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  1. Article ; Online: Immune evasion strategy involving propionylation by the KSHV interferon regulatory factor 1 (vIRF1).

    Jiale Shi / Xuemei Jia / Yujia He / Xinyue Ma / Xiaoyu Qi / Wan Li / Shou-Jiang Gao / Qin Yan / Chun Lu

    PLoS Pathogens, Vol 19, Iss 4, p e

    2023  Volume 1011324

    Abstract: Post-translational modifications (PTMs) are essential for host antiviral immune response and viral immune evasion. Among a set of novel acylations, lysine propionylation (Kpr) has been detected in both histone and non-histone proteins. However, whether ... ...

    Abstract Post-translational modifications (PTMs) are essential for host antiviral immune response and viral immune evasion. Among a set of novel acylations, lysine propionylation (Kpr) has been detected in both histone and non-histone proteins. However, whether protein propionylation occurs in any viral proteins and whether such modifications regulate viral immune evasion remain elusive. Here, we show that Kaposi's sarcoma-associated herpesvirus (KSHV)-encoded viral interferon regulatory factor 1 (vIRF1) can be propionylated in lysine residues, which is required for effective inhibition of IFN-β production and antiviral signaling. Mechanistically, vIRF1 promotes its own propionylation by blocking SIRT6's interaction with ubiquitin-specific peptidase 10 (USP10) leading to its degradation via a ubiquitin-proteasome pathway. Furthermore, vIRF1 propionylation is required for its function to block IRF3-CBP/p300 recruitment and repress the STING DNA sensing pathway. A SIRT6-specific activator, UBCS039, rescues propionylated vIRF1-mediated repression of IFN-β signaling. These results reveal a novel mechanism of viral evasion of innate immunity through propionylation of a viral protein. The findings suggest that enzymes involved in viral propionylation could be potential targets for preventing viral infections.
    Keywords Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2023-04-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Artemisinin Alleviates Intestinal Inflammation and Metabolic Disturbance in Ulcerative Colitis Rats Induced by DSS

    Xuemei Jia / Yunxiao Gao / Liran Liu / Yuxi Guo / Jie Wang / Hongyu Ma / Runyuan Zhao / Bolin Li / Yao Du / Qian Yang

    Evidence-Based Complementary and Alternative Medicine, Vol

    2022  Volume 2022

    Abstract: Objective. This study is aimed to reveal the possible mechanisms of artemisinin in the treatment of ulcerative colitis (UC) through bioinformatics analysis and experimental verification in UC model rats. Methods. Firstly, we searched two microarray data ... ...

    Abstract Objective. This study is aimed to reveal the possible mechanisms of artemisinin in the treatment of ulcerative colitis (UC) through bioinformatics analysis and experimental verification in UC model rats. Methods. Firstly, we searched two microarray data of the Gene Expression Omnibus (GEO) database to explore the differentially expressed genes (DEGs) between UC samples and normal samples. Then, we selected DEGs for gene ontology (GO) function enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. The acute UC model of rats was established by using 3.5% dextran sulfate sodium (DSS) for 10 days to verify the core pathway. Finally, we evaluated the therapeutic effect of artemisinin at the molecular level and used metabonomics to study the endogenous metabolites in the rat serum. Results. We screened in the GEO database and selected two eligible microarray datasets, GSE36807 and GSE9452. We performed GO function and KEGG pathway enrichment analyses of DEGs and found that these DEGs were mainly enriched in the inflammatory response, immune response, and IL-17 and NF-κB signaling pathways. Finally, we verified the IL-17 signaling pathway and key cytokines, and ELISA and immunohistochemical results showed that artemisinin could downregulate the expression of proinflammatory cytokines such as IL-1β and IL-17 in the IL-17 signaling pathway and upregulate the expression of the anti-inflammatory cytokine PPAR-γ. Metabolomics analysis showed that 33 differential metabolites were identified in the artemisinin group (AG) compared to the model group (MG). Differential metabolites were mainly involved in alanine, aspartate, and glutamate metabolism and synthesis and degradation of ketone bodies. Conclusion. In this study, we found that artemisinin can significantly inhibit the inflammatory response in UC rats and regulate metabolites and related metabolic pathways. This study provides a foundation for further research on the mechanism of artemisinin in the treatment of UC.
    Keywords Other systems of medicine ; RZ201-999
    Subject code 570
    Language English
    Publishing date 2022-01-01T00:00:00Z
    Publisher Hindawi Limited
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Correction

