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Xiufen Lei

Researcher at University of Texas Health Science Center at San Antonio

Publications -  14
Citations -  911

Xiufen Lei is an academic researcher from University of Texas Health Science Center at San Antonio. The author has contributed to research in topics: Lytic cycle & Kaposi's sarcoma-associated herpesvirus. The author has an hindex of 8, co-authored 12 publications receiving 849 citations. Previous affiliations of Xiufen Lei include University of Texas at San Antonio & Greehey Children's Cancer Research Institute.

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Journal ArticleDOI

Regulation of NF-kappaB inhibitor IkappaBalpha and viral replication by a KSHV microRNA.

TL;DR: It is shown that deletion of a 14 microRNA cluster from the KSHV genome significantly enhances viral lytic replication as a result of reduced NF-κB activity.
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Mechanisms of Kaposi's Sarcoma-Associated Herpesvirus Latency and Reactivation

TL;DR: The cellular and molecular basis of Kaposi's sarcoma-associated herpesvirus latency and reactivation is reviewed with a focus on the most recent advancements in the field.
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Reactive oxygen species hydrogen peroxide mediates Kaposi's sarcoma-associated herpesvirus reactivation from latency.

TL;DR: It is shown that the reactive oxygen species (ROS) hydrogen peroxide (H2O2) induces KSHV reactivation from latency through both autocrine and paracrine signaling, and indicates that antioxidants and anti-inflammation drugs could be promising preventive and therapeutic agents for effectively targeting K SHV replication and KSHv-related malignancies.
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Kaposi's Sarcoma-Associated Herpesvirus Latent Gene vFLIP Inhibits Viral Lytic Replication through NF-κB-Mediated Suppression of the AP-1 Pathway: a Novel Mechanism of Virus Control of Latency

TL;DR: It is shown that the KSHV latent gene vFLIP promotes viral latency by inhibiting viral lytic replication and indicates that the effect of the NF-κB pathway on K SHV replication is determined by the status of the AP-1 pathway, providing a mechanistic explanation for the contradictory role of the NPKB pathway.