肌醇六磷酸焦磷酸化介导的 AP3B1 焦磷酸化调节 HIV-1 Gag 释放。
Inositol pyrophosphate mediated pyrophosphorylation of AP3B1 regulates HIV-1 Gag release.
机构信息
Cell Biology Unit, Medical Research Council Laboratory for Molecular Cell Biology, and Department of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, United Kingdom.
出版信息
Proc Natl Acad Sci U S A. 2009 Dec 15;106(50):21161-6. doi: 10.1073/pnas.0909176106. Epub 2009 Nov 23.
High-energy inositol pyrophosphates, such as IP(7) (diphosphoinositol pentakisphosphate), can directly donate a beta-phosphate to a prephosphorylated serine residue generating pyrophosphorylated proteins. Here, we show that the beta subunit of AP-3, a clathrin-associated protein complex required for HIV-1 release, is a target of IP(7)-mediated pyrophosphorylation. We have identified Kif3A, a motor protein of the kinesin superfamily, as an AP3B1-binding partner and demonstrate that Kif3A, like the AP-3 complex, is involved in an intracellular process required for HIV-1 Gag release. Importantly, IP(7)-mediated pyrophosphorylation of AP3B1 modulates the interaction with Kif3A and, as a consequence, affects the release of HIV-1 virus-like particles. This study identifies a cellular process that is regulated by IP(7)-mediated pyrophosphorylation.
高能量肌醇六磷酸，如 IP（7）（二磷酸肌醇五磷酸），可以直接将β-磷酸基团供体给预先磷酸化的丝氨酸残基，生成焦磷酸化蛋白。在这里，我们表明，AP-3 的β亚基，一种 HIV-1 释放所需的网格蛋白相关蛋白复合物，是 IP（7）介导的焦磷酸化的靶标。我们已经鉴定出 Kif3A，一种驱动蛋白超家族的马达蛋白，作为 AP3B1 的结合伴侣，并证明 Kif3A 与 AP-3 复合物一样，参与 HIV-1 Gag 释放所需的细胞内过程。重要的是，AP3B1 的 IP（7）介导的焦磷酸化调节与 Kif3A 的相互作用，并因此影响 HIV-1 病毒样颗粒的释放。这项研究确定了一种受 IP（7）介导的焦磷酸化调节的细胞过程。
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