Institution
UPRRP College of Natural Sciences
About: UPRRP College of Natural Sciences is a based out in . It is known for research contribution in the topics: Apoptosis & Population. The organization has 9323 authors who have published 11826 publications receiving 284172 citations.
Topics: Apoptosis, Population, Gene, Oxidative stress, Signal transduction
Papers published on a yearly basis
Papers
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TL;DR: Hemin and CO-releasing molecules (CORM) promote Erastin-induced ferroptotic cell death, not by biliverdin and bilirubin, but by hemin and CORM accelerate the HO-1 expression in the presence of Erastsin and increase membranous lipid peroxidation.
Abstract: The oncogenic RAS-selective lethal small molecule Erastin triggers a unique iron-dependent form of nonapoptotic cell death termed ferroptosis. Ferroptosis is dependent upon the production of intracellular iron-dependent reactive oxygen species (ROS), but not other metals. However, key regulators remain unknown. The heme oxygenase (HO) is a major intracellular source of iron. In this study, the role of heme oxygenase in Erastin-triggered ferroptotic cancer cell death has been investigated. Zinc protoporphyrin IX (ZnPP), a HO-1 inhibitor, prevented Erastin-triggered ferroptotic cancer cell death. Furthermore, Erastin induced the protein and mRNA levels of HO-1 in HT-1080 fibrosarcoma cells. HO-1+/+ and HO-1-/- fibroblast, HO-1 overexpression, and chycloheximide-treated experiments revealed that the expression of HO-1 has a decisive effects in Erastin-triggered cell death. Hemin and CO-releasing molecules (CORM) promote Erastin-induced ferroptotic cell death, not by biliverdin and bilirubin. In addition, hemin and CORM accelerate the HO-1 expression in the presence of Erastin and increase membranous lipid peroxidation. Thus, HO-1 is an essential enzyme for iron-dependent lipid peroxidation during ferroptotic cell death.
376 citations
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TL;DR: It is found that postsynaptic proteins were degraded in the hippocampus by polyubiquitination after retrieval of contextual fear memory, and the infusion of proteasome inhibitor into the CA1 region immediately after retrieval prevented anisomycin-induced memory impairment, as well as the extinction of fear memory.
Abstract: Reactivated memory undergoes a rebuilding process that depends on de novo protein synthesis. This suggests that retrieval is dynamic and serves to incorporate new information into preexisting memories. However, little is known about whether or not protein degradation is involved in the reorganization of retrieved memory. We found that postsynaptic proteins were degraded in the hippocampus by polyubiquitination after retrieval of contextual fear memory. Moreover, the infusion of proteasome inhibitor into the CA1 region immediately after retrieval prevented anisomycin-induced memory impairment, as well as the extinction of fear memory. This suggests that ubiquitin- and proteasome-dependent protein degradation underlies destabilization processes after fear memory retrieval. It also provides strong evidence for the existence of reorganization processes whereby preexisting memory is disrupted by protein degradation, and updated memory is reconsolidated by protein synthesis.
375 citations
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367 citations
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University of Bristol1, University of Oregon2, Macquarie University3, Imperial College London4, University of Wyoming5, University of Exeter6, Centre national de la recherche scientifique7, Osaka City University8, University of Wisconsin-Madison9, University of New South Wales10, American Museum of Natural History11, Australian National University12, University of Bern13, Slovenian Academy of Sciences and Arts14, Sofia University15, University of Göttingen16, University of Montpellier17, Canadian Forest Service18, Geological Survey of Denmark and Greenland19, University of Newcastle20, École Polytechnique Fédérale de Lausanne21, Monash University22, Australian Nuclear Science and Technology Organisation23, University of Bremen24, UPRRP College of Natural Sciences25, University of Calgary26, University of Tennessee27, University of Cologne28, Virginia Tech29, Russian Academy of Sciences30, University of Wisconsin–Oshkosh31, Sapienza University of Rome32, Katholieke Universiteit Leuven33, University of Chile34, University of Queensland35, University of the Witwatersrand36, University of Münster37, Stockholm University38, Laval University39, Geode40, University of Franche-Comté41, University of Plymouth42, Fordham University43, University of the Free State44, Kyoto Prefectural University45, University of Orléans46, University of Kansas47, University of Geneva48, Central Washington University49, Chinese Academy of Sciences50
TL;DR: This article analyzed sedimentary charcoal records to show that the changes in fire regime over the past 21,000 yrs are predictable from changes in regional climates and showed that fire increases monotonically with changes in temperature and peaks at intermediate moisture levels.
