Analysis of SOCS/CSI family in skin
Analysis of SOCS/CSI family in skin
批准号:
13470173
负责人:
HASHIMOTO Koji
金额:
$9.47万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B)
财政年份:
2001
资助国家:
日本
项目状态:
已结题
起止时间:
2001 至 2002
中文摘要
细胞因子信号传导抑制因子(SOCS)/含丝氨酸诱导型SH 2(CIS)蛋白是丝氨酸诱导型的,并且是STAT信号传导途径的负调节因子。我们研究了细胞因子的主要靶细胞之一角质形成细胞中STATs和SOCS/CIS家族的调控机制,发现SOCS 1 mRNA在IFNγ作用后3 h上调,IFN γ作用后48 h上调8.1倍。SOCS 3 mRNA也从IFN γ后1 h开始上调,SOCS 3/CIS 3 mRNA在IFN γ后6 - 12 h增加6.7倍。IL-6处理1h后,SOCS 3/CIS 3 mRNA表达增强,而SOCS 1/JAB mRNA表达不受IL-6诱导; IL-4处理1h后,SOCS 1/JAB和CIS 1 mRNA表达分别增加3.4倍和5.1倍。相反,表皮生长因子(EGF)磷酸化STAT 3,不影响SOCS/CIS家族mRNA的表达水平。表达SOCS 1/JAB的腺病毒载体(AxCALNLJAB)的转染完全抑制IFNγ依赖的STAT 1磷酸化和IL-4依赖的STAT 6磷酸化。AxCANNLJAB的转染并不抑制IL-6依赖性STAT 3磷酸化--多份报告显示SOCS 1/JAB是骨髓白血病M1细胞中STAT 3信号传导的有效抑制剂。转染表达SOCS 3/CIS的腺病毒载体(AxCACIS 3)完全抑制IL-6依赖性STAT 3磷酸化,部分抑制IFNγ依赖性STAT 1磷酸化。然而,AxCACIS 3的转染不抑制IL-4依赖性STAT 6磷酸化。表达CIS 1的腺病毒载体(AxCALNLCIS 1)的转染对正常角质形成细胞中的STAT 1、STAT 3和STAT 6信号传导没有影响。因此,STAT和SOCS之间的关系在角质形成细胞中是独特的,并且SOCS调节这些细胞中的细胞因子信号。
英文摘要
The suppressor of cytokine signaling (SOCS)/cytokine-inducible SH2 containing (CIS) proteins are cytokine-inducible and are negative regulators of the STAT signaling pathway. We investigated the mechanism regulating STATs and the SOCS/CIS family in keratinocytes, one of the major target cells for cytokines.SOCS1 mRNA was upregulated 3 h post- interferon γ(IFNγ), and a 8.1-fold increase in SOCS1 mRNA occurred 48 h post-IFNγ. SOCS3 mRNA was also upregulated from 1 h post-IFNγ, and a 6.7-fold increase in SOCS3/CIS3 mRNA occurred between 6 and 12 h post-INFγ. Interleukin-6 (IL-6) exposure for 1 h enhanced the expression of SOCS3/CIS3 mRNA, but SOCS1/JAB mRNA was not induced by IL-6, IL-4 upregulated SOCS1/JAB and CIS1 mRNA, with 3.4-and 5.1-fold increases in mRNA observed at 1 h post-IL-4, respectively. In contrast, epidermal growth factor(EGF), which phosphorylates STAT3, did not influence the level of SOCS/CIS family mRNA expression.Transfection of an adenovirus vector expressing SOCS1/JAB(AxCALNLJAB)completely inhibited IFNγ-dependent STAT1 phosphorylation and IL-4-dependent STAT6 phosphorylation. Transfection of AxCALNLJAB did not inhibit IL-6-dependent STAT3 phosphorylation-several reports show SOCS1/JAB is a potent inhibitor of STAT3 signaling in the myeloid leukemia Ml cell. Transfection of the adenovirus vector expressing SOCS3/CIS(AxCACIS3)completely inhibited IL-6-dependent STAT3 phosphorylation and partially inhibited IFNγ-dependent STAT1 phosphorylation. However, transfection of AxCACIS3 did not inhibit IL-4-dependent STAT6 phosphorylation. Transfection of the adenovirus vector expressing CIS1(AxCALNLCISl)had no effect on STAT1, STAT3, and STAT6 signaling in normal keratinocytes. Therefore, the relationship between STAT and SOCS is unique in the keratinocytes, and SOCS regulates cytokine signals in these cells.
