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HGNC Genes

SARS-CoV-2 proteins

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    SARS-CoV-2 protein Nsp1 HGNC alters actomyosin cytoskeleton and phenocopies arrhythmogenic cardiomyopathy-related PKP2 HGNC mutant

    Authors: Cristina Marquez-Lopez; Marta Roche-Molina; Nieves García-Quintáns; Silvia Sacristan; David Siniscalco; Andrés Gonzalez-Guerra; Emilio Camafeita; Mariya Lytvyn; María Isabel Guillén; David Sanz-Rosa; Daniel Martín-Pérez; Cristina Sanchez-Ramos; Ricardo Garcia; Juan Antonio Bernal; Sijia Tao; Tristan R Horton; Elizabeth N Beagle; Ernestine A Mahar; Michelle YH Lee; Joyce Cohen; Sherrie Jean; Jennifer S Wood; Fawn Connor-Stroud; Rachelle L Stammen; Olivia M Delmas; Shelly Wang; Kimberly A Cooney; Michael N Sayegh; Lanfang Wang; Daniela Weiskopf; Peter D Filev; Jesse Waggoner; Anne Piantadosi; Sudhir P Kasturi; Hilmi Al-Shakhshir; Susan P Ribeiro; Rafick P Sekaly; Rebecca D Levit; Jacob D Estes; Thomas H Vanderford; Raymond F Schinazi; Steven E Bosinger; Mirko Paiardini

    doi:10.1101/2020.09.14.296178 Date: 2020-09-16 Source: bioRxiv

    Mutations in desmosomal Plakophilin-2 HGNC ( PKP2 HGNC) are the most prevalent drivers of arrhythmogenic-cardiomyopathy MESHD ( ACM MESHD) and a common cause of sudden death MESHD in young athletes. However, partner proteins that elucidate PKP2 HGNC cellular mechanism behind cardiac dysfunction MESHD in ACM MESHD are mostly unknown. Here we identify the actin-based motor proteins Myh9 HGNC and Myh10 HGNC as key PKP2 HGNC interactors and demonstrate that expression of the ACM MESHD-related PKP2 HGNC mutant R735X alters actin fiber organization and cell mechanical stiffness. We also show that SARS-CoV-2 Nsp1 HGNC protein acts similarly to this known pathogenic R735X mutant, altering the actomyosin component distribution on cardiac cells. Our data reveal that Nsp1 HGNC hijacks PKP2 HGNC into the cytoplasm and mimics the effect of delocalized R735X mutant. These results demonstrate that cytoplasmic PKP2 HGNC drives actomyosin deregulation and structural collapse, validating a critical role of PKP2 HGNC localization in the regulation of actomyosin architecture. The fact that Nsp1 HGNC and R735X share similar phenotypes also suggests that direct SARS-CoV-2 heart infection MESHD could induce a transient ACM MESHD-like disease in COVID-19 MESHD patients, which may contribute to right ventricle dysfunction, observed in patients with poor prognosis.

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MeSH Disease
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