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10.3390/ijms22105336

http://scihub22266oqcxt.onion/10.3390/ijms22105336
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34069441!8159090!34069441
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suck abstract from ncbi


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pmid34069441      Int+J+Mol+Sci 2021 ; 22 (10): ä
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  • Contribution of Syndecans to the Cellular Entry of SARS-CoV-2 #MMPMID34069441
  • Hudak A; Letoha A; Szilak L; Letoha T
  • Int J Mol Sci 2021[May]; 22 (10): ä PMID34069441show ga
  • The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel emerging pathogen causing an unprecedented pandemic in 21st century medicine. Due to the significant health and economic burden of the current SARS-CoV-2 outbreak, there is a huge unmet medical need for novel interventions effectively blocking SARS-CoV-2 infection. Unknown details of SARS-CoV-2 cellular biology hamper the development of potent and highly specific SARS-CoV-2 therapeutics. Angiotensin-converting enzyme-2 (ACE2) has been reported to be the primary receptor for SARS-CoV-2 cellular entry. However, emerging scientific evidence suggests the involvement of additional membrane proteins, such as heparan sulfate proteoglycans, in SARS-CoV-2 internalization. Here, we report that syndecans, the evolutionarily conserved family of transmembrane proteoglycans, facilitate the cellular entry of SARS-CoV-2. Among syndecans, the lung abundant syndecan-4 was the most efficient in mediating SARS-CoV-2 uptake. The S1 subunit of the SARS-CoV-2 spike protein plays a dominant role in the virus's interactions with syndecans. Besides the polyanionic heparan sulfate chains, other parts of the syndecan ectodomain, such as the cell-binding domain, also contribute to the interaction with SARS-CoV-2. During virus internalization, syndecans colocalize with ACE2, suggesting a jointly shared internalization pathway. Both ACE2 and syndecan inhibitors exhibited significant efficacy in reducing the cellular entry of SARS-CoV-2, thus supporting the complex nature of internalization. Data obtained on syndecan specific in vitro assays present syndecans as novel cellular targets of SARS-CoV-2 and offer molecularly precise yet simple strategies to overcome the complex nature of SARS-CoV-2 infection.
  • |*Virus Internalization[MESH]
  • |Amiloride/pharmacology[MESH]
  • |Angiotensin-Converting Enzyme 2/antagonists & inhibitors/metabolism[MESH]
  • |Angiotensin-Converting Enzyme Inhibitors/pharmacology[MESH]
  • |COVID-19/*metabolism/virology[MESH]
  • |Cell Line[MESH]
  • |Cell Survival/drug effects[MESH]
  • |Epithelial Sodium Channel Blockers/pharmacology[MESH]
  • |Humans[MESH]
  • |Peptides/pharmacology[MESH]
  • |Protein Domains[MESH]
  • |Receptors, Coronavirus/*metabolism[MESH]
  • |SARS-CoV-2/metabolism/*pathogenicity[MESH]
  • |Spike Glycoprotein, Coronavirus/*metabolism[MESH]
  • |Syndecan-4/antagonists & inhibitors/metabolism[MESH]


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