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Wentao Qiao

Researcher at Nankai University

Publications -  85
Citations -  1508

Wentao Qiao is an academic researcher from Nankai University. The author has contributed to research in topics: Virus & Transactivation. The author has an hindex of 19, co-authored 80 publications receiving 1278 citations. Previous affiliations of Wentao Qiao include Chinese Ministry of Education.

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The N-Terminal Region of IFITM3 Modulates Its Antiviral Activity by Regulating IFITM3 Cellular Localization

TL;DR: It is found that deleting this 21-amino-acid region relocates IFITM3 from the endosomal compartments to the cell periphery and suggests that its N-terminal region is specifically required for controlling pH-dependent viruses.
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Identification of an endocytic signal essential for the antiviral action of IFITM3

TL;DR: A critical sorting signal, namely 20‐YEML‐23, is identified that controls both the endocytic trafficking and the antiviral action of IFITM3 and reveals that as an endocytosed protein, IFITm3 first arrives at the plasma membrane before it is endocyTosed and further traffics to the late endosomes where it acts to impede virus entry.
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The MOV10 Helicase Inhibits LINE-1 Mobility

TL;DR: It is demonstrated that a helicase named MOV10 contributes to the cellular control of LINE-1 replication, and Mutating the helicase motifs impairs this function of MOV10, suggesting that MOV10 requires its helicase activity to suppress LINE- 1 replication.
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Design, synthesis and antiviral activity of novel quinazolinones.

TL;DR: A series of quinazolinones were designed and synthesized as novel HIV-1 inhibitors and found to exhibit good anti-TMV activity, of which compo und 9a showed similar in vivo anti- TMV activity to commercial plant virucide Ribavirin.
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The highly polymorphic cyclophilin A-binding loop in HIV-1 capsid modulates viral resistance to MxB.

TL;DR: The results demonstrate the existence of MxB-resistant T/F HIV-1 strains and indicates the significant selective pressure of M xB on HIV- 1 replication in vivo especially given that this viral resistance mechanism operates at expense of losing CypA.