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Shanping He

Researcher at University of Southern California

Publications -  5
Citations -  286

Shanping He is an academic researcher from University of Southern California. The author has contributed to research in topics: Pattern recognition receptor & Deamidation. The author has an hindex of 5, co-authored 5 publications receiving 215 citations. Previous affiliations of Shanping He include Hunan Normal University.

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Species-Specific Deamidation of cGAS by Herpes Simplex Virus UL37 Protein Facilitates Viral Replication.

TL;DR: It is reported that variation of a single amino acid residue in the innate immune sensor cGAS determines species-specific inactivation by HSV-1, and a single asparagine in human and mouse cG AS that is not conserved in many non-human primates is identified.
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Recent advances on viral manipulation of NF-κB signaling pathway.

TL;DR: This work summarizes recent studies concerning viral manipulation of the NF-κB signaling pathway downstream of pattern recognition receptors and indicates that signal transduction mediated by pattern Recognition receptors is a research frontier for both infectious disease and innate immunology.
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Viral Pseudo-Enzymes Activate RIG-I via Deamidation to Evade Cytokine Production

TL;DR: A surprising mechanism of RIG-I activation that is mediated by an enzyme is described, and it is shown that viral homologs of phosphoribosylformylglycinamidine synthetase (PFAS), although lacking intrinsic enzyme activity, recruit cellular PFAS to deamidate and activate Rig-I.
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Herpesviral G Protein-Coupled Receptors Activate NFAT to Induce Tumor Formation via Inhibiting the SERCA Calcium ATPase

TL;DR: It is reported that GPCRs of human Kaposi’s sarcoma-associated herpesvirus (kGPCR) and cytomegalovirus (US28) shortcut NFAT activation by inhibiting the sarcoplasmic reticulum calcium ATPase (SERCA), which is necessary for viral GPCR tumorigenesis.
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An Internally Translated MAVS Variant Exposes Its Amino-terminal TRAF-Binding Motifs to Deregulate Interferon Induction

TL;DR: The results collectively identify a new means by which signaling events is differentially regulated via exposing key internally embedded interaction motifs, implying a more ubiquitous regulatory role of truncated proteins arose from internal translation and other related mechanisms.