检索结果-南通市图书馆

NF-κB Signaling Pathway, Inflammation and Colorectal Cancer

Cellular & Molecular Immunology 2009年第5期6卷 327-334页

作者： Soly Wang Zhanjie Liu Lunshan Wang xiaoren zhang Key Laboratory of Stem Cell Biology Institute of Health Sciences Shanghai Institutes for Biological Sciences Chinese Academy of Sciences/Shanghai Jiao Tong University School of Medicine Shanghai 200025 China Department of Pathology Soochow University School of Medicine Suzhou215123 China Key Laboratory of Stem Cell Biology Laboratory of Immunoregulation and Tolerance Institute of Health Sciences Shanghai Institutes for Biological Sciences Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine Shanghai 200025 China

There is growing evidence for a connection between inflammation and tumor development, and the nuclear factor kappa B （NF-κB）, a proinflammatory transcription factor, is hypothesized to promote tumorigenesis. Although the genetic evidence for the hypothesis has been lacking, recent papers have lent credence to this hypothesis. It has been reported that constitutive NF-κB activation in inflammatory bowel diseases （IBDs） increases risk of colorectal cancer （CRC） in the patients with the number of years of active disease. NF-κB activation might induce cellular transformation, mediate cellular proliferation, prevent the elimination of pre-neoplastic and fully malignant cells by up-regulating the anti-apoptosis proteins. Furthermore, NF-κB may contribute to the progression of CRC by regulating the expression of diverse target genes that are involved in cell proliferation （Cyclin D1）, angiogenesis （VEGF, IL-8, COX2）, and metastasis （MMP9）. These findings implicate NF-κB inhibition as an important therapeutic target in CRC. However, due to lack of knowledge about the specific roles of different NF-r,B subunits in different stage of carcinogenesis, and compounds to block specific subunits of NF-κB family, it will be a long time before the coming of targeting NF-κB in CRC therapy.

关键词： NF-κB inflammation colorectal cancer

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Chitinase-3 like-protein-1 function and its role in diseases

引用

Signal Transduction and Targeted Therapy 2020年第1期5卷 820-839页

作者： Ting Zhao Zhongping Su Yingchang Li xiaoren zhang Qiang You Affiliated Cancer Hospital&Institute Guangzhou Medical UniversityGuangzhouChina Department of Biotherapy Department of GeriatricsSecond Affiliated Hospital of Nanjing Medical UniversityNanjingChina Key Laboratory of Cell Homeostasis and Cancer Research of Guangdong Higher Education Institutes Guangzhou Medical UniversityGuangzhouChina

Non-enzymatic chitinase-3 like-protein-1(CHI3L1)belongs to glycoside hydrolase family 18.It binds to chitin,heparin,and hyaluronic acid,and is regulated by extracellular matrix changes,cytokines,growth factors,drugs,and stress.CHI3L1 is synthesized and secreted by a multitude of cells including macrophages,neutrophils,synoviocytes,chondrocytes,fibroblast-like cells,smooth muscle cells,and tumor cells.It plays a major role in tissue injury,inflammation,tissue repair,and remodeling responses.CHI3L1 has been strongly associated with diseases including asthma,arthritis,sepsis,diabetes,liver fibrosis,and coronary artery disease.Moreover,following its initial identification in the culture supernatant of the MG63 osteosarcoma cell line,CHI3L1 has been shown to be overexpressed in a wealth of both human cancers and animal tumor models.To date,interleukin-13 receptor subunit alpha-2,transmembrane protein 219,galectin-3,chemo-attractant receptor-homologous 2,and CD44 have been identified as CHI3L1 receptors.CHI3L1 signaling plays a critical role in cancer cell growth,proliferation,invasion,metastasis,angiogenesis,activation of tumor-associated macrophages,and Th2 polarization of CD4+T cells.Interestingly,CHI3L1-based targeted therapy has been increasingly applied to the treatment of tumors including glioma and colon cancer as well as rheumatoid arthritis.This review summarizes the potential roles and mechanisms of CHI3L1 in oncogenesis and disease pathogenesis,then posits investigational strategies for targeted therapies.

