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- W4366245498 abstract "Zika virus (ZIKV) is a mosquito-borne flavivirus and causes an infection that is associated with neurological manifestations, including microcephaly and Guillain-Barre syndrome. The mechanism of ZIKV-mediated neuropathogenesis is not well understood. In this study, we discovered that ZIKV induces the degradation of the Numb protein, which plays a crucial role in neurogenesis by allowing asymmetric cell division during embryonic development. Our data show that ZIKV reduced the Numb protein level in a time- and dose-dependent manner. However, ZIKV infection appears to have minimal effect on the Numb transcript. Treatment of ZIKV-infected cells with a proteasome inhibitor restores the Numb protein level, which suggests the involvement of the ubiquitin-proteasome pathway. In addition, ZIKV infection shortens the half-life of the Numb protein. Among the ZIKV proteins, the capsid protein significantly reduces the Numb protein level. Immunoprecipitation of the Numb protein co-precipitates the capsid protein, indicating the interaction between these two proteins. These results provide insights into the ZIKV-cell interaction that might contribute to its impact on neurogenesis." @default.
- W4366245498 created "2023-04-20" @default.
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- W4366245498 date "2023-04-17" @default.
- W4366245498 modified "2023-10-08" @default.
- W4366245498 title "Zika Virus Induces the Degradation of the Numb Protein that is Required through Embryonic Neurogenesis" @default.
- W4366245498 doi "https://doi.org/10.20944/preprints202304.0435.v1" @default.
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