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10.18632/aging.103524

http://scihub22266oqcxt.onion/10.18632/aging.103524
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32575076!7343490!32575076
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suck abstract from ncbi


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pmid32575076      Aging+(Albany+NY) 2020 ; 12 (12): 11277-11286
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  • Re-analysis of SARS-CoV-2-infected host cell proteomics time-course data by impact pathway analysis and network analysis: a potential link with inflammatory response #MMPMID32575076
  • Bock JO; Ortea I
  • Aging (Albany NY) 2020[Jun]; 12 (12): 11277-11286 PMID32575076show ga
  • Coronavirus disease 2019 (COVID-19), caused by an outbreak of the severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) in Wuhan, China, has led to an unprecedented health and economic crisis worldwide. To develop treatments that can stop or lessen the symptoms and severity of SARS-CoV-2 infection, it is critical to understand how the virus behaves inside human cells, and so far studies in this area remain scarce. A recent study investigated translatome and proteome host cell changes induced in vitro by SARS-CoV-2. Here, we use the publicly available proteomics data from this study to re-analyze the in vitro cellular consequences of SARS-CoV-2 infection by impact pathways analysis and network analysis. Notably, proteins linked to the inflammatory response, but also proteins related to chromosome segregation during mitosis, were found to be altered in response to viral infection. Upregulation of inflammatory response proteins is in line with the propagation of inflammatory reaction and lung injury that is observed in advanced stages of COVID-19 patients and which worsens with age.
  • |*Proteomics[MESH]
  • |Aging[MESH]
  • |Angiotensin-Converting Enzyme 2[MESH]
  • |Betacoronavirus/*physiology[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/*virology[MESH]
  • |Gene Expression Regulation[MESH]
  • |Gene Regulatory Networks[MESH]
  • |Humans[MESH]
  • |Inflammation[MESH]
  • |Pandemics[MESH]
  • |Peptidyl-Dipeptidase A/metabolism[MESH]
  • |Pneumonia, Viral/*virology[MESH]
  • |SARS-CoV-2[MESH]


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