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10.1016/j.gene.2020.145325

http://scihub22266oqcxt.onion/10.1016/j.gene.2020.145325
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33253796!7695578!33253796
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suck abstract from ncbi


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pmid33253796      Gene 2021 ; 768 (ä): 145325
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  • The potential involvement of JAK-STAT signaling pathway in the COVID-19 infection assisted by ACE2 #MMPMID33253796
  • Luo J; Lu S; Yu M; Zhu L; Zhu C; Li C; Fang J; Zhu X; Wang X
  • Gene 2021[Feb]; 768 (ä): 145325 PMID33253796show ga
  • COVID-19, a novel identified coronavirus disease due to Severe Acute Respiratory Syndrome coronaviruses 2 (SARS-Cov-2) infection, has posed a significant threat to public health worldwide. It has been reported COVID-19 keeps substantial nucleotide similarity and shares common receptor, Angiotensin-converting enzyme 2 (ACE2) with Severe Acute Respiratory Syndrome coronaviruses (SARS-Cov). Here, we investigated the gene expression of ACE2 and identified associated pathways of SARS-Cov as a useful reference for a deepening understanding of COVID-19. The results indicated the ACE2 was overexpressed in human airway epithelial cells (HAEs), especially at 72 h after SARS-Cov infection. We found ACE2 might regulate immune response through immunological activation-associated pathways in the process of in both SARS-Cov and SARS-Cov-2 infection, where the activation of B cells, macrophages, helper T cells 1 (Th1 cells) and the inhibition of Foxp3 + regulatory T (Treg) cells and CD8 + T cells were found to be prominent. Finally, significant correlation between ACE2 and JAK-STAT signaling pathway was identified which indicate that JAK-STAT signaling pathway might involve in the downstream action of the overactivation of ACE2. These findings are expected to gain a further insight into the action mechanism of COVID-19 infection and provide a promising target for designing effective therapeutic strategies.
  • |Angiotensin-Converting Enzyme 2/*metabolism[MESH]
  • |COVID-19/genetics/*metabolism[MESH]
  • |Case-Control Studies[MESH]
  • |Humans[MESH]
  • |Janus Kinases/*metabolism[MESH]
  • |Lung/immunology/virology[MESH]
  • |STAT Transcription Factors/*metabolism[MESH]
  • |Signal Transduction[MESH]


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