<scp>RIP</scp>
            1 negatively regulates basal autophagic flux through
            <scp>TFEB</scp>
            to control sensitivity to apoptosis

Yonekawa, Tohru; Gamez, Graciela; Kim, Jihye; Tan, Aik Choon; Thorburn, Jackie; Gump, Jacob M.; Thorburn, Andrew; Morgan, Michael J.

doi:10.15252/embr.201439496

Cited by 58 publications

(39 citation statements)

References 23 publications

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“…Recently, it has been shown that RIP1 negatively regulates basal levels of autophagy in a kinase-independent manner (Yonekawa et al, 2015). The negative regulation of autophagy by RIP1 was accomplished through the phosphorylation and consequent negative regulation of TFEB, a transcription factor that induces expression of autophagy-related genes (Yonekawa et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

“…The negative regulation of autophagy by RIP1 was accomplished through the phosphorylation and consequent negative regulation of TFEB, a transcription factor that induces expression of autophagy-related genes (Yonekawa et al, 2015). Whereas RIP1 is required for TNFα-induced RIP3-dependent necroptosis, recent evidence has shown that RIP1 negatively regulates TRIF-mediated, IFN-mediated and spontaneous RIP3-dependent necroptosis in a kinase independent fashion (Dillon et al, 2014; Kaiser et al, 2014; Rickard et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

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RIP3 Regulates Autophagy and Promotes Coxsackievirus B3 Infection of Intestinal Epithelial Cells

Harris

Morosky

Drummond

et al. 2015

Cell Host & Microbe

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Summary Receptor Interacting Protein Kinase-3 (RIP3) is an essential kinase for necroptotic cell death signaling and has been implicated in antiviral cell death signaling upon DNA virus infection. Here, we performed high-throughout RNAi screening and identified RIP3 as a positive regulator of coxsackievirus B3 (CVB) replication in intestinal epithelial cells (IECs). RIP3 regulates autophagy, a process utilized by CVB for viral replication factory assembly, and depletion of RIP3 inhibits autophagic flux and leads to the accumulation of autophagosomes and amphisomes. Additionally, later in infection, RIP3 is cleaved by the CVB-encoded cysteine protease 3Cpro, which serves to abrogate RIP3-mediated necrotic signaling and induce a non-necrotic form of cell death. Taken together, our results show that temporal targeting of RIP3 allows CVB to benefit from its roles in regulating autophagy while inhibiting the induction of necroptotic cell death.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

RIP3 Regulates Autophagy and Promotes Coxsackievirus B3 Infection of Intestinal Epithelial Cells

Harris

Morosky

Drummond

et al. 2015

Cell Host & Microbe

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show abstract

“…Although autophagy can protect against cell death, apoptosis can suppress autophagy, inducing caspase-mediated cleavage of essential autophagy proteins such as Beclin 1 56 . Moreover, RIP1 also represses basal autophagy by activating ERK and subsequently inhibits TFEB-mediated expression of autophagy-related and lysosome genes 57 .…”

Section: Interactions Of Apoptosis Necrosis and Autophagymentioning

confidence: 99%

Linking Pathogenic Mechanisms of Alcoholic Liver Disease With Clinical Phenotypes

et al. 2016

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Alcoholic liver disease (ALD) develops in approximately 20% of alcoholics, with a higher prevalence in females. ALD progression is marked by fatty liver and hepatocyte necrosis, as well as apoptosis, inflammation, regenerating nodules, fibrosis, and cirrhosis 1. ALD develops via a complex process involving parenchymal and non-parenchymal cells, as well as recruitment of other cell types to the liver in response to damage and inflammation. Hepatocytes are damaged by ethanol, via generation of reactive oxygen species and induction of endoplasmic reticulum stress and mitochondrial dysfunction. Hepatocyte cell death via apoptosis and necrosis are markers of ethanol-induced liver injury. We review the mechanisms by which alcohol injures hepatocytes and the response of hepatic sinusoidal cells to alcohol-induced injury. We also discuss how recent insights into the pathogenesis of ALD will affect treatment and management of patients.

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“…In addition, RIP1 also activates ERK and represses basal autophagy by inhibiting TFEB-mediated expression of autophagy-related and lysosomal genes (Yonekawa et al, 2015). Therefore, there is a complicated mutual regulatory network among autophagy, apoptosis and necroptosis.…”

Section: Other Forms Of Regulated Programmed Cell Death In Aldmentioning

confidence: 99%

A Mechanistic Review of Cell Death in Alcohol‐Induced Liver Injury

Wang

Pacher

et al. 2016

Alcoholism Clin & Exp Res

108

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Alcoholic liver disease is a major health problem in the United States and worldwide without successful treatments. Chronic alcohol consumption can lead to alcoholic liver disease (ALD), which is characterized by steatosis, inflammation, fibrosis, cirrhosis and even liver cancer. Recent studies suggest that alcohol induces both cell death and adaptive cell survival pathways in the liver, and the balance of cell death and cell survival ultimately decides the pathogenesis of ALD. This review summarizes the recent progress on the role and mechanisms of apoptosis, necroptosis and autophagy in the pathogenesis of ALD. Understanding the complex regulation of apoptosis, necrosis and autophagy may help to develop novel therapeutic strategies by targeting all three pathways simultaneously.

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RIP 1 negatively regulates basal autophagic flux through TFEB to control sensitivity to apoptosis

Cited by 58 publications

References 23 publications

RIP3 Regulates Autophagy and Promotes Coxsackievirus B3 Infection of Intestinal Epithelial Cells

RIP3 Regulates Autophagy and Promotes Coxsackievirus B3 Infection of Intestinal Epithelial Cells

Linking Pathogenic Mechanisms of Alcoholic Liver Disease With Clinical Phenotypes

A Mechanistic Review of Cell Death in Alcohol‐Induced Liver Injury

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