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| 1 | The molecular machinery of regulated cell death显示文摘Cells may die from accidental cell death(ACD)or regulated cell death(RCD).ACD is a biologically uncontrolled process,whereas RCD involves tightly structured signaling cascades and molecularly defined effector mechanisms.A growing number of novel nonapoptotic forms of RCD have been identified and are increasingly being implicated in various human pathologies.Here,we critically review the current state of the art regarding non-apoptotic types of RCD,including necroptosis,pyroptosis,ferroptosis,entotic cell death,netotic cell death,parthanatos,lysosome-dependent cell death,autophagy-dependent cell death,alkaliptosis and oxeiptosis.The in-depth comprehension of each of these lethal subroutines and their intercellular consequences may uncover novel therapeutic targets for the avoidanee of pathogenic cell loss. | Daolin Tang Rui Kang Tom Vanden Berghe Peter Vandenabeele Guido Kroemer | 2019 | Cell Research2019，29，5： | 143 |
| 2 | Ferroptosis:molecular mechanisms and health implications显示文摘Cell death can be executed through different subroutines.Since the description of ferroptosis as an iron-dependent form of nonapoptotic cell death in 2012,there has been mounting interest in the process and function of ferroptosis.Ferroptosis can occur through two major pathways,the extrinsic or transporter-dependent pathway and the intrinsic or enzyme-regulated pathway.Ferroptosis is caused by a redox imbalance between the production of oxidants and antioxidants,which is driven by the abnormal expression and activity of multiple redox-active enzymes that produce or detoxify free radicals and lipid oxidation products.Accordingly,ferroptosis is precisely regulated at multiple levels,including epigenetic,transcriptional,posttranscriptional and posttranslational layers.The transcription factor NFE2L2 plays a central role in upregulating anti-ferroptotic defense,whereas selective autophagy may promote ferroptotic death.Here,we review current knowledge on the integrated molecular machinery of ferroptosis and describe how dysregulated ferroptosis is involved in cancer,neurodegeneration,tissue injury,inflammation,and infection. | Daolin Tang Xin Chen Rui Kang Guido Kroemer | 2021 | Cell Research2021，31，2： | 182 |
| 3 | Intracellular HMGB1 as a novel tumor suppressor of pancreatic cancer显示文摘尽管有最近的进展, oncogenic K 地岬驾驶的胰腺的 ductal 腺癌(PDAC ) 在最致命的人的癌症之中留在现代医学。PDAC 的致病对内在的染色体不稳定性和外来的发炎激活部分可归因。然而,在在胰腺的 tumorigenesis 的这二个事件之间的分子的连接充分还没被建立了。这里,我们证明(HMGB1 ) 细胞内部的高活动性组盒子 1 显著地压制 oncogenic 由禁止染色体的 K-Ras-driven 胰腺的 tumorigenesis 调停不稳定性的支持 inflammatory nucleosome 版本。任何一个单身者的有条件的基因脱离或在胰的 HMGB1 的两等位基因在出生使老鼠变为极其敏感到先锋损害的 oncogenic K-Ras-driven 开始,包括胰腺的 intraepithelial 瘤, intraductal 乳突的 mucinous 瘤,和 mucinous 膀胱的瘤。在胰的 HMGB1 的损失与染色体重新整理和 telomere 畸形描绘的氧化 DNA 损坏和 chromosomal 不稳定性被联系。这些导致煽动性的 nucleosome 版本并且宣传 K-Ras-driven 胰腺的 tumorigenesis。细胞外的 nucleosomes 支持 interleukin 6 (IL-6 ) 由渗入 macrophages/neutrophils 的分泌物并且提高在胰腺的损害表明激活的 oncogenic K 地岬。到 IL-6 或 histone H3 或为先进 glycation 的受体的大美人的抵销的抗体结束产品都限制表明激活的 K 地岬,阻止癌症开发和转移 / 侵略,并且延长在 Pdx1-Cre 的动物幸存; K 地岬 G12D/+;Hmgb1/ 鼠标。由 glycyrrhizin 的 HMGB1 损失的药理学抑制在煽动性的条件下面在老鼠限制 oncogenic K-Ras-driven tumorigenesis。减少在 PDAC 病人的 HMGB1 的原子、全部的细胞的表示与差的全面幸存相关,在 PDAC 与预示、治疗学的关联作为新奇肿瘤 suppressor 支持细胞内部的 HMGB1。 | Rui Kang Yangchun Xie Qiuhong Zhang Wen Hou Qingping Jiang Shan Zhu Jinbao Liu Dexing Zeng Haichao Wang David L Bartlet Timothy R Billiar Herbert J Zeh III Michael T Lotze Daolin Tang | 2017 | Cell Research2017，27，7： | 22 |