关键词： diseases invasion drugs

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Reversible acetylation modulates dishevelled-2 puncta formation in canonical Wnt signaling activation

引用

Signal Transduction and Targeted Therapy 2020年第1期5卷 1437-1440页

作者： Jinhong Shen Lin Hu Li Yang Mengshi zhang Weihong Sun Xiaomei Lu Gufa Lin Chao Huang xiaoren zhang Y.Eugene Chin CAS Key Laboratory of Tissue Microenvironment and Tumor Institute of Health SciencesShanghai Jiao Tong University School of Medicine&Shanghai Institutes for Biological SciencesChinese Academy of SciencesUniversity of Chinese Academy of Sciences200031 ShanghaiChina Institutes of Biology and Medical Sciences Soochow University Medical College215000 SuzhouJiangsuChina Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education Orthopaedic Department of Tongji HospitalSchool of Life Sciences and TechnologyTongji University200065 ShanghaiChina Clinical Medical Research Institute First Affiliated Hospital of Xinjiang Medical University830054 UrumuqiXinjiangChina

Dear Editor,Dishevelled-2(DVL2)is a central adaptor protein that propagates signals from upstream receptors to downstream effectorβ-catenin in canonical Wnt signaling.At high local concentration,DVL2 assembles into signalosomes through DIX domain-mediated homo-polymerization to provide a docking platform for the recruitment of signaling components,which is critical for Wnt signaling transduction and activation;1 however,the exact underlying mechanism remains inconclusive.Although the roles of phosphorylation and ubiquitination in DVL2-puncta formation have been discussed before,2 the impact of lysine acetylation of DVL2 on this process remains elusive.Here we investigated the effect of acetylation on DVL2-puncta formation.

关键词： activation canonical upstream

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Elevating H3K27me3 level sensitizes colorectal cancer to oxaliplatin

引用

Journal of Molecular Cell Biology 2020年第2期12卷 125-137页

作者： Qi Wang Xi Chen Yuhang Jiang Sanhong Liu Hanshao Liu Xiaohua Sun Haohao zhang Zhi Liu Yu Tao Cuifeng Li Yiming Hu Dandan Liu Deji Ye Yongzhong Liu Mingliang Wang xiaoren zhang The Key Laboratory of Stem Cell Biology Shanghai Jiao Tong University School of Medicine&Shanghai Institutes for Biological SciencesChinese Academy of SciencesShanghai 200025227 Chongqing South RoadShanghaiChina Affiliated Cancer Hospital&Institute Guangzhou Medical UniversityGuangzhou 510000195 Dongfeng West RoadGuangzhouChina Shanghai Institute for Advanced Immunochemical Studies ShanghaiTech UniversityShanghai 201210393 Huaxia Middle RoadShanghaiChina State Key Laboratory of Oncogenes and Related Genes Shanghai Cancer InstituteRenji HospitalShanghai Jiao Tong University School of MedicineShanghai 200032Ruijin 2nd RoadShanghaiChin Department of General Surgery Ruijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025Ruijin 2nd RoadShanghaiChina

Histone methylation is a context-dependent modification that regulates gene expression,and the trimethylation of histone H3 lysine 27(H3K27me3)usually induces gene silencing.Overcoming colorectal cancer(CRC)chemoresistance is currently a huge challenge,but the relationship between H3K27me3 modification and chemoresistance remains largely unclear.Here,we found that H3K27me3 levels positively correlated with the metastasis-free survival of CRC patients and a low H3K27me3 level predicted a poor outcome upon chemotherapeutic drug treatment.Oxaliplatin stimulation significantly induced the expression of H3K27 lysine demethylase 6A/6B(KDM6A/6B),thus decreasing the level of H3K27me3 in CRC cells.Elevation of H3K27me3 level through KDM6A/6B depletion or GSK-J4(a KDM6A/6B inhibitor)treatment significantly enhanced oxaliplatin-induced apoptosis.Conversely,when inhibiting the expression of H3K27me3 by EPZ-6438,an inhibitor of the histone methyltransferase EZH2,the proportion of apoptotic cells remarkably decreased.In addition,the combination of GSK-J4 and oxaliplatin significantly inhibited tumor growth in an oxaliplatin-resistant patient-derived xenograft model.Importantly,we revealed that oxaliplatin treatment dramatically induced NOTCH2 expression,which was caused by downregulation of H3K27me3 level on the NOTCH2 transcription initiation site.Thus,the activated NOTCH signaling promoted the expression of stemness-related genes,which resulted in oxaliplatin resistance.Furthermore,oxaliplatin-induced NOTCH signaling could be interrupted by GSK-J4 treatment.Collectively,our findings suggest that elevating H3K27me3 level can improve drug sensitivity in CRC patients.

