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Ubiquitin-specific protease 47 regulates intestinal inflammation through deubiquitination of TRAF6 in epithelial cells

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Science China(Life Sciences) 2022年第8期65卷 1624-1635页

作者： Hu Lei Li Yang Hanzhang Xu Zhengting Wang Xiangyun Li Meng Liu yingli wu Hongqiao International Institute of Medicine Shanghai Tongren Hospital/Faculty of Basic MedicineKey Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of EducationShanghai Jiao Tong University School of MedicineShanghai 200025China Department of Gastroenterology Ruijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025China

Deubiquitinates(DUBs) alter the stabilities, localizations or activities of substrates by removing their ubiquitin conjugates,which are closely related to the development of inflammatory response. Here, we show that ubiquitin-specific protease 47(USP47) prevents inflammation development in inflammatory bowel disease(IBD). Compared with wild-type mice, Usp47 knockout mice are more susceptible to dextran sodium sulfate(DSS)-induced acute and chronic colitis with higher inflammatory cytokines expression and severe intestinal tissue damage. Chimeric mouse experiments suggest that non-hematopoietic cells mainly contribute to the phenotype. And, DSS-induced colitis of the Usp47 knockout mice depends on commensal ***, down-regulation of USP47 aggravates the activation of NF-κB signaling pathway by increasing the K63-linked poly-ubiquitination of tumor necrosis factor receptor-associated factor 6(TRAF6) in intestinal epithelial cells. Furthermore, the expression of USP47, negatively correlated with the degree of inflammation, is lower at colonic inflammatory lesions than that non-inflammatory sites from the intestine from ulcerative colitis(UC) and Crohn's disease(CD) patients. These data, taken together, indicate that USP47 regulates intestinal inflammation through de-ubiquitination of K63-linked poly-ubiquitination TRAF6 in intestinal epithelial cells.

关键词： ubiquitin-specific protease 47 TRAF6 intestinal epithelial cell inflammation inflammatory bowel disease

Research review of the cement sand and gravel(CSG)dam

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Frontiers of Structural and Civil Engineering 2012年第1期6卷 19-24页

作者： Xin CAI yingli wu Xingwen GUO Yu MING College of Water Conservancy and Hydropower Engineering Hohai UniversityNanjing 210098China Nanjing Hydraulic Research Institute Nanjing 210098China College of Mechanics and Materials Hohai UniversityNanjing 210098China

The cement sand and gravel(CSG)dam is a new style of dam that owes the advantages both of the concrete faced rock-fill dam(CRFD)and roller compacted concrete(RCC)gravity dam,because of which it has attracted much attention of experts home and *** present,some researches on physic-mechanical property of CSG material and work behavior of CSG dam have been *** papcr introduces the development and characteristics of CSG dam systematically,and summarizes the progress of the study on basic tests,constitutive relation of CSG material and numerical analysis of CSG dam,in addition,indicates research and application aspect of the dam.

关键词： cement sand and gravel(CSG)dam cement sand and gravel(CSG)material research review

JaponiconeA induces apoptosis of bortezomib-sensitive and -resistant myeloma cells in vitro and in vivo by targeting IKKβ

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Cancer Biology & Medicine 2022年第5期19卷 651-668页

作者： Zilu Zhang Chenjing Ye Jia Liu Wenbin Xu Chao wu Qing Yu Xiaoguang Xu Xinyi Zeng Huizi Jin yingli wu Hua Yan Shanghai Institute of Hematology Affiliated Ruijin Hospital of Shanghai Jiao Tong University School of MedicineShanghai 200025China VIP Health Center Affiliated Ruijin Hospital of Shanghai Jiao Tong University School of MedicineShanghai 200025China Shanghai Key Laboratory for Molecular Engineering of Chiral Drugs School of PharmacyShanghai Jiao Tong UniversityShanghai 200240China Hongqiao International Institute of Medicine Shanghai Tongren Hospital/Faculty of Basic MedicineChemical Biology Division of Shanghai Universities E-InstitutesKey Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of EducationShanghai Jiao Tong University School of MedicineShanghai 200025China