| 4 | Cuproptosis:a copper-triggered modality of mitochondrial cell death显示文摘Various heavy metals can induce regulated cell death through different subroutines.A recent study published in Science found that intracellular copper accumulation triggers the aggregation of mitochondrial lipoylated proteins and the destabilization of Fe–S cluster proteins,leading to a unique type of cell death termed cuproptosis.Beyond classical apoptosis,several forms of regulated cell death(RCD)have been identified.These RCD subroutines differ in the initiating stimuli,intermediate activation events,and end effectors.1 Heavy metal ions are essential micronutrients,but either insufficient or excessive abundance of metals can trigger cell death.For example,ferroptosis has been defined as an iron-dependent form of oxidative cell death caused by unrestricted lipid peroxidation.2 Surprisingly,a recent study by Tsvetkov and colleagues showed that intracellular copper(Cu)induces a novel form of RCD that is different from oxidative stress-related cell death(e.g.,apoptosis,ferroptosis,and necroptosis)and has been termed“cuproptosis”.3 In contrast,mitochondrial stress,especially the aggregation of lipoylated mitochondrial enzymes and the loss of Fe–S cluster proteins,ignites cuproptosis(Fig.1). | Daolin Tang Xin Chen Guido Kroemer | 2022 | Cell Research2022，32，5： | 19 |
| 5 | Distribution,Frequency and Variation of Stripe Rust Resistance Loci Yr10,Lr34/Yr18 and Yr36 in Chinese Wheat Cultivars显示文摘Wheat stripe rust is a devastating disease in many regions of the world.In wheat,49 resistance genes for stripe rust have been officially documented,but only three genes are cloned,including the race-specific resistance Yr10 candidate gene(Yr10_(CG)) and slow-rusting genes Lr34/Yr18(hereafter designated as Yr18) and Yr36.In this study,we developed gene-specific markers for these genes and used them to screen a collection of 659 wheat accessions,including 485 Chinese cultivars.Thirteen percent and eleven percent of the tested Chinese cultivars were positive for the markers for Yr10_(CG) and Yr18_(RH)(the resistant haplotype of Yr18),respectively,but none were positive for the Yr36 marker.Since there is a limited use of the Yr10 gene in Chinese wheat,the relatively high frequency of wheat varieties with the Yr10_(CG) marker suggests that the identity of the Yr10 gene is unknown.With regards to the Yr18 gene,29%of the tested cultivars that are used in the Middle and Lower Yangtze Valleys' winter wheat zone were positive for Yr18_(RH) markers.A non-functional allele of Yr18_(RH) was identified in 'Mingxian 169',a commonly used susceptible check for studying stripe rust.The data presented here will provide useful information for marker-assisted selection for wheat stripe rust resistance. | Cuiling Yuan Hui Jiang Honggang Wang Kun Li Heng Tang Xianbin Li Daolin Fu | 2012 | Journal of Genetics and Genomics2012，39，11： | 12 |
| 6 | Cellular and molecular mechanisms of perineural invasion of pancreatic ductal adenocarcinoma显示文摘Pancreatic ductal adenocarcinoma(PDAC)is an aggressive malignant disease with a unique tumor microenvironment surrounded by an interlaced network of cancer and noncancerous cells.Recent works have revealed that the dynamic interaction between cancer cells and neuronal cells leads to perineural invasion(PNI),a clinical pathological feature of PDAC.The formation and function of PNI are dually regulated by molecular(e.g.,involving neurotrophins,cytokines,chemokines,and neurotransmitters),metabolic(e.g.,serine metabolism),and cellular mechanisms(e.g.,involving Schwann cells,stromal cells,T cells,and macrophages).Such integrated mechanisms of PNI not only support tumor development,growth,invasion,and metastasis but also mediate the formation of pain,all of which are closely related to poor disease prognosis in PDAC.This review details the modulation,signaling pathways,detection,and clinical relevance of PNI and highlights the opportunities for further exploration that may benefit PDAC patients. | Jingbo Li Rui Kang Daolin Tang | 2021 | Cancer Communications2021，41，8： | 4 |
