Research Topics
Genomes and Genes | Daolin TangSummaryAffiliation: University of Pittsburgh Country: USA Publications
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Publications
Endogenous HMGB1 regulates autophagyDaolin Tang
Damage Associated Molecular Pattern Molecule Laboratory, Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA 15219, USA
J Cell Biol 190:881-92. 2010..Thus, endogenous HMGB1 is a critical pro-autophagic protein that enhances cell survival and limits programmed apoptotic cell death...
Apoptosis promotes early tumorigenesisD Tang
Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA 15213, USA
Oncogene 30:1851-4. 2011..These findings provide important insights into the multifaceted roles of apoptosis in tumorigenesis...- High-mobility group box 1 is essential for mitochondrial quality controlDaolin Tang
Department of Surgery, G 27A Hillman Cancer Center, University of Pittsburgh Cancer Institute, Pittsburgh, PA 15219, USA
Cell Metab 13:701-11. 2011..Our findings reveal an essential role for HMGB1 in autophagic surveillance with important effects on mitochondrial quality control... - A Janus tale of two active high mobility group box 1 (HMGB1) redox statesDaolin Tang
Department of Surgery, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, United States of America
Mol Med 18:1360-2. 2012..Reduced HMGB1 protein promotes autophagy, whereas oxidized HMGB1 promotes apoptosis. Thus, the differential activity of HMGB1 in immunity, inflammation and cell death depends on the cellular redox status within tissues... - High mobility group box 1 (HMGB1) activates an autophagic response to oxidative stressDaolin Tang
Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, 5117 Centre Avenue, Pittsburgh, PA 15213, USA
Antioxid Redox Signal 15:2185-95. 2011..Autophagy, the process by which cells break down spent biochemical and damaged components, plays an important role in cell survival following stress. High mobility group box 1 (HMGB1) regulates autophagy in response to oxidative stress... - The redox protein HMGB1 regulates cell death and survival in cancer treatmentDaolin Tang
The DAMP Laboratory, Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA
Autophagy 6:1181-3. 2010..This suggests a new function for HMGB1 within the tumor microenvironment, regulating cell death and survival and suggests that it plays an important functional role in cross-regulating apoptosis and autophagy... - HMGB1 release and redox regulates autophagy and apoptosis in cancer cellsD Tang
The DAMP Laboratory, Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA
Oncogene 29:5299-310. 2010..HMGB1 release, as well as its redox state, thus links autophagy and apoptosis, representing a suitable target when coupled with conventional tumor treatments... - The expression of the receptor for advanced glycation endproducts (RAGE) is permissive for early pancreatic neoplasiaRui Kang
Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, Pittsburgh, PA 15219, USA
Proc Natl Acad Sci U S A 109:7031-6. 2012..Our results suggest a critical role for RAGE expression in the earliest stages of pancreatic carcinogenesis, potentially acting as the "autophagic switch," regulating mitochondrial STAT3 signaling... - Metabolic regulation by HMGB1-mediated autophagy and mitophagyRui Kang
The DAMP Laboratory, Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, University of Pittsburgh, PA, USA
Autophagy 7:1256-8. 2011..These findings reveal a novel pathway coupling autophagy and cellular energy metabolism... - Autophagy is required for IL-2-mediated fibroblast growthRui Kang
Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15219, USA
Exp Cell Res 319:556-65. 2013..These findings suggest that autophagy is an important pro-survival regulator for IL-2-induced cell growth in fibroblasts... - The Receptor for Advanced Glycation End-products (RAGE) protects pancreatic tumor cells against oxidative injuryRui Kang
Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, 5117 Centre Avenue, Pittsburgh, PA 15213, USA
Antioxid Redox Signal 15:2175-84. 2011..Taken together, these results suggest that RAGE is an important regulator of oxidative injury... - High-mobility group box 1, oxidative stress, and diseaseDaolin Tang
The DAMP Laboratory, Department of Surgery, G 27 Hillman Cancer Center, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania, USA
Antioxid Redox Signal 14:1315-35. 2011.... - Direct molecular interactions between HMGB1 and TP53 in colorectal cancerKristen M Livesey
Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA
Autophagy 8:846-8. 2012..Thus, HMGB1 and TP53 are critical in the cross-regulation of apoptosis and autophagy and central to colon cancer biology... 