期刊论文(46)
专著(0)
科研奖励(0)
会议论文
登录
查看更多内容
白方裕司, 橋本公二 等: "表皮細胞とシグナル伝達"現代医療. Vol.34. 1815-1822 (2002)
Yuji Shirakata、Koji Hashimoto 等:“表皮细胞和信号转导”现代医学第 34 卷(2002 年)。
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
Shouda T, Yoshida T, Hanada T, Wakioka T, Oishi M, Miyoshi K, Komiya S, Kosai K, Hanakawa Y, Hashimoto K, Nagata K, Yoshimura A: "Induction of the cytokine signal regulator SOC3/CIS3 as a therapeutic strategy for treating inflammatory arthritis"J Clin Inv
Shouda T、Yoshida T、Hanada T、Wakioka T、Oishi M、Miyoshi K、Komiya S、Kosai K、Hanakawa Y、Hashimoto K、Nagata K、Yoshimura A:“诱导细胞因子信号调节剂 SOC3/CIS3 作为治疗策略
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
Yamasaki K, Hashimoto K. et al.: "Keratinocyte growth inhibition by high-dose epidermal growth factor is mediated by transforming growth factor β autoinduction"J Invest Dermatol. Vol.120(In press). (2003)
Yamasaki K、Hashimoto K. 等人:“高剂量表皮生长因子对角质细胞生长的抑制是由转化生长因子 β 自诱导介导的”J Invest Dermatol 第 120 卷(出版中)。
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
Sayama K., Hashimoto K.et al.: "Phosphatidyl inositol 3 kinase is a key regulator of early phase differentiation in keratinocytes"J Biol Chem. Vol.277. 40390-40396 (2002)
Sayama K.、Hashimoto K.等人:“磷脂酰肌醇 3 激酶是角质形成细胞早期分化的关键调节因子”J Biol Chem。
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
Sayama K, Hashimoto K. et al.: "Phosphatidyl inositol 3 kinase is a key regulator of early phase differentiation in keratinocytes"J Biol Chem. Vol.277. 40390-40396 (2002)
Sayama K、Hashimoto K. 等人:“磷脂酰肌醇 3 激酶是角质形成细胞早期分化的关键调节因子”J Biol Chem。
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
共 22 条
Development of cerebral infarction regenerative treatment by neural stem cell transplant targeting microRNA
-
批准号:16K10715
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$3.0万
-
财政年份:2016
-
负责人:HASHIMOTO Koji
-
依托单位:
The role of a novel platelet activated receptor CLEC-2 in the carotid plaque
-
批准号:25861265
-
项目类别:Grant-in-Aid for Young Scientists (B)
-
资助金额:$2.5万
-
财政年份:2013
-
负责人:HASHIMOTO Koji
-
依托单位:
Construction of new description of atomic nuclei using superstring theory
-
批准号:23654096
-
项目类别:Grant-in-Aid for Challenging Exploratory Research