| 7 | The BET family in immunity and disease显示文摘Innate immunity serves as the rapid and frst-line defense against invading pathogens,and this process can be regulated at various levels,including epigenetic mechanisms.The bromodomain and extraterminal domain(BET)family of proteins consists of four conserved mammalian members(BRD2,BRD3,BRD4,and BRDT)that regulate the expression of many immunity-associated genes and pathways.In particular,in response to infection and sterile inflammation,abnormally expressed or dysfunctional BETs are involved in the activation of pattern recognition receptor(e.g,TLR,NLR,and CGAS)pathways,thereby linking chromatin machinery to innate immunity under disease or pathological conditions.Mechanistically,the BET family controls the transcription of a wide range of proinflammatory and immunoregulatory genes by recognizing acetylated histones(mainly H3 and H4)and recruiting transcription factors(e.g.,RELA)and transcription elongation complex(e.g.P-TEFb)to the chromatin,thereby promoting the phosphorylation of RNA polymerase II and subsequent transcription initiation and elongation.This review covers the accumulating data about the roles of the BET family in innate immunity,and discusses the attractive prospect of manipulating the BET family as a new treatment for disease. | Nian Wang Runliu Wu Daolin Tang Rui Kang | 2021 | Signal Transduction and Targeted Therapy2021，6，2： | 4 |
| 8 | HMGB1 in health and disease显示文摘 | Rui Kang Ruochan Chen Qiuhong Zhang Wen Hou Sha Wu Lizhi Cao Jin Huang Yan Yu Xue-gong Fan Zhengwen Yan Xiaofang Sun Haichao Wang Qingde Wang Allan Tsung Timothy R. Billiar Herbert J. Zeh Michael T. Lotze Daolin Tang | 2014 | Molecular Aspects of Medicine2014，，： | 2 |
| 9 | The STING 1 network regulates autophagy and cell death显示文摘Cell death and immune response are at the core of life.In past decades,the endoplasmic reticulum(ER)protein STING!(also known as STING or TMEM173)was found to play a fundamental role in the production of type I interferons(IFNs)and pro-inflammatory cytokines in response to DNA derived from invading microbial pathogens or damaged hosts by activating multiple transcription factors.In addition to this well-known function in infection,inflammation,and immunity,emerging evidence suggests that the STING 1-dependent signaling network is implicated in health and disease by regulating autophagic degradation or various cell death modalities(e.g.,apoptosis,necroptosis,pyroptosis,ferroptosis,mitotic cell death,and immunogenic cell death[ICD]).Here,we outline the latest advances in our understanding of the regulating mechanisms and signaling pathways of STING1 in autophagy and cell death,which may shed light on new targets for therapeutic interventions. | Ruoxi Zhang Rui Kang Daolin Tang | 2021 | Signal Transduction and Targeted Therapy2021，6，7： | 2 |
| 10 | High-mobility group box 1 and cancer显示文摘 | Daolin Tang Rui Kang Herbert J. Zeh Michael T. Lotze | 2009 | BBA - Gene Regulatory Mechanisms2009，，1： | 1 |
| 11 | HMGB1 release and re- dox regulates autophagy and apoptosis in Cancer cells 显示文摘 | Tang Daolin Kang Rui Cheh CW | 2010 | Onco- gene2010，29，38： | 1 |