RAGE regulates autophagy and apoptosis following oxidative injuryRui Kang
The DAMP Laboratory, Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA
Autophagy 7:442-4. 2011..These findings provide insight into how crosstalk between apoptosis and autophagy is mediated via ROS signaling with a process involving RAGE...- The receptor for advanced glycation end products promotes pancreatic carcinogenesis and accumulation of myeloid-derived suppressor cellsPhilip J Vernon
Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, Pittsburgh, PA 15219, USA
J Immunol 190:1372-9. 2013..KCR mice also maintained a significantly less suppressive milieu evidenced by marked decreases in CCL22 in relation to CXCL10 and diminished serum levels of IL-6... - AGER/RAGE-mediated autophagy promotes pancreatic tumorigenesis and bioenergetics through the IL6-pSTAT3 pathwayRui Kang
The DAMP Laboratory, Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA
Autophagy 8:989-91. 2012..Thus, AGER is an important inflammatory mediator that modulates crosstalk between prosurvival pathways, IL6-pSTAT3 and autophagy, in PDA tumor cells, and contributes to early PanIN formation... - HMGB1: a novel Beclin 1-binding protein active in autophagyRui Kang
The DAMP Laboratory, Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA
Autophagy 6:1209-11. 2010..Taken together, these findings indicate that endogenous HMGB1 functions as an autophagy effector by regulation of autophagosome formation... - HMGB1 as an autophagy sensor in oxidative stressRui Kang
DAMP Laboratory, Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, University of Pittsburgh, PA, USA
Autophagy 7:904-6. 2011..These findings provide insight into how HMGB1, a damage associated molecular pattern (DAMP), triggers autophagy as defense mechanism under conditions of cellular stress... - p53/HMGB1 complexes regulate autophagy and apoptosisKristen M Livesey
Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania 15213, USA
Cancer Res 72:1996-2005. 2012..These insights provide a novel link between HMGB1 and p53 in the cross-regulation of apoptosis and autophagy in the setting of cell stress, providing insights into their reciprocal roles in carcinogenesis... - High-mobility group box 1 and cancerDaolin Tang
The DAMP Laboratory, Department of Surgery, G 27 Hillman Cancer Center, University of Pittsburgh Cancer Institute, 5117 Centre Ave, Pittsburgh, PA 15213, USA
Biochim Biophys Acta 1799:131-40. 2010..Here, we focus on the role of HMGB1 in cancer, the mechanisms by which it contributes to carcinogenesis, and therapeutic strategies based on targeting HMGB1... - Autophagy inhibition in combination cancer treatmentKristen M Livesey
University of Pittsburgh, G 27A Hillman Cancer Center, 5117 Centre Avenue, Pittsburgh, PA 15213, USA
Curr Opin Investig Drugs 10:1269-79. 2009..Screening for new agents is ongoing, which, coupled with conventional chemotherapeutic compounds, may usher in a new generation of autophagy-inhibiting agents... - PAMPs and DAMPs: signal 0s that spur autophagy and immunityDaolin Tang
Department of Surgery, University of Pittsburgh Cancer Institute, Pittsburgh, PA 15213, USA
Immunol Rev 249:158-75. 2012..Here, we review recent advances in our understanding of autophagic molecular mechanisms and functions in emergent immunity... - DAMPs and autophagy: cellular adaptation to injury and unscheduled cell deathQiuhong Zhang
Department of Surgery, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA
Autophagy 9:451-8. 2013..Since both autophagy and DAMPs are important for pathogenesis of human disease, it is crucial to understand how they interplay to sustain homeostasis in stressful or dangerous environments... - PKR-dependent inflammatory signalsRui Kang
Department of Surgery, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA 15213, USA
Sci Signal 5:pe47. 2012..Thus, the cell stress kinase PKR has multifaceted roles in the regulation of inflammatory immune responses, and PKR and HMGB1 are attractive targets for inflammasome-associated diseases... - Damage associated molecular pattern molecule-induced microRNAs (DAMPmiRs) in human peripheral blood mononuclear cellsSebnem Unlu
Department of Surgery, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America
PLoS ONE 7:e38899. 2012..Our findings demonstrate that a specific microRNA expression signature is associated with the inflammatory response to damaged/injured cells and carries implications for many acute and chronic inflammatory disorders... - Apoptosis to autophagy switch triggered by the MHC class III-encoded receptor for advanced glycation endproducts (RAGE)Rui Kang
The DAMP Laboratory, Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA
Autophagy 7:91-3. 2011..These findings provide insight into how autophagy- and apoptosis-crossregulatory molecules interact in response to cellular stress including tumor therapy... - RAGE (Receptor for Advanced Glycation Endproducts), RAGE ligands, and their role in cancer and inflammationLouis J Sparvero
Departments of Surgery and Bioengineering, University of Pittsburgh Cancer Institute, Pittsburgh, USA
J Transl Med 7:17. 2009..Understanding the molecular structure and function of it and its ligands in the setting of inflammation is critically important in understanding the role of this receptor in tumor biology... - Life after death: targeting high mobility group box 1 in emergent cancer therapiesZ Sheng Guo
The University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine Pittsburgh, PA 15213, USA Departments of Surgery, University of Pittsburgh School of Medicine Pittsburgh, PA 15213, USA
Am J Cancer Res 3:1-20. 2013..This has significant implications for developing novel cancer therapeutics... - HMGB1 promotes drug resistance in osteosarcomaJun Huang
Departments of Orthopaedics, The Second Xiangya Hospital, Central South University, Changsha, Hunan, People s Republic of China
Cancer Res 72:230-8. 2012..Therefore, through its role as a regulator of autophagy, HMGB1 is a critical factor in the development of chemoresistance, and it offers a novel target for improving osteosarcoma therapy... - The receptor for advanced glycation end products (RAGE) sustains autophagy and limits apoptosis, promoting pancreatic tumor cell survivalR Kang
Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, Pittsburgh, PA 15232, USA
Cell Death Differ 17:666-76. 2010..Our data suggest that targeted inhibition of RAGE or its ligands may serve as novel targets to enhance current cancer therapies...