基本信息
章海兵  男  博导  中国科学院上海营养与健康研究所
电子邮件: hbzhang@sibs.ac.cn
通信地址: 上海市岳阳路320号
邮政编码:

招生信息

   
招生专业
100104-病理学与病理生理学
071009-细胞生物学
招生方向
病理学与病理生理学-细胞死亡与免疫代谢
细胞生物学-细胞死亡与免疫代谢

教育背景

2000-09--2005-07   中科院上海生科院   博士学位
1993-09--1997-07   山东大学生命科学学院   学士学位

工作经历

   
工作简历
2013-04~现在, 中国科学院上海营养与健康研究所, 研究员/课题组长
2012-04~2013-04,Children's Hospital of Philadelphia, 博士后
2006-02~2012-03,Thomas Jefferson University, 博士后
2000-09~2005-07,中科院上海生科院, 博士学位
1993-09~1997-07,山东大学生命科学学院, 学士学位

专利与奖励

   
专利成果
( 1 ) sgRNA筛选系统和方法, 2020, 第 1 作者, 专利号: CN106636154B

出版信息

   
发表论文
(1) A novel RIPK1 inhibitor reduces GVHD in mice via a nonimmunosuppressive mechanism that restores intestinal homeostasis, BLOOD, 2023, 第 30 作者
(2) Crucial Roles of the RIP Homotypic Interaction Motifs of RIPK3 in RIPK1-Dependent Cell Death and Lymphoproliferative Disease, CELL REPORTS, 2020, 通讯作者
(3) Protein Tyrosine Phosphatase Receptor S Acts as a Metastatic Suppressor in Malignant Peripheral Nerve Sheath Tumor via Profilin 1-Induced Epithelial-Mesenchymal Transition, FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY, 2020, 第 8 作者
(4) Gut epithelial TSC1/mTOR controls RIPK3-dependent necroptosis in intestinal inflammation and cancer, JOURNAL OF CLINICAL INVESTIGATION, 2020, 第 23 作者
(5) A necroptotic-independent function of MLKL in regulating endothelial cell adhesion molecule expression, CELL DEATH & DISEASE, 2020, 第 8 作者
(6) Catalytically inactive RIP1 and RIP3 deficiency protect against acute ischemic stroke by inhibiting necroptosis and neuroinflammation, CELL DEATH & DISEASE, 2020, 通讯作者
(7) Identification of the Raf kinase inhibitor TAK-632 and its analogues as potent inhibitors of necroptosis by targeting RIPK1 and RIPK3, British Journal of Pharmacology, 2019, 第11作者
(8) MLKL attenuates colon inflammation and colitis-tumorigenesis via suppression of inflammatory responses, CANCER LETTERS, 2019, 通讯作者
(9) Ubiquitination of RIPK1 suppresses programmed cell death by regulating RIPK1 kinase activation during embryogenesis, NATURE COMMUNICATIONS, 2019, 通讯作者
(10) Neonatal lethality and recycling defect of transferrin receptor in mice with Syntaxin12/13 disruption, Neonatal lethality and recycling defect of transferrin receptor in mice with Syntaxin12/13 disruption, PROTEIN & CELL, 2019, 第 7 作者
(11) Metabolic benefits of inhibition of p38 alpha in white adipose tissue in obesity, PLOS BIOLOGY, 2018, 其他(合作组作者)
(12) Chemotherapy drugs induce pyroptosis through caspase-3-dependent cleavage of GSDME, SCIENCE CHINA-LIFE SCIENCES, 2018, 通讯作者
(13) Embryonic Lethality and Host Immunity of RelA-Deficient Mice Are Mediated by Both Apoptosis and Necroptosis, JOURNAL OF IMMUNOLOGY, 2018, 通讯作者
(14) Chemotherapy drugs induce pyroptosis through caspase-3-dependent cleavage of GSDME, Chemotherapy drugs induce pyroptosis through caspase-3-dependent cleavage of GSDME, 中国科学:生命科学英文版, 2018, 第 2 作者
(15) RIPK3 Mediates Necroptosis during Embryonic Development and Postnatal Inflammation in Fadd-Deficient Mice, CELL REPORTS, 2017, 通讯作者
(16) RIP1 kinase activity-dependent roles in embryonic development of Fadd -deficient mice, CELL DEATH AND DIFFERENTIATION, 2017, 通讯作者
(17) RIP1 kinase activity-dependent roles in embryonic development of Fadd -deficient mice, CELL DEATH AND DIFFERENTIATION, 2017, 通讯作者
(18) Celastrol ameliorates inflammation through inhibition of NLRP3 inflammasome activation, ONCOTARGET, 2017, 通讯作者
(19) 3. A novel sgRNA selection system for CRISPR-Cas9 in mammalian cells, Biochem Biophys Res Commun, 2016, 通讯作者
(20) MLKL and FADD are Critical for Suppressing Progressive Lymphoaccumulative Disease and Activating NLRP3 Inflammasome, Cell Reports, 2016, 通讯作者
(21) 1. Gambogenic acid inhibits LPS-simulated inflammatory response by suppressing NF-κB and MAPK in macrophages, Acta Biochim Biophys Sin, 2016, 通讯作者
(22) Gambogenic acid inhibits LPS-simulated inflammatory response by suppressing NF-kappa B and MAPK in macrophages, ACTA BIOCHIMICA ET BIOPHYSICA SINICA, 2016, 通讯作者
(23) MLKL and FADD Are Critical for Suppressing Progressive Lymphoproliferative Disease and Activating the NLRP3 Inflammasome, CELL REPORTS, 2016, 通讯作者
(24) Lack of FADD in Tie-2 expressing cells causes RIPK3-mediated embryonic lethality, CELL DEATH & DISEASE, 2016, 通讯作者

科研活动

   
科研项目
( 1 ) RIPK3/MLKL介导细胞程序性坏死的分子机制及其在肠道炎症中的作用机理研究, 负责人, 国家任务, 2016-01--2019-12
( 2 ) 蛋白激酶RIP1泛素化修饰调控胚胎发育与免疫炎症的机制 研究, 负责人, 国家任务, 2018-01--2021-12
( 3 ) 环境与遗传致病因素导致2型糖尿病发生发展的机制研究, 参与, 国家任务, 2016-09--2020-12
( 4 ) Caspase8和RIP3调控细胞程序性坏死的关键机制研究, 负责人, 国家任务, 2020-01--2023-12
( 5 ) CYLD剪切调控细 胞死亡与炎症的作用机制研究, 负责人, 国家任务, 2023-01--2026-12
( 6 ) 不同细胞死亡方式互作机制及协同调控组织微环境的作用机理研 究, 负责人, 地方任务, 2022-06--2025-05
( 7 ) 组织器官发育与稳态维持的关键脂质代谢物及其调控网络, 参与, 国家任务, 2022-12--2027-11
( 8 ) 构建基于基因组标签的重要器官精准蛋白质图谱, 参与, 地方任务, 2023-01--2027-12
参与会议
(1)MLKL and FADD are Critical for Suppressing Progressive Lymphoaccumulative Disease and Activating the NLRP3 Inflammasome   冷泉港亚洲会议-细胞死亡与疾病   2015-11-10