Abstract: Climate is an important control on biomass burning, but the sensitivity of fire to changes in temperature and moisture balance has not been quantified. We analyze sedimentary charcoal records to show that the changes in fire regime over the past 21,000 yrs are predictable from changes in regional climates. Analyses of paleo- fire data show that fire increases monotonically with changes in temperature and peaks at intermediate moisture levels, and that temperature is quantitatively the most important driver of changes in biomass burning over the past 21,000 yrs. Given that a similar relationship between climate drivers and fire emerges from analyses of the interannual variability in biomass burning shown by remote-sensing observations of month-by-month burnt area between 1996 and 2008, our results signal a serious cause for concern in the face of continuing global warming.
362 citations
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TL;DR: How IR- induced EMT/CSC/oncogenic metabolism may promote resistance to radiotherapy is discussed and efforts to develop therapeutic approaches to eliminate these IR-induced adverse effects are reviewed.
Abstract: Radiation therapy is one of the major tools of cancer treatment, and is widely used for a variety of malignant tumours. Radiotherapy causes DNA damage directly by ionization or indirectly via the generation of reactive oxygen species (ROS), thereby destroying cancer cells. However, ionizing radiation (IR) paradoxically promotes metastasis and invasion of cancer cells by inducing the epithelial-mesenchymal transition (EMT). Metastasis is a major obstacle to successful cancer therapy, and is closely linked to the rates of morbidity and mortality of many cancers. ROS have been shown to play important roles in mediating the biological effects of IR. ROS have been implicated in IR-induced EMT, via activation of several EMT transcription factors—including Snail, HIF-1, ZEB1, and STAT3—that are activated by signalling pathways, including those of TGF-β, Wnt, Hedgehog, Notch, G-CSF, EGFR/PI3K/Akt, and MAPK. Cancer cells that undergo EMT have been shown to acquire stemness and undergo metabolic changes, although these points are debated. IR is known to induce cancer stem cell (CSC) properties, including dedifferentiation and self-renewal, and to promote oncogenic metabolism by activating these EMT-inducing pathways. Much accumulated evidence has shown that metabolic alterations in cancer cells are closely associated with the EMT and CSC phenotypes; specifically, the IR-induced oncogenic metabolism seems to be required for acquisition of the EMT and CSC phenotypes. IR can also elicit various changes in the tumour microenvironment (TME) that may affect invasion and metastasis. EMT, CSC, and oncogenic metabolism are involved in radioresistance; targeting them may improve the efficacy of radiotherapy, preventing tumour recurrence and metastasis. This study focuses on the molecular mechanisms of IR-induced EMT, CSCs, oncogenic metabolism, and alterations in the TME. We discuss how IR-induced EMT/CSC/oncogenic metabolism may promote resistance to radiotherapy; we also review efforts to develop therapeutic approaches to eliminate these IR-induced adverse effects.
362 citations
Authors
Showing all 9323 results
Name | H-index | Papers | Citations |
---|---|---|---|
Hyun-Chul Kim | 176 | 4076 | 183227 |
Alfred L. Goldberg | 156 | 474 | 88296 |
Stephen J. O'Brien | 153 | 1062 | 93025 |
Taeghwan Hyeon | 139 | 563 | 75814 |
Keiji Tanaka | 129 | 594 | 82885 |
Csaba Szabó | 123 | 958 | 61791 |
Young Hee Lee | 122 | 1168 | 61107 |
Angus C. Nairn | 118 | 469 | 44330 |
John P. Giesy | 114 | 1162 | 62790 |
Graham L. Collingridge | 103 | 353 | 51160 |
Ki-Hyun Kim | 99 | 1911 | 52157 |
Andrew D. Ellington | 96 | 569 | 43262 |
Nam-Gyu Park | 94 | 420 | 48648 |
Steven J. Cooke | 93 | 937 | 34644 |
Lenore Fahrig | 89 | 246 | 40968 |