scholarly journals Flow Cytometric Characterization of Accidental Cell Death Highlights Connections to Regulated Cell Death

2020 ◽  
Keyword(s):  
Cell Death ◽  
Flow Cytometric ◽  
Regulated Cell Death

scholarly journals Discovery and molecular characterization of a Bcl-2-regulated cell death pathway in schistosomes

2011 ◽  
Vol 108 (17) ◽  
pp. 6999-7003 ◽  
Author(s):  
E. F. Lee ◽  
O. B. Clarke ◽  
M. Evangelista ◽  
Z. Feng ◽  
T. P. Speed ◽  
...  
Keyword(s):  
Cell Death ◽  
Molecular Characterization ◽  
Cell Death Pathway ◽  
Regulated Cell Death

scholarly journals Simultaneous polychromatic flow cytometric detection of multiple forms of regulated cell death

APOPTOSIS ◽  
2019 ◽  
Vol 24 (5-6) ◽  
pp. 453-464 ◽  
Author(s):  
D. Bergamaschi ◽  
A. Vossenkamper ◽  
W. Y. J. Lee ◽  
P. Wang ◽  
E. Bochukova ◽  
...  
Keyword(s):  
Cell Death ◽  
Multiple Forms ◽  
Flow Cytometric ◽  
Regulated Cell Death

scholarly journals Flow Cytometry Reveals the Nature of Oncotic Cells

2019 ◽  
Vol 20 (18) ◽  
pp. 4379
Author(s):  
Anna Vossenkamper ◽  
Gary Warnes
Keyword(s):  
Cell Death ◽  
Sodium Azide ◽  
Caspase 3 ◽  
Flow Cytometric Analysis ◽  
Flow Cytometric ◽  
Regulated Cell Death ◽  
Damage Response ◽  
Induced Apoptosis ◽  
Apoptosis And Necrosis ◽  
Specific Pathway

The term necrosis is commonly applied to cells that have died via a non-specific pathway or mechanism but strictly is the description of the degradation processes involved once the plasma membrane of the cell has lost integrity. The signalling pathways potentially involved in accidental cell death (ACD) or oncosis are under-studied. In this study, the flow cytometric analysis of the intracellular antigens involved in regulated cell death (RCD) revealed the phenotypic nature of cells undergoing oncosis or necrosis. Sodium azide induced oncosis but also classic apoptosis, which was blocked by zVAD (z-Vla-Ala-Asp(OMe)-fluoromethylketone). Oncotic cells were found to be viability+ve/caspase-3–ve/RIP3+ve/–ve (Receptor-interacting serine/threonine protein kinase 3). These two cell populations also displayed a DNA damage response (DDR) phenotype pH2AX+ve/PARP–ve, cleaved PARP induced caspase independent apoptosis H2AX–ve/PARP+ve and hyper-activation or parthanatos H2AX+ve/PARP+ve. Oncotic cells with phenotype cell viability+ve/RIP3–ve/caspase-3–ve showed increased DDR and parthanatos. Necrostatin-1 down-regulated DDR in oncotic cells and increased sodium azide induced apoptosis. This flow cytometric approach to cell death research highlights the link between ACD and the RCD processes of programmed apoptosis and necrosis.

scholarly journals Characterization of dual effects induced by antimicrobial peptides: Regulated cell death or membrane disruption

2012 ◽  
Vol 1820 (7) ◽  
pp. 1062-1072 ◽  
Author(s):  
Edgar J. Paredes-Gamero ◽  
Marta N.C. Martins ◽  
Fábio A.M. Cappabianco ◽  
Jaime S. Ide ◽  
Antonio Miranda
Keyword(s):  
Cell Death ◽  
Antimicrobial Peptides ◽  
Membrane Disruption ◽  
Regulated Cell Death

Mechanisms of Regulated Cell Death: Current Perspectives

2021 ◽  
pp. 030098582110055
Author(s):  
Sara Francesca Santagostino ◽  
Charles-Antoine Assenmacher ◽  
James C. Tarrant ◽  
Adeyemi O. Adedeji ◽  
Enrico Radaelli
Keyword(s):  
Cell Death ◽  
Molecular Mechanisms ◽  
Regulated Cell Death ◽  
Morphologic Characteristics ◽  
Adaptive Processes ◽  
Molecular Machinery ◽  
Extracellular Microenvironment ◽  
Apoptosis And Necrosis ◽  
Microscopic Findings

Balancing cell survival and cell death is fundamental to development and homeostasis. Cell death is regulated by multiple interconnected signaling pathways and molecular mechanisms. Regulated cell death (RCD) is implicated in fundamental processes such as organogenesis and tissue remodeling, removal of unnecessary structures or cells, and regulation of cell numbers. RCD can also be triggered by exogenous perturbations of the intracellular or extracellular microenvironment when the adaptive processes that respond to stress fail. During the past few years, many novel forms of non-apoptotic RCD have been identified, and the characterization of RCD mechanisms at a molecular level has deepened our understanding of diseases encountered in human and veterinary medicine. Given the complexity of these processes, it has become clear that the identification of RCD cannot be based simply on morphologic characteristics and that descriptive and diagnostic terms presently used by pathologists—such as individual cell apoptosis or necrosis—appear inadequate and possibly misleading. In this review, the current understanding of the molecular machinery of each type of non-apoptotic RCD mechanisms is outlined. Due to the continuous discovery of new mechanisms or nuances of previously described processes, the limitations of the terms apoptosis and necrosis to indicate microscopic findings are also reported. In addition, the need for a standard panel of biomarkers and functional tests to adequately characterize the underlying RCD and its role as a mechanism of disease is considered.

scholarly journals Cryo-EM structural analysis of FADD:Caspase-8 complexes defines the catalytic dimer architecture for co-ordinated control of cell fate

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Joanna L. Fox ◽  
Michelle A. Hughes ◽  
Xin Meng ◽  
Nikola A. Sarnowska ◽  
Ian R. Powley ◽  
...  
Keyword(s):  
Cell Death ◽  
Structural Analysis ◽  
Cell Fate ◽  
Catalytic Domain ◽  
Caspase 8 ◽  
Type I ◽  
Signaling Complex ◽  
Catalytic Domains ◽  
Regulated Cell Death ◽  
Death Effector

AbstractRegulated cell death is essential in development and cellular homeostasis. Multi-protein platforms, including the Death-Inducing Signaling Complex (DISC), co-ordinate cell fate via a core FADD:Caspase-8 complex and its regulatory partners, such as the cell death inhibitor c-FLIP. Here, using electron microscopy, we visualize full-length procaspase-8 in complex with FADD. Our structural analysis now reveals how the FADD-nucleated tandem death effector domain (tDED) helical filament is required to orientate the procaspase-8 catalytic domains, enabling their activation via anti-parallel dimerization. Strikingly, recruitment of c-FLIPS into this complex inhibits Caspase-8 activity by altering tDED triple helix architecture, resulting in steric hindrance of the canonical tDED Type I binding site. This prevents both Caspase-8 catalytic domain assembly and tDED helical filament elongation. Our findings reveal how the plasticity, composition and architecture of the core FADD:Caspase-8 complex critically defines life/death decisions not only via the DISC, but across multiple key signaling platforms including TNF complex II, the ripoptosome, and RIPK1/RIPK3 necrosome.

Lytic regulated cell death in aquaculture fish

2021 ◽  
Author(s):  
Xiaojing Xia ◽  
Bin He ◽  
Xiulin Zhang ◽  
Zhe Cheng ◽  
Mingcheng Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Regulated Cell Death ◽  
Aquaculture Fish
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