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Literature summary for 2.3.2.27 extracted from

  • Ma-Lauer, Y.; Carbajo-Lozoya, J.; Hein, M.; Mueller, M.; Deng, W.; Lei, J.; Meyer, B.; Kusov, Y.; Von Brunn, B.; Bairad, D.; Huenten, S.; Drosten, C.; Hermeking, H.; Leonhardt, H.; Mann, M.; Hilgenfeld, R.; Von Brunn, A.
    P53 down-regulates SARS coronavirus replication and is targeted by the SARS-unique domain and PLpro via E3 ubiquitin ligase RCHY1 (2016), Proc. Natl. Acad. Sci. USA, 113, E5192-E5201 .
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Application

Application Comment Organism
medicine human coronaviruses antagonize the viral inhibitor p53 via stabilizing RCHY1 and promoting RCHY1-mediated p53 degradation Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens Q96PM5 isoform RCHY1
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Synonyms

Synonyms Comment Organism
RCHY1
-
 Homo sapiens

General Information

General Information Comment Organism
physiological function isoform RCHY1 is an interacting partner of the viral SARS-unique domain (SUD) and papain-like protease (PLpro). Residues 95-144 of RCHY1 and 389-652 of SUD (SUD-NM) are crucial for interaction. Association with SUD increases the stability of RCHY1 and augments RCHY1-mediated ubiquitination as well as degradation of p53. The calcium/calmodulin-dependent protein kinase II delta (CAMK2D) also binds to SUD. The PLpros from SARSCoV, MERS-CoV, and HCoV-NL63 also physically interact with and stabilize RCHY1, and thus trigger degradation of endogenous p53. A SUD-PLpro fusion interacts with RCHY1 more intensively and causes stronger p53 degradation than SARS-CoV PLpro alone. p53 inhibits replication of infectious SARS-CoV as well as of replicons and human coronavirus NL63 Homo sapiens