-
资助金额:$2.25万
-
财政年份:2011
-
负责人:HASHIMOTO Koji
-
依托单位:
Application of superstring theory to nuclear and quark physics
-
批准号:22340069
-
项目类别:Grant-in-Aid for Scientific Research (B)
-
资助金额:$11.9万
-
财政年份:2010
-
负责人:HASHIMOTO Koji
-
依托单位:
Role of signal transduction pathway of Bcl-3 and IkBNA in the pathogenesis of psoriasis
-
批准号:21390325
-
项目类别:Grant-in-Aid for Scientific Research (B)
-
资助金额:$11.48万
-
财政年份:2009
-
负责人:HASHIMOTO Koji
-
依托单位:
Research and development for basic technology of multipoint bidirectional relay system adapted to users' communication environments
-
批准号:21700085
-
项目类别:Grant-in-Aid for Young Scientists (B)
-
资助金额:$2.66万
-
财政年份:2009
-
负责人:HASHIMOTO Koji
-
依托单位:
Study of D-branes (non-perturbative effects in superstring theory) and solitons in field theories
-
批准号:19740125
-
项目类别:Grant-in-Aid for Young Scientists (B)
-
资助金额:$1.97万
-
财政年份:2007
-
负责人:HASHIMOTO Koji
-
依托单位:
Research of the fimction of SOCS3 in the pathogenesis ofpscriasis using keratinocyte specific SOCS3 knozkout mice
-
批准号:18390314
-
项目类别:Grant-in-Aid for Scientific Research (B)
-
资助金额:$11.14万
-
财政年份:2006
-
负责人:HASHIMOTO Koji
-
依托单位:
Regulation of skin innate immunity by epidermal differentiation
-
批准号:15209035
-
项目类别:Grant-in-Aid for Scientific Research (A)
-
资助金额:$31.45万
-
财政年份:2003
-
负责人:HASHIMOTO Koji
-
依托单位:
Research on inhibitors for autocrine and cross-induction mechanism in human keratinocytes
-
批准号:13557071
-
项目类别:Grant-in-Aid for Scientific Research (B)
-
资助金额:$7.87万
-
财政年份:2001
-
负责人:HASHIMOTO Koji
-
依托单位:
Nation wide survey of dental radiographic examination in Japan
-
批准号:13671984
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$0.96万
-
财政年份:2001
-
负责人:HASHIMOTO Koji
-
依托单位:
EPIDERMAL STEM CELL AND ITS CLINICAL APPLICATION
-
批准号:08407021
-
项目类别:Grant-in-Aid for Scientific Research (A)
-
资助金额:$5.25万
-
财政年份:1996
-
负责人:HASHIMOTO Koji
-
依托单位:
Tailoring of new amorphous alloy catalysts for conservation of atmosphere
-
批准号:07405032
-
项目类别:Grant-in-Aid for Scientific Research (A)
-
资助金额:$24.64万
-
财政年份:1995
-
负责人:HASHIMOTO Koji
-
依托单位:
A STUDY ON REGULATORY MECHANISM OF GROWTH AND DIFFERENTIATION IN HUMAN KERATINOCYTES BY GROWTH FACTORS.
