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Open AccessJournal ArticleDOI

Autoimmunity and the Clearance of Dead Cells

Shigekazu Nagata, +2 more
- 05 Mar 2010 - 
- Vol. 140, Iss: 5, pp 619-630
TLDR
How the endogenous components of dead cells activate the immune system through both extracellular and intracellular pathways is discussed.
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This article is published in Cell.The article was published on 2010-03-05 and is currently open access. It has received 769 citations till now. The article focuses on the topics: Innate immune system & Immune system.

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An overview of tissue and whole organ decellularization processes.

TL;DR: Tissue decellularization with preservation of ECM integrity and bioactivity can be optimized by making educated decisions regarding the agents and techniques utilized during processing.
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Control of apoptosis by the BCL-2 protein family: implications for physiology and therapy

TL;DR: The biochemical, structural and genetic studies that have clarified how the interplay between members of the BCL-2 family on mitochondria sets the apoptotic threshold are discussed, illuminating the physiological control of apoptosis, the pathological consequences of its dysregulation and the promising search for novel cancer therapies that target the BCA2 protein family.
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Programmed Cell Death in Animal Development and Disease

TL;DR: A growing body of work about the connections between apoptosis, stem cells, and cancer is explored, focusing on how apoptotic cells release a variety of signals to communicate with their cellular environment, including factors that promote cell division, tissue regeneration, and wound healing.
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Calcium-dependent phospholipid scrambling by TMEM16F

TL;DR: It is shown that TMEM16F (transmembrane protein 16F) is an essential component for the Ca2+-dependent exposure of PtdSer on the cell surface, which results from a defect in phospholipid scrambling activity and is found to carry a mutation at a splice-acceptor site of the gene encoding TMEM 16F, causing the premature termination of the protein.
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Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities

TL;DR: In advanced atherosclerotic lesions, the ratio between specialized pro-resolving mediators and pro-inflammatory lipids is strikingly low, providing a molecular explanation for the defective inflammation resolution features of these lesions.
References
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Journal ArticleDOI

Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics.

TL;DR: Apoptosis seems to be involved in cell turnover in many healthy adult tissues and is responsible for focal elimination of cells during normal embryonic development, and participates in at least some types of therapeutically induced tumour regression.
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Apoptosis by death factor.

TL;DR: This work was supported in part by Grants-in-Aid from the Ministry of Education, Science, and Culture of Japan and by a Research Grant from the Princess Takamatsu Cancer Research Fund, and performed in part through Special Coordination Funds of the Science and Technology Agency of the Japanese Government.
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Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonuclease activation

A. H. Wyllie
- 10 Apr 1980 - 
TL;DR: It is shown here that this morphological change is closely associated with excision of nucleosome chains from nuclear chromatin, apparently through activation of an intracellular, but non-lysosomal, endonuclease.
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Systemic lupus erythematosus

TL;DR: Systemic lupus erythematosus is a relapsing and remitting disease, and treatment aims are threefold: managing acute periods of potentially life-threatening ill health, minimizing the risk of flares during periods of relative stability, and controlling the less life- threatening, but often incapacitating day to day symptoms.
Journal Article

Exposure of phosphatidylserine on the surface of apoptotic lymphocytes triggers specific recognition and removal by macrophages.

TL;DR: The data suggest that macrophages specifically recognize phosphatidylserine that is exposed on the surface of lymphocytes during the development of apoptosis, and suggest that apoptotic lymphocytes lose membrane phospholipid asymmetry and expose phosphorus on the outer leaflet of the plasma membrane.
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