scholarly journals Disruption of the Toxoplasma gondii Parasitophorous Vacuole by IFNγ-Inducible Immunity-Related GTPases (IRG Proteins) Triggers Necrotic Cell Death

2009 ◽  
Vol 5 (2) ◽  
pp. e1000288 ◽  
Author(s):  
Yang O. Zhao ◽  
Aliaksandr Khaminets ◽  
Julia P. Hunn ◽  
Jonathan C. Howard
Keyword(s):  
Cell Death ◽  
Toxoplasma Gondii ◽  
Parasitophorous Vacuole ◽  
Necrotic Cell Death ◽  
Necrotic Cell

Oleanolic acid rich solubilized triterpene extracts from mistletoe induce apoptotic and necrotic cell death of murine B16. F10 melanoma cells

Planta Medica ◽  
2009 ◽  
Vol 75 (09) ◽  
Author(s):  
CM Strüh ◽  
S Jäger ◽  
CM Schempp ◽  
T Jakob ◽  
A Scheffler ◽  
...  
Keyword(s):  
Cell Death ◽  
Oleanolic Acid ◽  
Melanoma Cells ◽  
Necrotic Cell Death ◽  
Necrotic Cell

NADPH Oxidases: New Players in TNF-Induced Necrotic Cell Death

2007 ◽  
Vol 26 (6) ◽  
pp. 769-771 ◽  
Author(s):  
Tom Vanden Berghe ◽  
Wim Declercq ◽  
Peter Vandenabeele
Keyword(s):  
Cell Death ◽  
Necrotic Cell Death ◽  
Necrotic Cell ◽  
Nadph Oxidases

BNip3 is a mediator of TNF-induced necrotic cell death

APOPTOSIS ◽  
2010 ◽  
Vol 16 (2) ◽  
pp. 114-126 ◽  
Author(s):  
Jee-Youn Kim ◽  
Yong-Jun Kim ◽  
Sun Lee ◽  
Jae-Hoon Park
Keyword(s):  
Cell Death ◽  
Necrotic Cell Death ◽  
Necrotic Cell

scholarly journals Protein synthesis persists during necrotic cell death

2005 ◽  
Vol 168 (4) ◽  
pp. 545-551 ◽  
Author(s):  
Xavier Saelens ◽  
Nele Festjens ◽  
Eef Parthoens ◽  
Isabel Vanoverberghe ◽  
Michael Kalai ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
De Novo ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Necrotic Cell Death ◽  
Necrotic Cell ◽  
Proteolytic Activation ◽  
Double Stranded Rna ◽  
Molecular Events

Cell death is an intrinsic part of metazoan development and mammalian immune regulation. Whereas the molecular events orchestrating apoptosis have been characterized extensively, little is known about the biochemistry of necrotic cell death. Here, we show that, in contrast to apoptosis, the induction of necrosis does not lead to the shut down of protein synthesis. The rapid drop in protein synthesis observed in apoptosis correlates with caspase-dependent breakdown of eukaryotic translation initiation factor (eIF) 4G, activation of the double-stranded RNA-activated protein kinase PKR, and phosphorylation of its substrate eIF2-α. In necrosis induced by tumor necrosis factor, double-stranded RNA, or viral infection, de novo protein synthesis persists and 28S ribosomal RNA fragmentation, eIF2-α phosphorylation, and proteolytic activation of PKR are absent. Collectively, these results show that, in contrast to apoptotic cells, necrotic dying cells retain the opportunity to synthesize proteins.

scholarly journals Pegylated and nanoparticle-conjugated sulfonium salt photo triggers necrotic cell death

2016 ◽  
Vol Volume 11 ◽  
pp. 6161-6168 ◽  
Author(s):  
Alaa A Fadhel ◽  
Xiling Yue ◽  
Ebrahim H Ghazvini Zadeh ◽  
Mykhailo Bondar ◽  
Kevin D Belfield
Keyword(s):  
Cell Death ◽  
Necrotic Cell Death ◽  
Necrotic Cell ◽  
Sulfonium Salt

scholarly journals Pathogenic Connexin-31 Forms Constitutively Active Hemichannels to Promote Necrotic Cell Death

PLoS ONE ◽  
2012 ◽  
Vol 7 (2) ◽  
pp. e32531 ◽  
Author(s):  
Jingwei Chi ◽  
Li Li ◽  
Mujun Liu ◽  
Jieqiong Tan ◽  
Chengyuan Tang ◽  
...  
Keyword(s):  
Cell Death ◽  
Necrotic Cell Death ◽  
Necrotic Cell ◽  
Constitutively Active

scholarly journals Repurposing Cationic Amphiphilic Drugs and Derivatives to Engage Lysosomal Cell Death in Cancer Treatment

2020 ◽  
Vol 10 ◽  
Author(s):  
Michelle Hu ◽  
Kermit L. Carraway
Keyword(s):  
Cell Death ◽  
Tumor Cell ◽  
Cellular Transformation ◽  
Therapeutic Window ◽  
Cell Populations ◽  
Necrotic Cell Death ◽  
Necrotic Cell ◽  
Membrane Rupture ◽  
Cationic Amphiphilic Drugs ◽  
Amphiphilic Drugs

A major confounding issue in the successful treatment of cancer is the existence of tumor cell populations that resist therapeutic agents and regimens. While tremendous effort has gone into understanding the biochemical mechanisms underlying resistance to each traditional and targeted therapeutic, a broader approach to the problem may emerge from the recognition that existing anti-cancer agents elicit their cytotoxic effects almost exclusively through apoptosis. Considering the myriad mechanisms cancer cells employ to subvert apoptotic death, an attractive alternative approach would leverage programmed necrotic mechanisms to side-step therapeutic resistance to apoptosis-inducing agents. Lysosomal cell death (LCD) is a programmed necrotic cell death mechanism that is engaged upon the compromise of the limiting membrane of the lysosome, a process called lysosomal membrane permeabilization (LMP). The release of lysosomal components into the cytosol upon LMP triggers biochemical cascades that lead to plasma membrane rupture and necrotic cell death. Interestingly, the process of cellular transformation appears to render the limiting lysosomal membranes of tumor cells more fragile than non-transformed cells, offering a potential therapeutic window for drug development. Here we outline the concepts of LMP and LCD, and discuss strategies for the development of agents to engage these processes. Importantly, the potential exists for existing cationic amphiphilic drugs such as antidepressants, antibiotics, antiarrhythmics, and diuretics to be repurposed to engage LCD within therapy-resistant tumor cell populations.

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