-
批准号:06670863
-
项目类别:Grant-in-Aid for General Scientific Research (C)
-
资助金额:$1.28万
-
财政年份:1994
-
负责人:HASHIMOTO Koji
-
依托单位:
HOT SULFIDATION-AND OXIDATION-RESISTANT NEW ALLOYS
-
批准号:05044075
-
项目类别:Grant-in-Aid for international Scientific Research
-
资助金额:$3.2万
-
财政年份:1993
-
负责人:HASHIMOTO Koji
-
依托单位:
Tairoring Amorphous Surface Alloys Resistant against High Temperature Corrosion
-
批准号:05555187
-
项目类别:Grant-in-Aid for Developmental Scientific Research (B)
-
资助金额:$11.07万
-
财政年份:1993
-
负责人:HASHIMOTO Koji
-
依托单位:
ANALYSIS OF REGULATORY MECHANISM OF VIATAMIN D IN THE GROWTH AND DIFFERENTIATION OF EPIDERMAL KERATINOCYTES
-
批准号:04670641
-
项目类别:Grant-in-Aid for General Scientific Research (C)
-
资助金额:$1.34万
-
财政年份:1992
-
负责人:HASHIMOTO Koji
-
依托单位:
IN-SITU CHARACTERIZATION OF SURFACES ON NEW ELECTRODE FOR FUEL CELLS AND ELECTROLYSIS
-
批准号:03403012
-
项目类别:Grant-in-Aid for General Scientific Research (A)
-
资助金额:$17.41万
-
财政年份:1991
-
负责人:HASHIMOTO Koji
-
依托单位:
Preparation of Corrosion-Resistant Amorphous Surface Alloys
-
批准号:61850127
-
项目类别:Grant-in-Aid for Developmental Scientific Research
-
资助金额:$8.64万
-
财政年份:1986
-
负责人:HASHIMOTO Koji
-
依托单位:
国内基金
海外基金
登录
查看更多内容
去泛素化酶USP13稳定SOCS5调节自噬促进胶质母细胞瘤中的替莫唑胺耐药的机制研究
-
批准号:2026JJ80018
-
项目类别:省市级项目
-
资助金额:--
-
批准年份:2026
-
负责人:胡林旺
-
依托单位:
乌司他丁靶向抑制HDAC1通过SOCS1/JAK2/STAT3 轴调控小胶质细胞极化来减轻局灶性脑缺血再灌注损伤的机制研究
-
批准号:2026JJ81821
-
项目类别:省市级项目
-
资助金额:--
-
批准年份:2026
-
负责人:陈晓曦
-
依托单位:
去泛素化酶USP13通过调控SOCS1表达抑制小胶质细胞M1极化促进脑血管新生改善脑缺血再灌注损伤
-
批准号:2026JJ81103
-
项目类别:省市级项目
-
资助金额:--
-
批准年份:2026
-
负责人:王京微
-
依托单位:
SOCS1调控RORγt/Foxp3信号轴激活Th17细胞免疫诱导过敏性紫癜的作用及机制研究
-
批准号:
-
项目类别:省市级项目
-
资助金额:--
-
批准年份:2025
-
负责人:卢琴红
-
依托单位:
IFN- α 通过SOCS3/JAK2/STAT5通路调控
H3N2流感病毒引起的鼻黏膜嗜酸性粒细
胞浸润性炎症的分子机制研究
-
批准号:
-
项目类别:省市级项目
-
资助金额:10.0万元
-
批准年份:2025
-
负责人:洪海裕
-
依托单位:
急性胰腺炎 SOCS3/NF-κB 炎症轴机制解析与膈下逐瘀汤多模态调控策略研究
-
批准号:
-
项目类别:省市级项目
-
资助金额:--
-
批准年份:2025
-
负责人:韩俊刚
-
依托单位:
参附方靶向SOCS3/JAK2相互作用调控JAK2/STAT3通路改善肝缺血再灌注损伤的物质基础与作用机理研究
-
批准号:JCZRLH202500794
-
项目类别:省市级项目
-
资助金额:--
-
批准年份:2025
-
负责人:
-
依托单位:
SOCS3-HK3-葡萄糖代谢通路调控SOX9基因去甲基化介导椎间盘退变的机制研究
-
批准号:JCZRYB202500272
-
项目类别:省市级项目
-
资助金额:--
-
批准年份:2025
-
负责人:
-
依托单位:
Kallistatin协同IL-7激活SOCS家族信号
通路趋化难治性鼻窦炎Th2型炎症发生机
制的探索
-
批准号:
-
项目类别:省市级项目
-
资助金额:10.0万元
-
批准年份:2025
-
负责人:赖银妍
-
依托单位:
温针灸通过SOCS3负反馈调节JAK1/STAT3信号通路影响CAG小鼠胃黏膜炎症微环境的机制研究
-
批准号:2025JJ70548
-
项目类别:省市级项目
-
资助金额:--
-
批准年份:2025
-
负责人:冯芳
-
依托单位: