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| 1 | Mlkl knockout mice demonstrate the indispensable role of Mlkl in necroptosis显示文摘像域的蛋白质(Mlkl ) 最近被发现与受体交往交往的混合的系 kinase 蛋白质 3 (Rip3 ) 并且导致的坏死因素(TNF ) 在有教养的房间线规划了坏死(necroptosis ) 为肿瘤必要。我们由抄写产生了 Mlkl 缺乏的老鼠像使活跃之物的受动器核酸酶(TALEN ) 调停了基因混乱和发现 Mlkl 到为象有免疫力的房间开发一样的正常老鼠开发非必需。胚胎的成纤维细胞(MEF ) 和巨噬细胞两个都显示出的 Mlkl 缺乏的老鼠抵抗到坏死然而并非 apoptotic 刺激。Mlkl 缺乏的 MEF 和巨噬细胞与处于他们激活 NF-κ 的能力的野类型的房间难区分;响应 TNF 和 lipopolysaccharides (LPS ) 的 B,英皇家空军之阶级最低之兵, JNK,和 p38 分别地。一致地, Mlkl 缺乏的巨噬细胞和老鼠展出了正常 interleukin-1β(IL-1β) ,在 LPS 处理以后的 IL-6,和 TNF 生产。Mlkl 缺乏保护老鼠免受导致天蓝色的尖锐胰腺炎的伤害,坏死相关的疾病,但是没在 polymicrobial 上有效果腐败导致吃惊的动物死亡。我们的结果在 necroptosis 为 Mlkl 的角色提供基因证据。 | Jianfeng Wu Zhe Huang Junming Ren Zhirong Zhang Peng He Yangxin Li Jianhui Ma Wanze Chen Yingying Zhang Xiaojuan Zhou Zhentao Yang Su-Qin Wu Lanfen Chen Jiahuai Han | 2013 | Cell Research2013，23，8： | 35 |
| 2 | Circular RNA circStag1 promotes bone regeneration by interacting with HuR显示文摘Postmenopausal osteoporosis is a common bone metabolic disorder characterized by deterioration of the bone microarchitecture,leading to an increased risk of fractures.Recently,circular RNAs(circ RNAs)have been demonstrated to play pivotal roles in regulating bone metabolism.However,the underlying functions of circ RNAs in bone metabolism in postmenopausal osteoporosis remain obscure.Here,we report that circ Stag1 is a critical osteoporosis-related circ RNA that shows significantly downregulated expression in osteoporotic bone marrow mesenchymal stem cells(BMSCs)and clinical bone tissue samples from patients with osteoporosis.Overexpression of circ Stag1 significantly promoted the osteogenic capability of BMSCs.Mechanistically,we found that circ Stag1 interacts with human antigen R(Hu R),an RNA-binding protein,and promotes the translocation of Hu R into the cytoplasm.A high cytoplasmic level of Hu R led to the activation of the Wnt signaling pathway by stabilizing and enhancing low-density lipoprotein receptor-related protein 5/6(Lrp5/6)andβ-catenin expression,thereby stimulating the osteogenic differentiation of BMSCs.Furthermore,overexpression of circ Stag1 in vivo by circ Stag1-loaded adeno-associated virus(circ Stag1-AAV)promoted new bone formation,thereby preventing bone loss in ovariectomized rats.Collectively,we show that circ Stag1 plays a pivotal role in promoting the regeneration of bone tissue via Hu R/Wnt signaling,which may provide new strategies to prevent bone metabolic disorders such as postmenopausal osteoporosis. | Gaoyang Chen Canling Long Shang Wang Zhenmin Wang Xin Chen Wanze Tang Xiaoqin He Zhiteng Bao Baoyu Tan Jin Zhao Yongheng Xie Zhizhong Li Dazhi Yang Guozhi Xiao Songlin Peng | 2022 | Bone Research2022，10，3： | 7 |
| 3 | The Gβy-Src signaling pathway regulates TNF-induced necroptosis via control of necrosome translocation显示文摘 | Lisheng Li Wanze Chen Yaoji Liang Huabin Ma Wenjuan Li Zhenru Zhou Jie Li Yan Ding Junming Ren Juan Lin Felicia Han Jianfeng Wu Jiahuai Han | 2014 | Cell Research2014，24，4： | 2 |
| 4 | Targeting Kindlin-2 in adipocytes increases bone mass through inhibiting FAS/PPARγ/FABP4 signaling in mice显示文摘Osteoporosis(OP)is a systemic skeletal disease that primarily affects the elderly population,which greatly increases the risk of fractures.Here we report that Kindlin-2 expression in adipose tissue increases during aging and high-fat diet fed and is accompanied by decreased bone mass.Kindlin-2 specific deletion(K2KO)controlled by Adipoq-Cre mice or adipose tissue-targeting AAV(AAV-Rec2-CasRx-sgK2)significantly increases bone mass.Mechanistically,Kindlin-2 promotes peroxisome proliferator-activated receptor gamma(PPARγ)activation and downstream fatty acid binding protein 4(FABP4)expression through stabilizing fatty acid synthase(FAS),and increased FABP4 inhibits insulin expression and decreases bone mass.Kindlin-2 inhibition results in accelerated FAS degradation,decreased PPARγactivation and FABP4 expression,and therefore increased insulin expression and bone mass.Interestingly,we find that FABP4 is increased while insulin is decreased in serum of OP patients.Increased FABP4 expression through PPARγactivation by rosiglitazone reverses the high bone mass phenotype of K2KO mice.Inhibition of FAS by C75 phenocopies the high bone mass phenotype of K2KO mice.Collectively,our study establishes a novel Kindlin-2/FAS/PPARγ/FABP4/insulin axis in adipose tissue modulating bone mass and strongly indicates that FAS and Kindlin-2 are new potential targets and C75 or AAV-Rec2-CasRx-sgK2 treatment are potential strategies for OP treatment. | Wanze Tang Zhen Ding Huanqing Gao Qinnan Yan Jingping Liu Yingying Han Xiaoting Hou Zhengwei Liu Litong Chen Dazhi Yang Guixing Ma Huiling Cao | 2023 | Acta Pharmaceutica Sinica B2023，13，11： | 0 |
| 5 | 坏死激酶RIP1/RIP3通过特异性结合HSV-1的ICP6蛋白从而启动细胞坏死来抑制病毒在小鼠中的繁殖显示文摘2007年3月,细胞出版社正式推出《细胞-宿主与微生物》(月刊)。本刊出版的研究论文和综述文章重点关注对微生物与其宿主关系的理解。通过与作者、审稿人和科学编委的紧密合作,本刊的编辑人员以保持细胞出版社期刊一贯的高标准为使命,对该领域的研究结果予以及时报道。该杂志2015年公布的影响因子为12.328。 | Zhe Huang Su-Qin Wu 梁耀极 Xiaojuan Zhou Wanze Chen Lisheng Li Jianfeng Wu Qiuyu Zhuang Chang'an Chen Jingxian Li Chuan-Qi Zhong Weixiang Xia Rongbin Zhou Chunfu Zheng 韩家淮 | 2016 | 科学新闻2016，0，1： | 0 |
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