Viral control of mitochondrial apoptosis.
Lorenzo Galluzzi,Catherine Brenner,Eugenia Morselli,Eugenia Morselli,Eugenia Morselli,Zahia Touat,Guido Kroemer,Guido Kroemer,Guido Kroemer +8 more
TLDR
The current knowledge on the viral modulation of mitochondrial apoptosis is summarized, by focusing in particular on the mechanisms by which viral proteins control the host cell death apparatus.Abstract:
Throughout the process of pathogen–host co-evolution, viruses have developed a battery of distinct strategies to overcome biochemical and immunological defenses of the host. Thus, viruses have acquired the capacity to subvert host cell apoptosis, control inflammatory responses, and evade immune reactions. Since the elimination of infected cells via programmed cell death is one of the most ancestral defense mechanisms against infection, disabling host cell apoptosis might represent an almost obligate step in the viral life cycle. Conversely, viruses may take advantage of stimulating apoptosis, either to kill uninfected cells from the immune system, or to induce the breakdown of infected cells, thereby favoring viral dissemination. Several viral polypeptides are homologs of host-derived apoptosis-regulatory proteins, such as members of the Bcl-2 family. Moreover, viral factors with no homology to host proteins specifically target key components of the apoptotic machinery. Here, we summarize the current knowledge on the viral modulation of mitochondrial apoptosis, by focusing in particular on the mechanisms by which viral proteins control the host cell death apparatus.read more
Citations
More filters
Journal ArticleDOI
Immunogenic Cell Death in Cancer Therapy
TL;DR: It is postulate that ICD constitutes a prominent pathway for the activation of the immune system against cancer, which in turn determines the long-term success of anticancer therapies and its subversion by pathogens.
Journal ArticleDOI
Immunogenic cell death in cancer and infectious disease
TL;DR: Current knowledge on the mechanisms that underlie the activation of immune responses against dying cells and their pathophysiological relevance are reviewed.
Journal ArticleDOI
Decoding cell death signals in liver inflammation.
Catherine Brenner,Catherine Brenner,Lorenzo Galluzzi,Lorenzo Galluzzi,Oliver Kepp,Oliver Kepp,Guido Kroemer +6 more
TL;DR: The cellular and molecular mechanisms that account for the most deleterious effect of hepatic inflammation at the cellular level are discussed, that is, the initiation of a massive cell death response among hepatocytes.
Journal ArticleDOI
The eIF2α kinases: their structures and functions
TL;DR: While significant sequence similarity exists between the eIF2α kinases in their kinase domains, underlying their common role in phosphorylating eif2α, additional unique features determine the regulation of these four proteins, that is, what signals activate them.
Journal ArticleDOI
Virus Inhibition of RIP3-Dependent Necrosis
TL;DR: In this article, the authors found that a virus-encoded inhibitor of RIP activation (vIRA) targets RIP3 during infection and disrupts RIP3-RIP1 interactions characteristic of TNFα-induced necroptosis, thereby suppressing both death pathways.
References
More filters
Journal ArticleDOI
Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death
Michael C. Wei,Michael C. Wei,Wei-Xing Zong,Emily H. Cheng,Tullia Lindsten,Vily Panoutsakopoulou,Andrea J. Ross,Kevin A. Roth,Grant R. MacGregor,Craig B. Thompson,Stanley J. Korsmeyer +10 more
TL;DR: In this article, the authors found that doubly deficient cells are resistant to multiple apoptotic stimuli that act through disruption of mitochondrial function: staurosporine, ultraviolet radiation, growth factor deprivation, etoposide, and the endoplasmic reticulum stress stimuli thapsigargin and tunicamycin.
Journal ArticleDOI
The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53
TL;DR: It is demonstrated that the E6 proteins of the oncogenic HPVs that bind p53 stimulate the degradation of p53, which results in selective degradation of cellular proteins such as p53 with negative regulatory functions provides a novel mechanism of action for dominant-acting oncoproteins.
Journal ArticleDOI
Mitochondrial Membrane Permeabilization in Cell Death
TL;DR: Once MMP has been induced, it causes the release of catabolic hydrolases and activators of such enzymes (including those of caspases) from mitochondria, meaning that mitochondria coordinate the late stage of cellular demise.
Journal ArticleDOI
Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC
TL;DR: The results indicate that the Bcl-2 family of proteins bind to the VDAC in order to regulate the mitochondrial membrane potential and the release of cytochrome c during apoptosis.
Journal ArticleDOI
Direct activation of Bax by p53 mediates mitochondrial membrane permeabilization and apoptosis.
Jerry E. Chipuk,Tomomi Kuwana,Lisa Bouchier-Hayes,Nathalie Droin,Donald D. Newmeyer,Martin Schuler,Douglas R. Green +6 more
TL;DR: It is proposed that when p53 accumulates in the cytosol, it can function analogously to the BH3-only subset of proapoptotic Bcl-2proteins to activate Bax and trigger apoptosis.