    Wan Li / Fei Wang / Jiale Shi / Qi Feng / Yuheng Chen / Xiaoyu Qi / Cong Wang / Hongmei Lu / Zhongmou Lu / Xuemei Jia / Qin Yan / Shou-Jiang Gao / Chun Lu

    PLoS Pathogens, Vol 18, Iss 1, p e

    Sperm associated antigen 9 promotes oncogenic KSHV-encoded interferon regulatory factor-induced cellular transformation and angiogenesis by activating the JNK/VEGFA pathway.

    2022  Volume 1010232

    Abstract: This corrects the article DOI:10.1371/journal.ppat.1008730.]. ...

    Abstract [This corrects the article DOI:10.1371/journal.ppat.1008730.].
    Keywords Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2022-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Correction

    Wan Li / Fei Wang / Jiale Shi / Qi Feng / Yuheng Chen / Xiaoyu Qi / Cong Wang / Hongmei Lu / Zhongmou Lu / Xuemei Jia / Qin Yan / Shou-Jiang Gao / Chun Lu

    PLoS Pathogens, Vol 18, Iss

    Sperm associated antigen 9 promotes oncogenic KSHV-encoded interferon regulatory factor-induced cellular transformation and angiogenesis by activating the JNK/VEGFA pathway

    2022  Volume 1

    Keywords Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2022-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: CircRNA ARFGEF1 functions as a ceRNA to promote oncogenic KSHV-encoded viral interferon regulatory factor induction of cell invasion and angiogenesis by upregulating glutaredoxin 3.

    Shuihong Yao / Xuemei Jia / Fei Wang / Liuxue Sheng / Pengxia Song / Yanhui Cao / Hongjuan Shi / Weifei Fan / Xiangya Ding / Shou-Jiang Gao / Chun Lu

    PLoS Pathogens, Vol 17, Iss 2, p e

    2021  Volume 1009294

    Abstract: Circular RNAs (circRNAs) are novel single-stranded noncoding RNAs that can decoy other RNAs to inhibit their functions. Kaposi's sarcoma (KS), caused by oncogenic Kaposi's sarcoma-associated herpesvirus (KSHV), is a highly angiogenic and invasive ... ...

    Abstract Circular RNAs (circRNAs) are novel single-stranded noncoding RNAs that can decoy other RNAs to inhibit their functions. Kaposi's sarcoma (KS), caused by oncogenic Kaposi's sarcoma-associated herpesvirus (KSHV), is a highly angiogenic and invasive vascular tumor of endothelial origin commonly found in AIDS patients. We have recently shown that KSHV-encoded viral interferon regulatory factor 1 (vIRF1) induces cell invasion, angiogenesis and cellular transformation; however, the role of circRNAs is largely unknown in the context of KSHV vIRF1. Herein, transcriptome analysis identified 22 differentially expressed cellular circRNAs regulated by vIRF1 in an endothelial cell line. Among them, circARFGEF1 was the highest upregulated circRNA. Mechanistically, vIRF1 induced circARFGEF1 transcription by binding to transcription factor lymphoid enhancer binding factor 1 (Lef1). Importantly, upregulation of circARFGEF1 was required for vIRF1-induced cell motility, proliferation and in vivo angiogenesis. circARFGEF1 functioned as a competing endogenous RNAs (ceRNAs) by binding to and inducing degradation of miR-125a-3p. Mass spectrometry analysis demonstrated that glutaredoxin 3 (GLRX3) was a direct target of miR-125a-3p. Knockdown of GLRX3 impaired cell motility, proliferation and angiogenesis induced by vIRF1. Taken together, vIRF1 transcriptionally activates circARFGEF1, potentially by binding to Lef1, to promote cell oncogenic phenotypes via inhibiting miR-125a-3p and inducing GLRX3. These findings define a novel mechanism responsible for vIRF1-induced oncogenesis and establish the scientific basis for targeting these molecules for treating KSHV-associated cancers.
    Keywords Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2021-02-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Sperm associated antigen 9 promotes oncogenic KSHV-encoded interferon regulatory factor-induced cellular transformation and angiogenesis by activating the JNK/VEGFA pathway.