关键词： H3K27 trim ethylation colorectal cancer chem oresistance NOTCH signaling

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

基于全基因组关联分析的肾移植术后糖尿病发病风险预测模型的构建

引用

中华医学杂志 2024年第2期104卷 138-146页

作者：王依娜沈洲姬奚炜炜诸医蒙张孝认仉超裘晓蕙徐鹏杰胡雨韵王江东宁波大学附属李惠利医院肾内科宁波315040 浙江大学医学院附属邵逸夫医院肾内科杭州310018 宁波大学附属李惠利医院检验科宁波315040

目的探索肾移植术后糖尿病(PTDM)的临床危险因素及易感基因,构建PTDM发病风险预测模型。方法回顾性分析2001年1月至2022年12月期间在宁波大学附属李惠利医院和浙江大学医学院附属邵逸夫医院随访的肾移植受者资料,根据术后是否发生PTDM... 详细信息

目的探索肾移植术后糖尿病(PTDM)的临床危险因素及易感基因,构建PTDM发病风险预测模型。方法回顾性分析2001年1月至2022年12月期间在宁波大学附属李惠利医院和浙江大学医学院附属邵逸夫医院随访的肾移植受者资料,根据术后是否发生PTDM将其分为PTDM组和非PTDM组(Non-PTDM组),比较两组临床指标差异,筛选PTDM的危险因素,并通过全基因组关联分析(GWAS)筛选PTDM易感基因。分别建立仅基于临床指标(模型1)和临床指标结合易感基因(模型2)的PTDM发病风险预测模型,比较两种预测模型的预测效能。最后绘制较优模型的列线图,评价模型的校准度、区分度及临床实用性。结果纳入113例肾移植受者,男70例,女43例,年龄(46.2±10.8)岁。PTDM组51例,Non-PTDM组62例。通过GWAS和多因素logistic回归分析筛选出的相关因素包括糖尿病家族史(OR=88.912,95%CI:5.827~1356.601,P=0.001)、术前甘油三酯(OR=1.888,95%CI:1.150~3.098,P=0.012)、血尿酸(OR=1.011,95%CI:1.000~1.022,P=0.045)3个临床指标及rs802707基因位点(OR=10.046,95%CI:1.462~69.042,P=0.019)。模型1预测PTDM发生的受试者工作特征(ROC)曲线下面积(AUC)为0.891(95%CI:0.811~0.972),灵敏度为0.889,特异度为0.742;模型2预测PTDM发生的AUC为0.930(95%CI:0.864~0.995),灵敏度为0.885,特异度为0.900。结论糖尿病家族史、移植前甘油三酯、血尿酸这3个临床指标及rs802707基因位点与PTDM的发生有关联,联合易感基因能提高临床指标对PTDM发病风险的预测能力。

关键词：肾移植移植后糖尿病易感基因危险因素预测模型

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

The histone H3 lysine-27 demethylase Jmjd3 plays a critical role in specific regulation of Th17 cell differentiation

引用

分子细胞生物学报:英文版 2015年第6期7卷 505-516页

作者： Zhi Liu Wei Cao Longxia Xu Xi Chen Yu Zhan Qian Yang Sanhong Liu Pengfei Chen Yuhang Jiang Xiaohua Sun Yu Tao Yiming Hu Cuifeng Li Qi Wang Ying Wang Charlie Degui Chen Yufang Shi xiaoren zhang Key Laboratory of Stem Cell Biology Institute of Health SciencesShanghai Institutes for Biological SciencesChinese Academy of Sciences and Shanghai Jiao Tong University School of MedicineShanghai 200031China State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell BiologyShanghai Institutes for Biological SciencesChinese Academy of SciencesShanghai 200031China Collaborative Innovation Center of Systems Biomedicine Shanghai Jiao Tong University School of MedicineShanghai 200240China

