  Volume: 3 Issue: 10 Pages: e00436-e00436
- DOI
  10.1016/j.heliyon.2017.e00436
- Peer Reviewed / Open Access
- Data Source
  KAKENHI-PROJECT-17K07343, KAKENHI-PROJECT-17K08286, KAKENHI-PROJECT-17K08641
[Journal Article] Intracellular NF-HEV/IL-33 harbors essential roles in Ras-induced cellular transformation by contributing to cyclin D1 protein synthesis.2016
- Author(s)
  S. Ohta, K. Tago, M. Funakoshi-Tago, J. Matsugi, K. Yanagisawa
- Journal Title
  
  Cellular Signalling
  
  Volume: 0 Issue: 8 Pages: 0-0
- DOI
  10.1016/j.cellsig.2016.04.013
- Peer Reviewed / Acknowledgement Compliant / Int'l Joint Research
- Data Source
  KAKENHI-PROJECT-26460376, KAKENHI-PROJECT-26440062
[Presentation] Ras変異体が誘導する新規チロシンリン酸化シグナルにおけるSTK38/NDR1の役割2023
- Author(s)
  太田聡、多胡憲治、笠嶋克己、柳澤健、冨永薫
- Organizer
  第46回日本分子生物学会年会
- Data Source
  KAKENHI-PROJECT-22K06903
[Presentation] Ras変異体が誘導する細胞遊走シグナルにおけるSTK38/NDR1の役割2022
- Author(s)
  太田聡、多胡憲治、松儀実広、柳澤健、冨永薫
- Organizer
  第45回日本分子生物学会
- Data Source
  KAKENHI-PROJECT-22K06903
[Presentation] ST2Lの新規結合タンパク質IFITM3はST2Lのリソソーム分解を介してIL-33シグナルを制御する2019
- Author(s)
  多胡憲治、多胡めぐみ、太田聡、大村千尋、松儀実広、富永眞一、柳澤健
- Organizer
  第92回日本生化学会大会
- Data Source
  KAKENHI-PROJECT-17K08641
[Presentation] 細胞遊走を亢進する新規RasシグナルRas/IL-33/MerTK経路の解析2019
- Author(s)
  太田聡、多胡憲治、松儀実広、柳澤健
- Organizer
  第42回分子生物学会
- Data Source
  KAKENHI-PROJECT-17K08641
[Presentation] 神経線維腫症 I型由来細胞において Rasと ARFの機能的相互作用は miR-222-3pの発現を介して p27Kip1の発現を制御する2019
- Author(s)
  多胡憲治、多胡めぐみ、藤原研、小宮根真弓、太田聡、大村千尋、齊藤博司、大多和宏季、松儀実広、大槻マミ太郎、大野伸彦、山内淳司、柳澤健
- Organizer
  第42回分子生物学会
- Data Source
  KAKENHI-PROJECT-17K08641
[Presentation] 新規K-Ras変異体は独特なシグナル伝達系を介して細胞のがん化を誘導する2018
- Author(s)
  多胡憲治、多胡めぐみ、太田聡、大村千尋、松儀実広、柳澤健
- Organizer
  第41回日本分子生物学会年会（横浜）
- Data Source
  KAKENHI-PROJECT-17K08641
[Presentation] 受容体型チロシンキナーゼMer(MerTK)のがん化型Ras変異体が誘導する発がんシグナルにおける役割2018
- Author(s)
  太田聡、多胡憲治、松儀実広、柳澤健
- Organizer
  第41回日本分子生物学会年会（横浜）
- Data Source
  KAKENHI-PROJECT-17K08641
[Presentation] Ras変異体が誘導する発がんシグナルにおける受容体型チロシンキナーゼMer(MerTK)の機能解析2017
- Author(s)
  太田聡、多胡憲治、松儀実広、柳澤健
- Organizer
  第90回日本生化学会大会・第40回日本分子生物学会年会（神戸）
- Data Source
  KAKENHI-PROJECT-17K08641
[Presentation] K-Ras遺伝子の新しい突然変異は発がん活性を示す2017
- Author(s)
  多胡憲治、多胡めぐみ、太田聡、松儀実広、柳澤健
- Organizer
  第90回日本生化学会大会・第40回日本分子生物学会年会（神戸）
- Data Source
  KAKENHI-PROJECT-17K08641
[Presentation] IL-33前駆体は、がん化型Ras変異体が誘導する形質転換とサイクリンD1タンパク質合成に必須の役割を担う2015
- Author(s)
  太田　聡、多胡　憲治、多胡　めぐみ、松儀　実広、柳澤　健
- Organizer
  第38回日本分子生物学会年会　第88回日本生化学会大会　合同大会
- Place of Presentation
  神戸
- Year and Date
  2015-12-01
- Data Source
  KAKENHI-PROJECT-26460376
[Presentation] 新規IL-33シグナル調節蛋白質IFITM3の同定2015
- Author(s)
  多胡　憲治、多胡　めぐみ、太田　聡、松儀　実広、柳澤　健
- Organizer
  第38回日本分子生物学会年会　第88回日本生化学会大会　合同大会
- Place of Presentation
  神戸
- Year and Date
  2015-12-03
- Data Source
  KAKENHI-PROJECT-26460376
[Presentation] IL-33 induces inflammatory reaction in endothelial cells, and its receptor, ST2L is expressed in growth-dependent manner. (IL-33は内皮細胞に炎症反応を惹起し, その受容体のST2Lは増殖依存性に内皮細胞に発現する. )2009
- Author(s)
  柳澤健, 太田聡, 松儀実広, 富永眞一
- Organizer
  第32回日本分子生物学会年会
- Place of Presentation
  横浜
- Year and Date
  2009-12-12
- Data Source
  KAKENHI-PROJECT-19590318
[]

