Muscovy duck reovirus promotes virus replication by inhibiting autophagy-lysosomal degradation pathway

2021 ◽  
Vol 253 ◽  
pp. 108945
Author(s):  
Minghui Li ◽  
Ping Yan ◽  
Xia Shen ◽  
Zhenni Liu ◽  
Quanxi Wang ◽  
...  
Keyword(s):  
Virus Replication ◽  
Degradation Pathway ◽  
Muscovy Duck ◽  
Lysosomal Degradation ◽  
Muscovy Duck Reovirus

scholarly journals Muscovy duck reovirus σNS protein triggers autophagy enhancing virus replication

2017 ◽  
Vol 14 (1) ◽  
Author(s):  
Yijian Wu ◽  
Longping Cui ◽  
Erpeng Zhu ◽  
Wuduo Zhou ◽  
Quanxi Wang ◽  
...  
Keyword(s):  
Virus Replication ◽  
Muscovy Duck ◽  
Muscovy Duck Reovirus

scholarly journals SNX17 protects integrins from degradation by sorting between lysosomal and recycling pathways

2012 ◽  
Vol 197 (2) ◽  
pp. 219-230 ◽  
Author(s):  
Florian Steinberg ◽  
Kate J. Heesom ◽  
Mark D. Bass ◽  
Peter J. Cullen
Keyword(s):  
Isotope Labeling ◽  
Degradation Pathway ◽  
Lysosomal Degradation ◽  
Sorting Nexins ◽  
Retromer Complex ◽  
Proteomic Approach ◽  
Cytoplasmic Tails ◽  
Npxy Motif ◽  
Global Identification ◽  
Insight Into

The FERM-like domain–containing sorting nexins of the SNX17/SNX27/SNX31 family have been proposed to mediate retrieval of transmembrane proteins from the lysosomal pathway. In this paper, we describe a stable isotope labeling with amino acids in culture–based quantitative proteomic approach that allows an unbiased, global identification of transmembrane cargoes that are rescued from lysosomal degradation by SNX17. This screen revealed that several integrins required SNX17 for their stability, as depletion of SNX17 led to a loss of β1 and β5 integrins and associated a subunits from HeLa cells as a result of increased lysosomal degradation. SNX17 bound to the membrane distal NPXY motif in β integrin cytoplasmic tails, thereby preventing lysosomal degradation of β integrins and their associated a subunits. Furthermore, SNX17-dependent retrieval of integrins did not depend on the retromer complex. Consistent with an effect on integrin recycling, depletion of SNX17 also caused alterations in cell migration. Our data provide mechanistic insight into the retrieval of internalized integrins from the lysosomal degradation pathway, a prerequisite for subsequent recycling of these matrix receptors.

Development of a live attenuated vaccine against Muscovy duck reovirus infection

Vaccine ◽  
2018 ◽  
Vol 36 (52) ◽  
pp. 8001-8007 ◽  
Author(s):  
Shilong Chen ◽  
Fengqiang Lin ◽  
Shaoying Chen ◽  
Qilin Hu ◽  
Xiaoxia Cheng ◽  
...  
Keyword(s):  
Muscovy Duck ◽  
Live Attenuated Vaccine ◽  
Reovirus Infection ◽  
Attenuated Vaccine ◽  
Muscovy Duck Reovirus

scholarly journals Autophagy gene-dependent intracellular immunity triggered by interferon-γ

2021 ◽  
Author(s):  
Michael R McAllaster ◽  
Jaya Bhushan ◽  
Dale R Balce ◽  
Anthony Orvedahl ◽  
Arnold Park ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Interferon Γ ◽  
Degradation Pathway ◽  
Lysosomal Degradation ◽  
Cellular Processes ◽  
Binding Domains ◽  
New Genes ◽  
Autophagy Gene ◽  
Atg Genes ◽  
Dependent Processes

Genes required for the lysosomal degradation pathway of autophagy play key roles in topologically distinct cellular processes with significant physiologic importance. One of the first-described of these ATG gene-dependent processes is the requirement for a subset of ATG genes in interferon-γ (IFNγ)-induced inhibition of Norovirus and Toxoplasma gondii replication. Herein we identified new genes that are required for or that negatively regulate this immune mechanism. Enzymes involved in the conjugation of UFM1 to target proteins including UFC1 and UBA5, negatively regulated IFNγ-induced inhibition of norovirus replication via effects of Ern1. IFNγ-induced inhibition of norovirus replication required Wipi2b and Atg9a, but not Becn1 (encoding Beclin1), Atg14, or Sqstm1. The phosphatidylinositol-3-phosphate and ATG16L1 binding domains of WIPI2B were required for IFNγ-induced inhibition of norovirus replication. Both WIPI2 and SQSTM1 were required for IFN?-induced inhibition of Toxoplasma gondii replication in HeLa cells. These studies further delineate the mechanisms of a programmable form of cytokine-induced intracellular immunity that relies on an expanding cassette of essential ATG genes to restrict the growth of phylogenetically diverse pathogens.