Interleukin(IL)17-producing T helper(Th17)cells play critical roles in the clearance of extracellular bacteria and fungi as well as the pathogenesis of various autoimmune diseases,such as multiple sclerosis,psoriasis,and ulcerative colitis.Although a global transcriptional regulatory network of Th17 cell differentiation has been mapped recently,the participation of epigenetic modifications in the differentiation process has yet to be elucidated.We demonstrated here that histone H3 lysine-27(H3K27)demethylation,predominantly mediated by the H3K27 demethylase Jmjd3,crucially regulated Th17 cell differentiation.Activation of naı¨ve CD41 T cells immediately induced high expression of Jmjd3.Genetic depletion of Jmjd3 in CD41 T cells specifically impaired Th17 cell differentiation both in vitro and in vivo.Ectopic expression of Jmjd3 largely rescued the impaired differentiation of Th17 cells in vitro in Jmjd3-deficientCD41 T cells.Importantly,Jmjd3-deficient mice were resistant to the induction of experimental autoimmune encephalomyelitis(EAE).Furthermore,inhibition of the H3K27 demethylase activity with the specific inhibitor GSK-J4 dramatically suppressed Th17 cell differentiation in vitro.At the molecular level,Jmjd3 directly bound to and reduced the level of H3K27 trimethylation(me3)at the genomic sites ofRorc,which encodes the masterTh17 transcription factorRorgt,and Th17 cytokine genes such as Il17,Il17f,and Il22.Therefore,our studies established acritical role of Jmjd3-mediatedH3K27demethylation inTh17 cell differentiation andsuggest that Jmjd3 can be a novel therapeutic target for suppressing autoimmune responses.

关键词： histone H3K27 demethylation Jmjd3 Th17 cells autoimmune disease

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Bcl-3 promotes Wnt signaling by maintaining the acetylation ofβ-catenin at lysine 49 in colorectal cancer

引用

Signal Transduction and Targeted Therapy 2020年第1期5卷 1913-1924页

作者： Xi Chen Chen Wang Yuhang Jiang Qi Wang Yu Tao Haohao zhang Yongxu Zhao Yiming Hu Cuifeng Li Deji Ye Dandan Liu Wenxia Jiang Eugene Y.Chin Sheng Chen Yongzhong Liu Mingliang Wang Sanhong Liu xiaoren zhang CAS Key Laboratory of Tissue Microenvironment and Tumor Shanghai Institute of Nutrition and HealthShanghai Institutes for Biological SciencesUniversity of Chinese Academy of SciencesChinese Academy of SciencesShanghai 200025China Shanghai Institute for Advanced Immunochemical Studies ShanghaiTech UniversityShanghai 201210China Affiliated Cancer Hospital&Institute of Guangzhou Medical University Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and DegradationState Key Laboratory of Respiratory DiseaseGuangzhou 510000China Renji Hospital Shanghai Jiao Tong University School of MedicineShanghai 200025China State Key Laboratory of Oncogenes and Related Genes Shanghai Cancer InstituteRenji HospitalShanghai Jiao Tong University School of MedicineShanghai 200032China Department of General Surgery Ruijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025China

Wnt/β-catenin signaling plays a critical role in colorectal cancer(CRC)tumorigenesis and the homeostasis of colorectal cancer stem cells(CSCs),but its molecular mechanism remains unclear.B-cell lymphoma 3(Bcl-3),a member of the IκB family,is overexpressed in CRC and promotes tumorigenicity.Here,we report a novel function of Bcl-3 in maintaining colorectal CSC homeostasis by activating Wnt/β-catenin signaling.Silencing Bcl-3 suppresses the self-renewal capacity of colorectal CSCs and sensitizes CRC cells to chemotherapeutic drugs through a decrease in Wnt/β-catenin signaling.Moreover,our data show that Bcl-3 is a crucial component of Wnt/β-catenin signaling and is essential forβ-catenin transcriptional activity in CRC cells.Interestingly,Wnt3a increases the level and nuclear translocation of Bcl-3,which binds directly toβ-catenin and enhances the acetylation ofβ-catenin at lysine 49(Ac-K49-β-catenin)and transcriptional activity.Bcl-3 depletion decreases the Ac-K49-β-catenin level by increasing the level of histone deacetylase 1 to remove acetyl groups fromβ-catenin,thus interrupting Wnt/β-catenin activity.In CRC clinical specimens,Bcl-3 expression negatively correlates with the overall survival of CRC patients.A significantly positive correlation was found between the expression of Bcl-3 and Ac-K49-β-catenin.Collectively,our data reveal that Bcl-3 plays a crucial role in CRC chemoresistance and colorectal CSC maintenance via its modulation of the Ac-K49-β-catenin,which serves as a promising therapeutic target for CRC.