1. YANAGISAWA Ken (50182366)

# of Collaborated Projects: 2 results

# of Collaborated Products: 4 results
2. TOMINAGA Shinichi (70155571)

# of Collaborated Projects: 1 results

# of Collaborated Products: 1 results
3. TAKEZAKO Naoki (80424026)

# of Collaborated Projects: 1 results

# of Collaborated Products: 0 results
4. 多胡憲治 (20306111)

# of Collaborated Projects: 1 results

# of Collaborated Products: 5 results

Ohta Satoshi 太田 聡

太田 聡 オオタ サトシ

OHTA Satoshi 太田 聡

Research Projects

Research Products

Co-Researchers

Ras変異体が誘導する新規細胞遊走シグナルの分子基盤とがん悪性化への影響の解明Principal Investigator

Principal Investigator

Project Period (FY)

Research Category

Review Section

Research Institution

The novel oncogenic signal with tyrosine phosphorylation induced by RasPrincipal Investigator

Principal Investigator

Project Period (FY)

Research Category

Research Field

Research Institution

Investigation on inhibitory mechanism of soluble ST2 protein (secreted IL-33 receptor) against LPS signal

Principal Investigator

Project Period (FY)

Research Category

Research Field

Research Institution

Identification of functional regions the soluble ST2 protein against inflammation, and its possible application for novel drugs.

Principal Investigator

Project Period (FY)

Research Category

Research Field

Research Institution

[Journal Article] Oncogenic Ras mutant causes thehyper-activation of NF-kB via acceleration of its transcriptional activation.2019

Author(s)

Journal Title

Data Source

[Journal Article] STAT3 and ERK pathways are involved in cell growth stimulation of the ST2/IL1RL1 promoter2017

Author(s)

Journal Title

DOI

Data Source

[Journal Article] ST2 gene products critically contribute to cellular transformation caused by an oncogenic Ras mutant2017

Author(s)

Journal Title

DOI

Data Source

[Journal Article] Intracellular NF-HEV/IL-33 harbors essential roles in Ras-induced cellular transformation by contributing to cyclin D1 protein synthesis.2016

Author(s)

Journal Title

DOI

Data Source

[Presentation] Ras変異体が誘導する新規チロシンリン酸化シグナルにおけるSTK38/NDR1の役割2023

Author(s)

Organizer

Data Source

[Presentation] Ras変異体が誘導する細胞遊走シグナルにおけるSTK38/NDR1の役割2022

Author(s)

Organizer

Data Source

[Presentation] ST2Lの新規結合タンパク質IFITM3はST2Lのリソソーム分解を介してIL-33シグナルを制御する2019

Author(s)

Organizer

Data Source

[Presentation] 細胞遊走を亢進する新規RasシグナルRas/IL-33/MerTK経路の解析2019

Author(s)

Organizer

Data Source

[Presentation] 神経線維腫症 I型由来細胞において Rasと ARFの機能的相互作用は miR-222-3pの発現を介 して p27Kip1の発現を制御する2019

Author(s)

Organizer

Data Source

[Presentation] 新規K-Ras変異体は独特なシグナル伝達系を介して細胞のがん化を誘導する2018

Author(s)

Organizer

Data Source

[Presentation] 受容体型チロシンキナーゼMer(MerTK)のがん化型Ras変異体が誘導する発がんシグナルにおける役割2018

Author(s)

Organizer

Data Source

[Presentation] Ras変異体が誘導する発がんシグナルにおける受容体型チロシンキナーゼMer(MerTK)の機能解析2017

Author(s)

Organizer

Ohta Satoshi 太田聡

太田聡オオタサトシ

OHTA Satoshi 太田聡

[Presentation] 神経線維腫症 I型由来細胞において Rasと ARFの機能的相互作用は miR-222-3pの発現を介して p27Kip1の発現を制御する2019