    Wan Li / Fei Wang / Jiale Shi / Qi Feng / Yuheng Chen / Xiaoyu Qi / Cong Wang / Hongmei Lu / Zhongmou Lu / Xuemei Jia / Qin Yan / Shou-Jiang Gao / Chun Lu

    PLoS Pathogens, Vol 16, Iss 8, p e

    2020  Volume 1008730

    Abstract: Kaposi's sarcoma (KS), caused by Kaposi's sarcoma-associated herpesvirus (KSHV), is a highly angioproliferative disseminated tumor of endothelial cells commonly found in AIDS patients. We have recently shown that KSHV-encoded viral interferon regulatory ... ...

    Abstract Kaposi's sarcoma (KS), caused by Kaposi's sarcoma-associated herpesvirus (KSHV), is a highly angioproliferative disseminated tumor of endothelial cells commonly found in AIDS patients. We have recently shown that KSHV-encoded viral interferon regulatory factor 1 (vIRF1) mediates KSHV-induced cell motility (PLoS Pathog. 2019 Jan 30;15(1):e1007578). However, the role of vIRF1 in KSHV-induced cellular transformation and angiogenesis remains unknown. Here, we show that vIRF1 promotes angiogenesis by upregulating sperm associated antigen 9 (SPAG9) using two in vivo angiogenesis models including the chick chorioallantoic membrane assay (CAM) and the matrigel plug angiogenesis assay in mice. Mechanistically, vIRF1 interacts with transcription factor Lef1 to promote SPAG9 transcription. vIRF1-induced SPAG9 promotes the interaction of mitogen-activated protein kinase kinase 4 (MKK4) with JNK1/2 to increase their phosphorylation, resulting in enhanced VEGFA expression, angiogenesis, cell proliferation and migration. Finally, genetic deletion of ORF-K9 from KSHV genome abolishes KSHV-induced cellular transformation and impairs angiogenesis. Our results reveal that vIRF1 transcriptionally activates SPAG9 expression to promote angiogenesis and tumorigenesis via activating JNK/VEGFA signaling. These novel findings define the mechanism of KSHV induction of the SPAG9/JNK/VEGFA pathway and establish the scientific basis for targeting this pathway for treating KSHV-associated cancers.
    Keywords Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2020-08-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article: Effects of DuPont Tyvek® non-woven material mulching on fruit quality and chlorophyll fluorescence in Wanzhou Rose Orange

    Xuemei, Jia / Deng Lie / He Shaolan / Liu Yanmei / Lv Qiang / Ma Yanyan / Wang Ya / Xie Rangjin / Yang Qiong / Yi Shilai / Zheng Yongqiang

    Scientia horticulturae. 2017 May 17, v. 219

    2017  

    Abstract: To provide a theoretical basis for cultivation measures for alleviating the effects of weak daylight on citrus fruit quality, the effects of DuPont Tyvek® Non-Woven Material Mulching on Fruit Quality and Chlorophyll Fluorescence in Wanzhou Rose Orange [ ... ...