Objective:Multiple myeloma(MM)remains incurable with high rates of *** therapeutic drugs are therefore urgently needed to improve the ***(JA),a natural product isolated from Inula japonica Thunb,has shown good anti-MM potential.A comprehensive study should therefore be conducted to identify both the in vitro and in vivo mechanisms of the anti-MM effects of ***:CCK8 assays and flow cytometry were used to detect the proliferation,apoptosis,and cell cycle of MM cell lines when treated with *** vivo experiments were conducted using subcutaneous xenograft mouse *** also identified possible targets and the mechanism of JA using RNA-seq and c-Map databases,and identified the specific targets of JA in bortezomib-sensitive and-resistant MM cell lines using CETSA,DARTS,and rescue ***,JA and bortezomib were used separately or together to characterize their possible synergistic ***:In vitro,JA inhibited proliferation,and induced apoptosis and G2/M phase arrest in MM cell lines,and selectively killed primary CD138+MM *** vivo,JA also demonstrated a strong anti-tumor effect with no observable *** addition,JA showed synergetic effects in combination with bortezomib,and enhanced the anti-tumor effect of bortezomib in bortezomibresistant *** and DARTS confirmed direct binding of JA to NF-κB inhibitor kinase beta(IKKβ),and overexpression of IKKβor knockdown of IκBαpartially rescued the apoptosis induced by ***:JA exhibited strong anti-tumor effects in *** sensitized myeloma cells to bortezomib and overcame NF-κB-induced drug resistance by inhibiting IKKβ,providing a new treatment strategy for MM patients.

关键词： Multiple myeloma NF-κB JaponiconeA bortezomib drug resistance

NES1/KLK10 and hNIS gene therapy enhanced iodine-131 internal radiation in PC3 proliferation inhibition

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Frontiers of Medicine 2019年第6期13卷 646-657页

作者： Jiajia Hu Wenbin Shen Qian Qu Xiaochun Fei Ying Miao Xinyun Huang Jiajun Liu yingli wu Biao Li Department of Nuclear Medicine Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200025China Department of Pathology Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200025China Hongqiao International Institute of Medicine Shanghai Tongren Hospital/Faculty of Basic MedicineChemical Biology Division of Shanghai Universities E-InstitutesKey Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of EducationShanghai Jiao Tong University School of MedicineShanghai 200025China

NES1 gene is thought to be a tumor-suppressor *** previous study found that overexpression of NES1 gene in PC3 cell line could slow down the tumor proliferation rate,associated with a mild decrease in BCL-2 *** BCL-2 decrease could increase the sensitivity of radiotherapy to ***,we supposed to have an“enhanced firepower”effect by combining overexpressed NES1 gene therapy and 131I radiation therapy uptake by overexpressed hNIS *** found a weak endogenous expression of hNIS protein in PC3 cells and demonstrated that the low expression of hNIS protein in PC3 cells might be the reason for the low iodine *** overexpressing hNIS in PC3,the radioactive iodine uptake ability was significantly *** of in vitro and in vivo tumor proliferation experiments and 18F-fluorothymidine(18F-FLT)micro-positron emission tomography/computed tomography(micro-PET/CT)imaging showed that the combined NES1 gene therapy and 131I radiation therapy mediated by overexpressed hNIS protein had the best tumor proliferative inhibition *** showed an obvious decrease of Ki-67 expression and the lowest BCL-2 *** data suggest that via inhibition of BCL-2 expression,overexpressed NES1 might enhance the effect of radiation therapy of 131I uptake in hNIS overexpressed PC3 cells.

关键词： androgen-independent prostate cancer normal epithelial cell-specific 1/kallikrein 10 sodium/iodide symporter radiation therapy proliferation

YL064 activates proteasomal-dependent degradation of c-Myc and synergistically enhances the anti-tumor activity of ABT-199 in diffuse large B cell lymphoma

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Signal Transduction and Targeted Therapy 2020年第1期5卷 1441-1444页