| 12 | Mitochondrial ACOD1/IRG1 in infection and sterile inflammation显示文摘Immunometabolism is a dynamic process involving the interplay of metabolism and immune response in health and diseases.Increasing evidence suggests that impaired immunometabolism contributes to infectious and inflammatory diseases.In particular,the mitochondrial enzyme aconitate decarboxylase 1(ACOD1,best known as immunoresponsive gene 1[IRG1])is upregulated under various inflammatory conditions and serves as a pivotal regulator of immunometabolism involved in itaconate production,macrophage polarization,inflammasome activation,and oxidative stress.Consequently,the activation of the ACOD1 pathway is implicated in regulating the pathogenic process of sepsis and septic shock,which are part of a clinical syndrome of life-threatening organ failure caused by a dysregulated host response to pathogen infection.In this review,we discuss the latest research advances in ACOD1 expression and function,with particular attention to how the ACOD1-itaconate pathway affects infection and sterile inflammation diseases.These new insights may give us a deeper understanding of the role of immunometabolism in innate immunity. | Runliu Wu Rui Kang Daolin Tang | 2022 | Journal of Intensive Medicine2022，2，2： | 1 |
| 13 | HMGB1 in Cancer: Good, Bad, or Both?显示文摘 | Rui Kang Qiuhong Zhang Herbert J. Zeh Michael T. Lotze Daolin Tang | 2013 | Clinical Cancer Research2013，，15： | 1 |
| 14 | Quercetin prevents LPS-induced high-mobility group Box 1 release and proinflammatory func-tion显示文摘 | Daolin Tang Rui Kang Weimin Xiao | 2009 | Am J Respir Cell Mol Biol2009，41，6： | 1 |
| 15 | THE INHIBITION OF LPS-INDUCED PRODUCTION OF INFLAMMATORY CYTOKINES BY HSP70 INVOLVES INACTIVATION OF THE NF-κB PATHWAY BUT NOT THE MAPK PATHWAYS显示文摘 | Yongzhong Shi Zizhi Tu Daolin Tang Huali Zhang Meidong Liu Kangkai Wang Stuart K. Calderwood Xianzhong Xiao | 2006 | Shock2006，，3： | 1 |
| 16 | ACOD1 in immunometabolism and disease显示文摘Immunometabolism plays a fundamental role in health and diseases and involves multiple genes and signals.Aconitate decarboxylase 1(ACOD1;also known as IRG1)is emerging as a regulator of immunometabolism in inflammation and infection.Upregulation of ACOD1 expression occurs in activated immune cells(e.g.,macrophages and monocytes)in response to pathogen infection(e.g.,bacteria and viruses),pathogen-associated molecular pattern molecules(e.g.,LPS),cytokines(e.g.,TNF and IFNs),and damage-associated molecular patterns(e.g.,monosodium urate).Mechanistically,several immune receptors(e.g.,TLRs and IFNAR),adapter proteins(e.g.,MYD88),ubiquitin ligases(e.g.,A20),and transcription factors(e.g.,NF-κB,IRFs,and STATs)form complex signal transduction networks to control ACOD1 expression in a context-dependent manner.Functionally,ACOD1 mediates itaconate production,oxidative stress,and antigen processing and plays dual roles in immunity and diseases.On the one hand,activation of the ACOD1 pathway may limit pathogen infection and promote embryo implantation.On the other hand,abnormal ACOD1 expression can lead to tumor progression,neurodegenerative disease,and immune paralysis.Further understanding of the function and regulation of ACOD1 is important for the application of ACOD1-based therapeutic strategies in disease. | Runliu Wu Feng Chen Nian Wang Daolin Tang Rui Kang | 2020 | Cellular & Molecular Immunology2020，17，8： | 1 |