scholarly journals Revealing the fate of cell surface human P-glycoprotein (ABCB1): The lysosomal degradation pathway

2015 ◽  
Vol 1853 (10) ◽  
pp. 2361-2370 ◽  
Author(s):  
Kazuhiro Katayama ◽  
Khyati Kapoor ◽  
Shinobu Ohnuma ◽  
Atish Patel ◽  
William Swaim ◽  
...  
Keyword(s):  
Cell Surface ◽  
Degradation Pathway ◽  
Lysosomal Degradation ◽  
P Glycoprotein

scholarly journals Molecular characterization and expression of the S3 gene of muscovy duck reovirus strain 89026.

1999 ◽  
Vol 80 (1) ◽  
pp. 195-203 ◽  
Author(s):  
G Le Gall-Recul√© ◽  
M Cherbonnel ◽  
C Arnauld ◽  
P Blanchard ◽  
A Jestin ◽  
...  
Keyword(s):  
Molecular Characterization ◽  
Muscovy Duck ◽  
Muscovy Duck Reovirus ◽  
S3 Gene

scholarly journals An Intervention Target for Myocardial Fibrosis: Autophagy

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Chunmiao Lu ◽  
Yusong Yang ◽  
Yaping Zhu ◽  
Shichao Lv ◽  
Junping Zhang
Keyword(s):  
Cardiovascular Diseases ◽  
Myocardial Fibrosis ◽  
Collagen Synthesis ◽  
Degradation Pathway ◽  
Lysosomal Degradation ◽  
Metabolic Imbalance

Myocardial fibrosis (MF) is the result of metabolic imbalance of collagen synthesis and metabolism, which is widespread in various cardiovascular diseases. Autophagy is a lysosomal degradation pathway which is highly conserved. In recent years, research on autophagy has been increasing and the researchers have also become cumulatively aware of the specified association between autophagy and MF. This review highlights the role of autophagy in MF and the potential effects through the administration of medicine.

A TaqMan-MGB real-time RT-PCR assay with an internal amplification control for rapid detection of Muscovy duck reovirus

2020 ◽  
Vol 52 ◽  
pp. 101575
Author(s):  
Min Zheng ◽  
Xiuqin Chen ◽  
Shao Wang ◽  
Jingxiang Wang ◽  
Meiqing Huang ◽  
...  
Keyword(s):  
Real Time ◽  
Rapid Detection ◽  
Internal Amplification Control ◽  
Muscovy Duck ◽  
Rt Pcr ◽  
Pcr Assay ◽  
Muscovy Duck Reovirus

scholarly journals Autophagy Modulation in Lymphocytes From COVID-19 Patients: New Therapeutic Target in SARS-COV-2 Infection

2020 ◽  
Vol 11 ◽  
Author(s):  
Marta Vomero ◽  
Cristiana Barbati ◽  
Tania Colasanti ◽  
Alessandra Ida Celia ◽  
Mariangela Speziali ◽  
...  
Keyword(s):  
Therapeutic Potential ◽  
Degradation Pathway ◽  
The Novel ◽  
Lysosomal Degradation ◽  
Tnf Α ◽  
Evolutionarily Conserved ◽  
Novel Coronavirus ◽  
Factor Α ◽  
Necrosis Factor ◽  
Pro Inflammatory Cytokines

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the novel coronavirus, causing coronavirus disease 2019 (COVID-19). During virus infection, several pro-inflammatory cytokines are produced, leading to the “cytokine storm.” Among these, interleukin (IL)-6, tumor necrosis factor‐α (TNF‐α), and IL-1β seem to have a central role in the progression and exacerbation of the disease, leading to the recruitment of immune cells to infection sites. Autophagy is an evolutionarily conserved lysosomal degradation pathway involved in different aspects of lymphocytes functionality. The involvement of IL-6, TNF‐α, and IL-1β in autophagy modulation has recently been demonstrated. Moreover, preliminary studies showed that SARS-CoV-2 could infect lymphocytes, playing a role in the modulation of autophagy. Several anti-rheumatic drugs, now proposed for the treatment of COVID-19, could modulate autophagy in lymphocytes, highlighting the therapeutic potential of targeting autophagy in SARS-CoV-2 infection.

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