关键词： colorectal homeostasis cancer

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

基于专利地图理论的我国商业银行专利比较研究

引用

情报杂志 2011年第6期30卷 30-35,13页

作者：章晓仁丁玲陈向东北京航空航天大学经济管理学院北京100083

专利地图是分析专利技术、制定专利战略的一种重要工具和方法,结合专利地图的主要方法,在对国内商业银行专利检索基础上,从专利地图视角对我国商业银行专利发展状况、年度走势、技术领域分布、IPC分类等进行了深入比较研究,分析国内商... 详细信息

专利地图是分析专利技术、制定专利战略的一种重要工具和方法,结合专利地图的主要方法,在对国内商业银行专利检索基础上,从专利地图视角对我国商业银行专利发展状况、年度走势、技术领域分布、IPC分类等进行了深入比较研究,分析国内商业银行的技术创新能力和产品研发能力。

关键词：专利地图 IPC分类商业银行技术创新

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

肾移植受者肠道菌群特征及其与糖代谢紊乱的关联

引用

肾脏病与透析肾移植杂志 2023年第3期32卷 231-237页

作者：诸医蒙王江东仉超张孝认徐鹏杰王依娜胡雨韵沈洲姬宁波大学附属李惠利医院肾脏内科宁波315040 宁波大学附属李惠利医院检验科宁波315040

目的:明确肾移植受者肠道菌群结构和代谢改变模式,评估差异菌群对肾移植后糖尿病(PTDM)的预测价值。方法:纳入2001年1月至2022年7月在宁波大学附属李惠利医院手术及随访的肾移植受者,分为移植后高血糖(PTHG)组[包括PTDM组和移植后糖尿... 详细信息

目的:明确肾移植受者肠道菌群结构和代谢改变模式,评估差异菌群对肾移植后糖尿病(PTDM)的预测价值。方法:纳入2001年1月至2022年7月在宁波大学附属李惠利医院手术及随访的肾移植受者,分为移植后高血糖(PTHG)组[包括PTDM组和移植后糖尿病前期(prePTDM)组]和血糖正常组,对其粪便标本进行16S rRNA基因V3-V4区域测序。比较PTHG组与血糖正常组粪便菌群结构及功能改变,分析差异菌群与临床理化指标之间的关联,并评估其辅助诊断PTHG的能力。结果:纳入肾移植受者92例,其中PTHG组36例(包括PTDM组29例,prePTDM组7例)。与血糖正常组相比,PTHG患者粪便菌群丰度和多样性的增加无统计学意义。PTHG组中芽孢杆菌属(Gemmiger)和亚诺杆菌属(Anaerobacterium)的相对丰度显著增加,而黄杆菌属(Flavonifractor)、双歧杆菌属(Bifidobacterium)和副沙门氏菌属(Parasutterella)的相对丰度显著减少(P0.3且P<0.05)。联合上述6种菌属绘制ROC曲线(AUC=0.830),并将菌群联合空腹血糖进行分析(AUC=0.962),大于空腹血糖的单独诊断效能。PTHG组氨基糖、核苷酸糖和半乳糖代谢等糖代谢途径以及胆汁酸生物合成显著减少。亚组分析显示,脱硫弧菌属(Desulfovibrio)、Anaerobacterium菌属和芽孢杆菌属在PTDM、prePTDM和血糖正常三组间呈递减趋势,但趋势并不显著。结论:PTDM患者肠道菌群结构和功能发生显著改变,差异菌群与糖代谢显著相关。部分菌群在PTDM、prePTDM和血糖正常三组间呈递减趋势。

关键词：肠道微生物移植后糖尿病 16S rRNA基因测序肾移植

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

基于ANP的复杂产品系统创新集成能力研究

引用

科技进步与对策 2010年第24期27卷 96-99页

作者：章晓仁陈向东丁玲北京航空航天大学经济管理学院北京100191

根据复杂产品系统的特征,设计创新过程中集成能力的评估指标体系,运用网络层次分析理论分析评估影响因素各层次间及同一层元素间的依赖与反馈关系,建立网络层次结构模型,应用super decision软件计算指标的影响权重,为提高复杂产品系统... 详细信息

根据复杂产品系统的特征,设计创新过程中集成能力的评估指标体系,运用网络层次分析理论分析评估影响因素各层次间及同一层元素间的依赖与反馈关系,建立网络层次结构模型,应用super decision软件计算指标的影响权重,为提高复杂产品系统创新集成能力提供一种定量化的决策方法和依据。

关键词：企业能力评估指标体系网络层次分析法复杂产品系统系统集成能力

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：