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Open AccessJournal ArticleDOI

RIP3: a molecular switch for necrosis and inflammation.

TLDR
The current understanding of the mechanisms that drive RIP3-dependent necrosis and its role in different inflammatory diseases is reviewed.
Abstract
The receptor-interacting protein kinase 3 (RIP3/RIPK3) has emerged as a critical regulator of programmed necrosis/ necroptosis, an inflammatory form of cell death with important functions in pathogen-induced and sterile inflammation. RIP3 activation is tightly regulated by phosphorylation, ubiquitination, and caspase-mediated cleavage. These post-translational modifications coordinately regulate the assembly of a macromolecular signaling complex termed the necrosome. Recently, several reports indicate that RIP3 can promote inflammation independent of its pronecrotic activity. Here, we review our current understanding of the mechanisms that drive RIP3-dependent necrosis and its role in different inflammatory diseases.

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Journal ArticleDOI

Necroptosis in Hepatosteatotic Ischaemia-Reperfusion Injury

TL;DR: The effect of hepatic steatosis during liver transplantation as well as molecular mechanisms of necroptosis and its involvement during liver IR injury are focused on.
Journal ArticleDOI

Dynamin-Related Protein 1 Deficiency Leads to Receptor-Interacting Protein Kinase 3-Mediated Necroptotic Neurodegeneration.

TL;DR: Testing whether neurodegeneration involves necrotic cell death by generating Purkinje cell-specific Drp1-knockout mice that lack the receptor-interacting protein kinase 3 (Rip3), which regulates necroptosis found that the loss of Rip3 significantly delays the degeneration of Drp 1-KOPurkinje neurons.
Journal ArticleDOI

NLRP3 inflammasome in NMDA-induced retinal excitotoxicity.

TL;DR: Results indicate that NMDA‐mediated retinal excitotoxicity induces immune cell recruitment and NLRP3 inflammasome activity even though inflammaome‐mediated neuroinflammation is not a leading contributing factor to cell death in this type of retinal injury.
Journal ArticleDOI

A novel function of RIP1 in postnatal development and immune homeostasis by protecting against RIP3-dependent necroptosis and FADD-mediated apoptosis

TL;DR: The data show that the postnatal developmental defect in rip1−/− mice is due in part to FADD-mediated apoptosis as well as RIP3-dependent necroptosis, and the function of RIP1 contributes to development of lpr diseases.
Journal ArticleDOI

Necrosis and necroptosis in germ cell depletion from mammalian ovary.

TL;DR: Prevention of necrosis and necroptosis pathways using their specific inhibitors could enhance growth/differentiation factor‐9 expression, improve survivability as well as the meiotic competency of oocytes, and prevent decline of reproductive potential in several mammalian species and early onset of menopause in women.
References
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Journal ArticleDOI

Hallmarks of cancer: the next generation.

TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.
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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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Cancer-related inflammation.

TL;DR: The molecular pathways of this cancer-related inflammation are now being unravelled, resulting in the identification of new target molecules that could lead to improved diagnosis and treatment.
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An endotoxin-induced serum factor that causes necrosis of tumors

TL;DR: It is proposed that TNF mediates endotoxin-induced tumor necrosis, and that it may be responsible for the suppression of transformed cells by activated macrophages.
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Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death

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.
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