| 17 | The dual role of ferroptosis in pancreatic cancer: a narrative review显示文摘Pancreatic ductal adenocarcinoma is the main cause of cancer-related mortality,with a lack of effective treatments and overall survival rates far lower than other solid cancers.This clinical challenge is related to late diagnosis as well as primary or acquired resistance to therapy-induced apoptosis.Targeting nonapoptotic cell death pathways may provide alternative therapeutic strategies to overcome drug resistance.In particular,recent studies have suggested that ferroptosis,a type of iron-dependent nonapoptotic cell death,is a promising target for pancreatic ductal adenocarcinoma.Ferroptosis can be triggered by inhibiting or activating the redox or iron metabolism-related pathways,mediated by extrinsic/membrane transports(e.g.,solute carrier family 7 member 11)or intrinsic/enzymes(e.g.,glutathione peroxidase 4).Although the exact effector molecule remains obscure,reactive oxygen species-induced lipid peroxidation and subsequent plasma membrane damage appears to play a central role in mediating ferroptotic death.While treatment-induced ferroptosis is beneficial to suppress tumor growth,inflammation-related immunosuppression caused by ferroptotic damage may promote the occurrence of pancreatic ductal adenocarcinoma.In this review,we outline the latest knowledge about the regulation and function of ferroptosis in pancreatic tumorigenesis and therapy. | Daolin Tang Xin Chen Paul B.Comish Rui Kang | 2021 | Journal of Pancreatology2021，4，2： | 1 |
| 18 | Quercetin Prevents LPS-Induced High-Mobility Group Box 1 Release and Proin? ammatory Function显示文摘 | DAOLIN TANG RUI KANG WEIMIN XIAO | 2009 | Am J Respir Cell Mol Bi- ol2009，，41： | 1 |
| 19 | Hypoxia induced HMGB1 and mitochondrial DNA interactions mediate tumor growth in hepatocellular carcinoma through Toll-like receptor 9显示文摘 | Yao Liu Wei Yan Samer Tohme Man Chen Yu Fu Dean Tian Michael Lotze Daolin Tang Allan Tsung | 2015 | Journal of Hepatology2015，，： | 1 |
| 20 | Bilirubin inhibits the anticancer activity of sorafenib by blocking MCL-1 degradation in hepatocellular carcinoma cells显示文摘Objective:Sorafenib is a first-line drug for advanced hepatocellular carcinoma(HCC).Unfortunately,most patients with HCC do not respond to sorafenib,mainly because of the frequent development of drug resistance.Bilirubin is an end metabolite of heme catabolism and an indicator of liver function,but its direct role in regulating the anticancer activity of sorafenib in HCC cells is unclear.In the current study,we aimed to investigate the mechanism of action of bilirubin in sorafenib-mediated tumor suppression in HCC.Methods:A retrospective observational cohort of 100 patients receiving sorafenib was conducted to evaluate the potential role of bilirubin in predicting the prognosis of patients with HCC.Human HCC cell lines were treated with sorafenib in the absence or presence of bilirubin,and cell proliferation,apoptosis,and signaling pathways were assayed.The antagonistic effect of bilirubin toward sorafenib was assessed in nude mice bearing HCC xenografts.Results:Serum levels of bilirubin(including total,direct,and indirect bilirubin)negatively correlated with the overall survival of patients with HCC treated with sorafenib(P<0.05).Both in vitro and in vivo analyses demonstrated that bilirubin significantly abrogated sorafenib-mediated proliferation inhibition and apoptosis induction in HCC cells(P<0.05).Mechanically,bilirubin inhibited sorafenib-induced activation of GSK-3βand subsequent downstream MCL-1 degradation.Conclusions:Our study provides experimental evidence of the antagonistic effect of bilirubin toward sorafenib-mediated anticancer activity in HCC,and it suggests that bilirubin could be used to predict the efficacy of sorafenib treatment. | Leyi Yao Qian Zhao Ding Yan Ziying Lei Yali Hao Jinghong Chen Qian Xue Xiaofen Li Qingtian Huang Daolin Tang QPing Dou Xin Chen Jinbao Liu | 2022 | Cancer Biology & Medicine2022，19，7： | 0 |
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