A Transmembrane Serine Protease Is Linked to the Severe Acute Respiratory Syndrome Coronavirus Receptor and Activates Virus Entry

By Ana Shulla, T. Heald-Sargent, G. Subramanya, Jincun Zhao, S. Perlman, T. Gallagher. Journal of Virology, 2010

664 citations recorded by the source corpus.

Subfields: Epidemiology, Infectious Diseases

View Paper: https://www.semanticscholar.org/paper/2c9e704a16a25f8af034e895794dd36899ed7b52

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Citations in the corpus

SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor (2020, background): “, 2005) and the serine protease TMPRSS2 (Glowacka et al., 2011; Matsuyama et al., 2010; Shulla et al., 2011) for S protein priming in cell lines, and inhibition of both proteases is required for robust blockade of viral entry (Kawase et al.”
Mechanisms of Coronavirus Cell Entry Mediated by the Viral Spike Protein (2012, background): “TMPRSS2 likely plays a key role in the initial infection and spread of the virus; however the importance of this protease on SARS-CoV infection results from a fine balance between two antagonist effects on infection: shedding of the receptor and fusion activation.”
Tracking Changes in SARS-CoV-2 Spike: Evidence that D614G Increases Infectivity of the COVID-19 Virus (2020, positive): “TMPRSS2, a type-II transmembrane serine protease, cleaves the viral Spike after receptor binding to enhance entry of MERSCoV, SARS-CoV, and SARS-CoV-2 (Hoffmann et al., 2020b; Kleine-Weber et al., 2018; Matsuyama et al., 2020; Millet and Whittaker, 2014; Park et al., 2016; Shulla et al., 2011; Zang ”
SARS-CoV-2 and Coronavirus Disease 2019: What We Know So Far (2020, background): “It has been suggested that cells in which ACE-2 and TMPRSS2 are simultaneously present are most susceptible to entry by SARS-CoV [23] .”
Enhanced isolation of SARS-CoV-2 by TMPRSS2-expressing cells (2020, background): “greatly promotes replication and syncytium formation in these viruses in vitro and in vivo (5, 6, 11, 12, 15).”
Structural insights into coronavirus entry (2019, background): “…activity and/or virus entry into host cells using experiments of inhibition of intracellular proteases (Burkard et al., 2014; Frana et al., 1985; Simmons et al., 2005; Yamada and Liu, 2009) and/or substitutions of residues at the S1/S2 or S2’ cleavage sites (Belouzard et al., 2009; Li et al.,…”
SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues (2020, positive): “Activation events proximal to the plasma membrane have been shown to be most effective for SARS-CoV entry (Shulla et al., 2011).”
A Multibasic Cleavage Site in the Spike Protein of SARS-CoV-2 Is Essential for Infection of Human Lung Cells (2020, positive): “Our previous work revealed that the activity of the cellular serine protease TMPRSS2, which activates several coronaviruses (Bertram et al., 2013; Gierer et al., 2013; Glowacka et al., 2011; Matsuyama et al., 2010; Shirato et al., 2013, 2016; Shulla et al., 2011), is also required for robust SARS-Co”