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    HEVgp9 hypothetical protein [ Hepeviridae ]

    Gene ID: 9725255, updated on 7-May-2023

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Via homophilic interactions ORF3 forms multimeric complexes associated with intracellular endoplasmic-reticulum-derived membranes. ORF3's ion channel function is evidenced by its ability to mediate ionic currents when expressed in Xenopus laevis oocytes. Several positions in ORF3 are critical for its formation of multimeric complexes, ion channel activity, and, ultimately, release of infectious particles.

    Hepatitis E virus ORF3 is a functional ion channel required for release of infectious particles.
    Ding Q, Heller B, Capuccino JM, Song B, Nimgaonkar I, Hrebikova G, Contreras JE, Ploss A., Free PMC Article

    04/28/2018
    we found that ORF3 protein downregulates TLR3-mediated NF-kappaB signaling via TRADD and RIP1. Our findings provide a new perspective on the cellular response in HEV infection and expand our understanding of the molecular mechanisms of Hepatitis E virus (HEV) pathogenesis in innate immunity.

    The ORF3 Protein of Genotype 1 Hepatitis E Virus Suppresses TLR3-induced NF-κB Signaling via TRADD and RIP1.
    He M, Wang M, Huang Y, Peng W, Zheng Z, Xia N, Xu J, Tian D., Free PMC Article

    04/28/2018
    Here, we report that the HEV X-domain directly interacts with the viral methyltransferase and the ORF3 proteins.

    Identification of critical residues in Hepatitis E virus macro domain involved in its interaction with viral methyltransferase and ORF3 proteins.
    Anang S, Subramani C, Nair VP, Kaul S, Kaushik N, Sharma C, Tiwari A, Ranjith-Kumar CT, Surjit M., Free PMC Article

    01/27/2018
    ORF3 plays a functional role in virus-cell interactions by affecting the expression of integral membrane protein and basement membrane proteins and by altering the process of apoptosis and lipid metabolism in host cells

    Transcriptome Analysis of HepG2 Cells Expressing ORF3 from Swine Hepatitis E Virus to Determine the Effects of ORF3 on Host Cells.
    Xu K, Guo S, Zhao T, Zhu H, Jiao H, Shi Q, Pang F, Li Y, Li G, Peng D, Nie X, Cheng Y, Wu K, Du L, Cui K, Zhang W, Wang F., Free PMC Article

    03/11/2017
    These results demonstrated that hepatitis E virus ORF3 attenuated lipopolysaccharide-induced cytokine production and chemotactic factors, predominantly by inhibiting various pattern recognition receptor-mediated NF-kappaB signaling pathways.

    ORF3 of Hepatitis E Virus Inhibits the Expression of Proinflammatory Cytokines and Chemotactic Factors in LPS-Stimulated Human PMA-THP1 Cells by Inhibiting NF-κB Pathway.
    Lei Q, Li L, Cai J, Huang W, Qin B, Zhang S.

    12/17/2016
    PSAP motif of OFR3 is required for hepatitis E virus exit and interaction with host TSG101.

    Replacement of the hepatitis E virus ORF3 protein PxxP motif with heterologous late domain motifs affects virus release via interaction with TSG101.
    Kenney SP, Wentworth JL, Heffron CL, Meng XJ., Free PMC Article

    06/11/2016
    These results indicate that vp13, encoded by open reading frame 3, enhances RIG-I signaling and interferon-beta biosynthesis, which may play a role in hepatitis E virus invasion.

    Enhancement of interferon induction by ORF3 product of hepatitis E virus.
    Nan Y, Ma Z, Wang R, Yu Y, Kannan H, Fredericksen B, Zhang YJ., Free PMC Article

    10/4/2014
    identified three antigenic domains at amino acids (aa) 1-28, 55-74 and 75-88 in which aa 75-88 was a dominant domain

    Characterization of antigenic domains and epitopes in the ORF3 protein of a Chinese isolate of avian hepatitis E virus.
    Zhao Q, Sun YN, Hu SB, Wang XJ, Xiao YH, Hsu WH, Xiao SQ, Wang CB, Mu Y, Hiscox JA, Zhou EM.

    05/31/2014
    Hepatitis E virus ORF3-induced miR-221/222 downregulation enhances p27(kip1) expression in HEK293 cells.

    Identification of miR-221 and -222 as important regulators in genotype IV swine hepatitis E virus ORF3-expressing HEK 293 cells.
    Cheng Y, Du L, Shi Q, Jiao H, Zhang X, Hao Y, Rong H, Zhang J, Jia X, Guo S, Kuang W, Zhang H, Chen C, Wang F.

    02/22/2014
    Data suggest that the ORF3 protein is likely to lead to an imbalance of coagulation and fibrinolysis by interacting with host proteins and triggering the corresponding pathological processes.

    Virus host protein interaction network analysis reveals that the HEV ORF3 protein may interrupt the blood coagulation process.
    Geng Y, Yang J, Huang W, Harrison TJ, Zhou Y, Wen Z, Wang Y., Free PMC Article

    08/31/2013
    The PSAP motif within the ORF3 protein of avian hepatitis E virus is not critical for viral infectivity but plays a role in virus release.

    The PSAP motif within the ORF3 protein of an avian strain of the hepatitis E virus is not critical for viral infectivity in vivo but plays a role in virus release.
    Kenney SP, Pudupakam RS, Huang YW, Pierson FW, LeRoith T, Meng XJ., Free PMC Article

    06/23/2012
    ORF3 interacts with Tsg101. The PSAP motif in ORF3 acts as an L-domain for the release of membrane-associated HEV particles from infected cells.

    Tumour susceptibility gene 101 and the vacuolar protein sorting pathway are required for the release of hepatitis E virions.
    Nagashima S, Takahashi M, Jirintai S, Tanaka T, Nishizawa T, Yasuda J, Okamoto H.

    01/14/2012
    RNA interference with siRNA inhibited mRNA accumulation and protein expression of SHEV ORF3.

    RNA interference induces effective inhibition of mRNA accumulation and protein expression of SHEV ORF3 gene in vitro.
    Liu T, Lei M, Jiao H, Du L, Cheng Y, Zhang D, Hao Y, Man C, Wang F.

    07/16/2011
    Virus egress from cells depended on open reading frame 3 (ORF3) protein, and a proline-rich sequence in ORF3 was important for egress from cultured cells and for infection of macaques.

    Release of genotype 1 hepatitis E virus from cultured hepatoma and polarized intestinal cells depends on open reading frame 3 protein and requires an intact PXXP motif.
    Emerson SU, Nguyen HT, Torian U, Burke D, Engle R, Purcell RH., Free PMC Article

    09/27/2010
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