    Abstract To provide a theoretical basis for cultivation measures for alleviating the effects of weak daylight on citrus fruit quality, the effects of DuPont Tyvek® Non-Woven Material Mulching on Fruit Quality and Chlorophyll Fluorescence in Wanzhou Rose Orange [Citrus sinensis (L.) Osbeck cv Tarocco] was evaluated. At fructescence, soil surface of rose orange was applied full (FC) or half (HC) cover of DuPont Tyvek® non-woven materials, and relative light intensity, fruit quality, chlorophyll fluorescence, and other indexes were assessed. The experiment show that Tyvek® mulching significantly increased relative light intensity at different parts of the tree regardless of weather. Specifically, relative intensity of reflected light at the bottom was improved by more than 177.8%. In terms of fruit internal quality, the total soluble soiled (TSS) content of FC-treated trees was significantly increased compared with control values. However, titratable acid (TA) contents of HC-treated trees were significantly enhanced, delaying fruit ripening. Meanwhile, TA contents of FC-treated trees showed no significant changes, promoting fruit ripening. At the same time, FC and HC Tyvek® treatments significantly increased the final color index of fruits a/b. Both FC and HC treatments significantly improved peel uniformity and fresh coloring. Finally, HC and FC treatments significantly altered chlorophyll fluorescence transient and other leaf parameters; Fj, Vj, ABS/RC, RC/Cso and φDo in leaves of HC-treated trees were significantly increased, and ψo, φEo and Fv/Fo markedly decreased. Meanwhile, ABS/RC, RC/Cso and φDo in the FC group were significantly reduced, and ψo, φEo and Fv/Fo markedly increased, compared with control values. In conclusion, the FC method effectively decreases the effects of weak daylight on rose orange quality, and could improve its economic value.
    Keywords chlorophyll ; citrus fruits ; Citrus sinensis ; color ; economic valuation ; fluorescence ; fruit quality ; fruits ; leaves ; light intensity ; mulching ; ripening ; soil ; solar radiation ; titratable acidity ; trees
    Language English
    Dates of publication 2017-0517
    Size p. 31-36.
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 185557-8
    ISSN 0304-4238
    ISSN 0304-4238
    DOI 10.1016/j.scienta.2017.02.049
    Database NAL-Catalogue (AGRICOLA)

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  8. Article ; Online: Human Immunodeficiency Virus Type 1 Tat Accelerates Kaposi Sarcoma-Associated Herpesvirus Kaposin A-Mediated Tumorigenesis of Transformed Fibroblasts In Vitro as well as in Nude and Immunocompetent Mice

    Xiuying Chen / Lin Cheng / Xuemei Jia / Yi Zeng / Shuihong Yao / Zhigang Lv / Di Qin / Xin Fang / Yongliang Lei / Chun Lu

    Neoplasia : An International Journal for Oncology Research, Vol 11, Iss 12, Pp 1272-

    2009  Volume 1284

    Abstract: Kaposi sarcoma-associated herpesvirus (KSHV) is necessary but not sufficient to cause Kaposi sarcoma (KS). Coinfection with human immunodeficiency virus type 1 (HIV-1), in the absence of antiretroviral suppressive therapy, drastically increases the risk ... ...

    Abstract Kaposi sarcoma-associated herpesvirus (KSHV) is necessary but not sufficient to cause Kaposi sarcoma (KS). Coinfection with human immunodeficiency virus type 1 (HIV-1), in the absence of antiretroviral suppressive therapy, drastically increases the risk of KS. Previously, we identified that HIV-1 transactivative transcription protein (Tat) was an important cofactor that activated lytic cycle replication of KSHV. Here, we further investigated the potential of Tat to influence tumorigenesis induced by KSHV Kaposin A, a product of KSHV that was encoded by the open reading frame K12 (a KSHV-transforming gene). By using colony formation in soft agar, 3H-TdR incorporation, cell cycle, and microarray gene expression analyses, we demonstrated that Tat enhanced proliferation as well as mitogen-activated protein kinase, signal transducer and activator of transcription 3, and phosphatidylinositol 3-kinase/protein kinase B signaling induced by Kaposin A in NIH3T3 cells. Animal experiments further demonstrated that Tat accelerated tumorigenesis by Kaposin A in athymic nu/nu mice. Cells obtained from primary tumors of nude mice succeeded inducing tumors in immunocompetent mice. These data suggest that Tat can accelerate tumorigenesis induced by Kaposin A. Our data present the first line of evidence that Tat may participate in KS pathogenesis by collaborating with Kaposin A in acquired immunodeficiency syndrome (AIDS)-related KS (AIDS-KS) patients. Our data also suggest that the model for Kaposin and Tat-mediated oncogenesis will contribute to our understanding of the pathogenesis of AIDS-KS at the molecular level and may even be important in exploring a novel therapeutic method for AIDS-KS.
    Keywords Medicine ; R ; Internal medicine ; RC31-1245 ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282
    Subject code 571
    Publishing date 2009-12-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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