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10.1016/j.mehy.2020.109893

http://scihub22266oqcxt.onion/10.1016/j.mehy.2020.109893
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suck abstract from ncbi


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pmid32512290      Med+Hypotheses 2020 ; 143 (ä): 109893
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  • Expression of angiotensin-converting enzyme 2 and proteases in COVID-19 patients: A potential role of cellular FURIN in the pathogenesis of SARS-CoV-2 #MMPMID32512290
  • Drak Alsibai K
  • Med Hypotheses 2020[Oct]; 143 (ä): 109893 PMID32512290show ga
  • Recently, a mini-review was published in the Medical Hypotheses journal by Usul Afsar entitled 2019-nCoV-SARS-CoV-2 (COVID-19) infection: Cruciality of Furin and relevance with cancer. Previous studies have pointed out that disruption of the proteolytic cleavage of proteins can promote infectious and non-infectious diseases. The last few weeks have been marked by an important revelation concerning the pathophysiology of SARS-CoV-2. This new coronavirus disease (COVID-19) is a highly contagious and transmissible acute respiratory infectious disorder. SARS-CoV-2 is composed of RNA-dependent RNA polymerase and structural proteins including Spike protein (S protein). Interestingly, the FURIN, one of the proproteins of the convertase family, plays a crucial role in the maturation of viral glycoproteins. In addition, many viruses including coronaviruses, exploit FURIN for the activation of their glycoproteins. Recent data indicate that SARS-CoV-2 enters human cells by binding to angiotensin-converting enzyme 2. Subsequently, the S protein is cleaved by transmembrane protease serine 2 with the help of FURIN which facilitates the entry of the virus into the cell after binding. Furthermore, it seems that FURIN is implicated in the pathogenesis of SARS-CoV-2 and potentially in the increased rates of human-to-human transmission.
  • |*Betacoronavirus/pathogenicity/physiology[MESH]
  • |Angiotensin-Converting Enzyme 2[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/*enzymology/*etiology/immunology[MESH]
  • |Furin/genetics/*physiology[MESH]
  • |Host Microbial Interactions/physiology[MESH]
  • |Humans[MESH]
  • |Immune Tolerance[MESH]
  • |Immunity, Cellular[MESH]
  • |Pandemics[MESH]
  • |Peptidyl-Dipeptidase A/*physiology[MESH]
  • |Pneumonia, Viral/*enzymology/*etiology/immunology[MESH]
  • |Receptors, Virus/physiology[MESH]
  • |SARS-CoV-2[MESH]
  • |Spike Glycoprotein, Coronavirus/*physiology[MESH]
  • |T-Lymphocytes/immunology/physiology[MESH]


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  • suck abstract from ncbi

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