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10.1093/jmcb/mjab003

http://scihub22266oqcxt.onion/10.1093/jmcb/mjab003
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33493263!7928767!33493263
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suck abstract from ncbi


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pmid33493263      J+Mol+Cell+Biol 2021 ; 13 (3): 185-196
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  • Kidney injury molecule-1 is a potential receptor for SARS-CoV-2 #MMPMID33493263
  • Yang C; Zhang Y; Zeng X; Chen H; Chen Y; Yang D; Shen Z; Wang X; Liu X; Xiong M; Chen H; Huang K
  • J Mol Cell Biol 2021[Jul]; 13 (3): 185-196 PMID33493263show ga
  • COVID-19 patients present high incidence of kidney abnormalities, which are associated with poor prognosis and mortality. The identification of SARS-CoV-2 in the kidney of COVID-19 patients suggests renal tropism of SARS-CoV-2. However, whether there is a specific target of SARS-CoV-2 in the kidney remains unclear. Herein, by using in silico simulation, coimmunoprecipitation, fluorescence resonance energy transfer, fluorescein isothiocyanate labeling, and rational design of antagonist peptides, we demonstrate that kidney injury molecule-1 (KIM1), a molecule dramatically upregulated upon kidney injury, binds with the receptor-binding domain (RBD) of SARS-CoV-2 and facilitates its attachment to cell membrane, with the immunoglobulin variable Ig-like (Ig V) domain of KIM1 playing a key role in this recognition. The interaction between SARS-CoV-2 RBD and KIM1 is potently blockaded by a rationally designed KIM1-derived polypeptide AP2. In addition, our results also suggest interactions between KIM1 Ig V domain and the RBDs of SARS-CoV and MERS-CoV, pathogens of two severe infectious respiratory diseases. Together, these findings suggest KIM1 as a novel receptor for SARS-CoV-2 and other coronaviruses. We propose that KIM1 may thus mediate and exacerbate the renal infection of SARS-CoV-2 in a 'vicious cycle', and KIM1 could be further explored as a therapeutic target.
  • |COVID-19/*genetics/pathology/virology[MESH]
  • |Computer Simulation[MESH]
  • |Hepatitis A Virus Cellular Receptor 1/*genetics[MESH]
  • |Humans[MESH]
  • |Kidney/pathology/virology[MESH]
  • |Protein Binding/genetics[MESH]
  • |Receptors, Virus/*genetics[MESH]


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