| First Author | Staring J | Year | 2018 |
| Journal | Cell Host Microbe | Volume | 23 |
| Issue | 5 | Pages | 636-643.e5 |
| PubMed ID | 29681460 | Mgi Jnum | J:272726 |
| Mgi Id | MGI:6284937 | Doi | 10.1016/j.chom.2018.03.019 |
| Citation | Staring J, et al. (2018) KREMEN1 Is a Host Entry Receptor for a Major Group of Enteroviruses. Cell Host Microbe 23(5):636-643.e5 |
| abstractText | Human type A Enteroviruses (EV-As) cause diseases ranging from hand-foot-and-mouth disease to poliomyelitis-like disease. Although cellular receptors are identified for some EV-As, they remain elusive for the majority of EV-As. We identify the cell surface molecule KREMEN1 as an entry receptor for coxsackievirus A10 (CV-A10). Whereas loss of KREMEN1 renders cells resistant to CV-A10 infection, KREMEN1 overexpression enhances CV-A10 binding to the cell surface and increases susceptibility to infection, indicating that KREMEN1 is a rate-limiting factor for CV-A10 infection. Furthermore, the extracellular domain of KREMEN1 binds CV-A10 and functions as a neutralizing agent during infection. Kremen-deficient mice are resistant to CV-A10-induced lethal paralysis, emphasizing the relevance of Kremen for infection in vivo. KREMEN1 is also essential for infection by a phylogenetic and pathogenic related group of EV-As. Collectively these findings highlight the importance of KREMEN1 for these emerging pathogens and its potential as an antiviral therapeutic target. |
