claim: the papain-like protease of coronaviruses cleaves ulk1 to its host autophagy
evidence_1: autophagy modulators have emerged as potential therapeutic candidates against sars-cov-2 but recent clinical setbacks underline the urgent need for better understanding the mechanism of viral subversion of autophagy.", "in conclusion, our study identified a new mechanism by which plpro of betacoronaviruses induces viral pathogenesis by targeting cellular autophagic pathway (word count=250) importance the recent covid-19 global pandemic alongside the 2003 sars and 2012 mers outbreaks underscore an urgent need to better understand betacoronaviruses as pathogens that pose global challenge to human health.", 
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  "to investigate whether virus-encoded proteases target this protein, we conducted in vitro and cellular cleavage assays and identified ulk1 as a novel bona fide substrate of sars-cov-2 papain-like protease (plpro).", "using murine hepatitis virus-a59 (mhv-a59) as a model betacoronavirus , time-course infections revealed a significant loss in the protein level of ulk1, a canonical autophagy regulating serine-threonine kinase, and the concomitant appearance of a possible cleavage fragment.", "consistent with this, over-expression of sars-cov-2 plpro is sufficient to impair starvation-induced canonical autophagy and disrupt formation of ulk1-atg13 complex."
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  )