PPIases Par14/Par17 Affect HBV Replication in Multiple Ways.
PPIases Par14/Par17 Affect HBV Replication in Multiple Ways.
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DOI：
10.3390/v15020457
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发表时间：
2023-02-06
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影响因子：
--
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中科院分区：
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--
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人细小蛋白14（Par 14）和细小蛋白17（Par 17）是肽基脯氨酰顺/反异构酶，通过结合HBc和核心颗粒的保守133 Arg-Pro 134（RP）基序和HBx的19 RP 20 - 28 RP 29基序来上调B肝炎病毒（HBV）复制。在没有HBx的情况下，Par 14/Par 17对HBV复制没有影响。与Par 14/Par 17的相互作用增强了HBx、核心颗粒和HBc的稳定性。Par 14/Par 17结合核心颗粒的外部和内部，并参与HBc二聚体-二聚体相互作用以促进核心颗粒组装。尽管HBc RP基序对于HBV复制是重要的，但R133残基对于其与Par 14/Par 17的相互作用是唯一重要的。Par 14和Par 17与HBx的相互作用涉及两个底物结合残基，分别为Glu 46/Asp 74（E46/D 74）和E71/D99，并促进HBx转运到细胞核和线粒体。在HBx存在下，Par 14/Par 17被有效地募集到cccDNA，并通过特异性DNA结合残基Ser 19/44（S19/44）促进转录激活。Par 14的S19和E46/D 74以及Par 17的S44和E71/D99也参与HBc募集到cccDNA上。Par 14/Par 17通过多种作用上调HBV复制，这些作用部分通过HBx-Par 14/Par 17-cccDNA复合物和细胞核中的三重HBc、Par 14/Par 17和cccDNA相互作用以及细胞质中的核心颗粒-Par 14/Par 17相互作用介导。
Human parvulin 14 (Par14) and parvulin 17 (Par17) are peptidyl-prolyl cis/trans isomerases that upregulate hepatitis B virus (HBV) replication by binding to the conserved 133Arg-Pro134 (RP) motif of HBc and core particles, and 19RP20-28RP29 motifs of HBx. In the absence of HBx, Par14/Par17 have no effect on HBV replication. Interaction with Par14/Par17 enhances the stability of HBx, core particles, and HBc. Par14/Par17 binds outside and inside core particles and is involved in HBc dimer–dimer interaction to facilitate core particle assembly. Although HBc RP motif is important for HBV replication, R133 residue is solely important for its interaction with Par14/Par17. Interaction of Par14 and Par17 with HBx involves two substrate-binding residues, Glu46/Asp74 (E46/D74) and E71/D99, respectively, and promotes HBx translocation to the nucleus and mitochondria. In the presence of HBx, Par14/Par17 are efficiently recruited to cccDNA and promote transcriptional activation via specific DNA-binding residues Ser19/44 (S19/44). S19 and E46/D74 of Par14, and S44 and E71/D99 of Par17, are also involved in the recruitment of HBc onto cccDNA. Par14/Par17 upregulate HBV replication via various effects that are mediated in part through the HBx–Par14/Par17–cccDNA complex and triple HBc, Par14/Par17, and cccDNA interactions in the nucleus, as well as via core particle-Par14/Par17 interactions in the cytoplasm.
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