作者： Huizhuang Shan Yang Cao Xinhua Xiao Meng Liu Yunzhao wu Qi Zhu Hanzhang Xu Hu Lei Zhujun Yao yingli wu Hongqiao International Institute of Medicine Tongren Hospital/Faculty of Basic MedicineChemical Biology Division of Shanghai Universities E-InstitutesKey Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of EducationShanghai Jiao Tong University School of MedicineShanghai 200025China Department of Hematology The Third Affiliated Hospital of Soochow UniversityChangzhouJiangsu Province 213003PR China State Key Laboratory for Medical Genomics Shanghai Institute of HematologyCollaborative Innovation Center of HematologyNational Research Center for Translational MedicineRuijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025China Institute of Oncology Shanghai 9th People’s HospitalShanghai Jiao Tong University School of Medicine639 Zhizaoju RdShanghai 200011China State Key Laboratory of Coordination Chemistry Jiangsu Key Laboratory of Advanced Organic MaterialsSchool of Chemistry and Chemical EngineeringNanjing University163 Xianlin AvenueNanjingJiangsu 210023China

Dear Editor,c-Myc is highly associated with poor prognosis and aggressive progression of diffuse large B cell lymphoma(DLBCL)and is thus a desirable drug ***,studies indicate that 5–15%of DLBCL patients harbor MYC and BCL-2 translocations,while 20–35%DLBCL patients simultaneously overexpress of c-Myc and BCL-2 proteins without gene rearrangements.1 These two types of DLBCL are referred as“double-hit”lymphoma(DHL)and“double-expressor”lymphoma(DEL),*** DHL and DEL lymphomas have inferior clinical outcomes and are refractory to R-CHOP or even hematopoietic stem cell transplant.2 Thus,targeting both c-Myc and BCL-2 is a promising strategy to treat high-risk DLBCLs.3 Although BCL-2 inhibitors are clinically available,c-Myc remains to be“undruggable”owing to its lack of kinase activity and intrinsically disordered structure.4 Thus,developing clinically applicable c-Myc inhibitor remains challenging.

关键词： lymphoma synergistic harbor

Hsp90/C terminal Hsc70-interacting protein regulates the stability of Ikaros in acute myeloid leukemia cells

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Science China(Life Sciences) 2021年第9期64卷 1481-1490页

作者： Meng Liu Jin Jin Yanjie Ji Huizhuang Shan Zhihui Zou Yang Cao Li Yang Ligen Liu Li Zhou Hu Lei Yunzhao wu Hanzhang Xu yingli wu Hongqiao International Institute of Medicine Shanghai Tongren Hospital/Faculty of Basic MedicineChemical Biology Division of Shanghai Universities E-InstitutesKey Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of EducationShanghai Jiao Tong University School of MedicineShanghai 200025China Department of Ultrasound Second Affiliated Hospital of Zhejiang UniversityHangzhou 310009China Department of Hematology The Third Affiliated Hospital of Soochow UniversityChangzhou 213003China Shanghai Institute of Hematology State Key Laboratory of Medical GenomicsNational Research Center for Translational Medicine at ShanghaiRuijin Hospital affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200025China

The stability of Ikaros family zinc finger protein 1(Ikaros),a critical hematopoietic transcription factor,can be regulated by cereblon(CRBN)ubiquitin ligase stimulated by immunomodulatory drugs in multiple ***,other stabilization mechanisms of Ikaros have yet to be *** this study,we show that the pharmacologic inhibition or knockdown of Hsp90 downregulates Ikaros in acute myeloid leukemia(AML)*** inhibitor MG132 but not autophagy inhibitor chloroquine could suppress the Hsp90 inhibitor STA-9090-induced reduction of Ikaros,which is accompanied with the increased ubiquitination of ***,Ikaros interacts with E3 ubiquitin-ligase C terminal Hsc70 binding protein(CHIP),which mediates the STA-9090-induced ubiquitination of *** addition,the knockdown of Ikaros effectively inhibits the proliferation of leukemia cells,but this phenomenon could be rescued by Ikaros ***,our findings indicate that the interplay between HSP90 and CHIP regulates the stability of Ikaros in AML cells,which provides a novel strategy for AML treatment through targeting the HSP90/Ikaros/CHIP axis.

关键词： Ikaros CHIP Hsp90 AML STA-9090

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Brain-derived neurotrophic factor plays with TRiC:focus on synaptic dysfunction in Huntington’s disease

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Neural Regeneration Research 2025年第10期20卷 2919-2920页

作者： yingli Gu Kijung Sung Chengbiao wu Department of Neurosciences University of California San DiegoLa JollaCAUSA

Brain-derived neurotrophic factor(BDNF)exerts pleiotropic effects on brain processes including psychiatric disorders,aging,neurodegeneration,and metabolic homeostasis.A simple PubMed search using the key word“BDNF,”to date,yields over 33,000 *** fundamental biology to potential therapeutic applications,BDNF has clearly garnered extensive and significant attention in the field of neurobiology research.

关键词： Huntington homeostasis therapeutic

USP7 deubiquitinates and stabilizes NOTCH1 in T-cell acute lymphoblastic leukemia

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Signal Transduction and Targeted Therapy 2018年第1期3卷 52-61页

作者： Huizhuang Shan Xiangyun Li Xinhua Xiao Yuting Dai Jinyan Huang Junjun Song Meng Liu Li Yang Hu Lei Yin Tong Li Zhou Hanzhang Xu yingli wu Hongqiao International Institute of Medicine Shanghai Tongren Hospital/Faculty of Basic MedicineChemical Biology Division of Shanghai Universities E-InstitutesKey Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of EducationShanghai Jiao Tong University School of MedicineShanghai 200025China Department of Hematology Rui-Jin HospitalShanghai Jiao Tong University School of MedicineNo.197Ruijin Er RoadShanghaiChina Shanghai University of Medicine&Health Sciences No.279Zhouzhu RoadShanghaiChina Department of Hematology Shanghai First People’s HospitalShanghai Jiao Tong University School of MedicineShanghai 200080China

T-cell acute lymphoblastic leukemia(T-ALL)is a highly aggressive leukemia that is primarily caused by aberrant activation of the NOTCH1 signaling *** studies have revealed that posttranslational modifications,such as ubiquitination,regulate NOTCH1 stability,activity,and ***,the specific deubiquitinase that affects NOTCH1 protein stability remains ***,we report that ubiquitin-specific protease 7(USP7)can stabilize ***7 deubiquitinated NOTCH1 in vivo and in vitro,whereas knockdown of USP7 increased the ubiquitination of ***7 interacted with NOTCH1 protein in T-ALL cells,and the MATH and UBL domains of USP7 were responsible for this *** of USP7 significantly suppressed the proliferation of T-ALL cells in vitro and in vivo,accompanied by downregulation of the NOTCH1 protein ***,pharmacologic inhibition of USP7 led to apoptosis of T-ALL *** importantly,we found that USP7 was significantly upregulated in human T-ALL cell lines and patient samples,and a USP7 inhibitor exhibited cell cytotoxicity toward primary T-ALL cells,indicating the clinical relevance of these ***,our results demonstrate that USP7 is a novel deubiquitinase that stabilizes ***,USP7 may be a promising therapeutic target in the currently incurable T-ALL.

关键词： ubiquitin USP7 lymphoblastic

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旋转圆柱目标的动态散斑统计特性(英文)

强激光与粒子束 2012年第2期24卷 331-337页

作者：武颖丽吴振森张耿西安电子科技大学理学院西安710071

高斯光束照射以固定角速度旋转的粗糙圆柱体表面,反射空间形成随着被测表面运动变化的动态散斑。研究了照射面积大于圆柱曲面条件下在远场衍射区形成的动态散斑统计特性,得到了不同入射条件及不同圆柱时动态散斑强度起伏空间-时间归一... 详细信息

高斯光束照射以固定角速度旋转的粗糙圆柱体表面,反射空间形成随着被测表面运动变化的动态散斑。研究了照射面积大于圆柱曲面条件下在远场衍射区形成的动态散斑统计特性,得到了不同入射条件及不同圆柱时动态散斑强度起伏空间-时间归一化相关函数。结果表明:随着圆柱半径、旋转速度以及照射光斑有效面积的增大,动态散斑强度起伏相关性快速减小;当圆柱旋转速度恒定,动态散斑光强起伏相关函数的峰值随着探测点之间距离的增大而减小,但峰值的位置随之而增大;在近似点照射情况下随着圆柱半径的增大空间相关长度基本不变,而相关时间性明显增大。

关键词：动态散斑高斯光束相关函数旋转圆柱