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  1. Article ; Online: Protein S-palmitoylation in immunity

    Tandrila Das / Jacob S. Yount / Howard C. Hang

    Open Biology, Vol 11, Iss

    2021  Volume 3

    Abstract: S-palmitoylation is a reversible posttranslational lipid modification of proteins. It controls protein activity, stability, trafficking and protein–protein interactions. Recent global profiling of immune cells and targeted analysis have identified many S- ...

    Abstract S-palmitoylation is a reversible posttranslational lipid modification of proteins. It controls protein activity, stability, trafficking and protein–protein interactions. Recent global profiling of immune cells and targeted analysis have identified many S-palmitoylated immunity-associated proteins. Here, we review S-palmitoylated immune receptors and effectors, and their dynamic regulation at cellular membranes to generate specific and balanced immune responses. We also highlight how this understanding can drive therapeutic advances to pharmacologically modulate immune responses.
    Keywords s-palmitoylation ; adaptive immunity ; innate immune receptors ; innate immune effectors ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2021-03-01T00:00:00Z
    Publisher The Royal Society
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: BEX1 is a critical determinant of viral myocarditis.

    Colton R Martens / Lisa E Dorn / Adam D Kenney / Shyam S Bansal / Jacob S Yount / Federica Accornero

    PLoS Pathogens, Vol 18, Iss 2, p e

    2022  Volume 1010342

    Abstract: Viral infection of the heart is a common but underappreciated cause of heart failure. Viruses can cause direct cardiac damage by lysing infected cardiomyocytes. Inflammatory immune responses that limit viral replication can also indirectly cause damage ... ...

    Abstract Viral infection of the heart is a common but underappreciated cause of heart failure. Viruses can cause direct cardiac damage by lysing infected cardiomyocytes. Inflammatory immune responses that limit viral replication can also indirectly cause damage during infection, making regulatory factors that fine-tune these responses particularly important. Identifying and understanding these factors that regulate cardiac immune responses during infection will be essential for developing targeted treatments for virus-associated heart failure. Our laboratory has discovered Brain Expressed X-linked protein 1 (BEX1) as a novel stress-regulated pro-inflammatory factor in the heart. Here we report that BEX1 plays a cardioprotective role in the heart during viral infection. Specifically, we adopted genetic gain- and loss-of-function strategies to modulate BEX1 expression in the heart in the context of coxsackievirus B3 (CVB3)-induced cardiomyopathy and found that BEX1 limits viral replication in cardiomyocytes. Interestingly, despite the greater viral load observed in mice lacking BEX1, inflammatory immune cell recruitment in the mouse heart was profoundly impaired in the absence of BEX1. Overall, the absence of BEX1 accelerated CVB3-driven heart failure and pathologic heart remodeling. This result suggests that limiting inflammatory cell recruitment has detrimental consequences for the heart during viral infections. Conversely, transgenic mice overexpressing BEX1 in cardiomyocytes revealed the efficacy of BEX1 for counteracting viral replication in the heart in vivo. We also found that BEX1 retains its antiviral role in isolated cells. Indeed, BEX1 was necessary and sufficient to counteract viral replication in both isolated primary cardiomyocytes and mouse embryonic fibroblasts suggesting a broader applicability of BEX1 as antiviral agent that extended to viruses other than CVB3, including Influenza A and Sendai virus. Mechanistically, BEX1 regulated interferon beta (IFN-β) expression in infected cells. Overall, our study ...
    Keywords Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2022-02-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Rapalogs downmodulate intrinsic immunity and promote cell entry of SARS-CoV-2

    Guoli Shi / Abhilash I. Chiramel / Tiansheng Li / Kin Kui Lai / Adam D. Kenney / Ashley Zani / Adrian C. Eddy / Saliha Majdoul / Lizhi Zhang / Tirhas Dempsey / Paul A. Beare / Swagata Kar / Jonathan W. Yewdell / Sonja M. Best / Jacob S. Yount / Alex A. Compton

    The Journal of Clinical Investigation, Vol 132, Iss

    2022  Volume 24

    Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in immunocompromised individuals is associated with prolonged virus shedding and evolution of viral variants. Rapamycin and its analogs (rapalogs, including everolimus, temsirolimus, ... ...

    Abstract Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in immunocompromised individuals is associated with prolonged virus shedding and evolution of viral variants. Rapamycin and its analogs (rapalogs, including everolimus, temsirolimus, and ridaforolimus) are FDA approved as mTOR inhibitors for the treatment of human diseases, including cancer and autoimmunity. Rapalog use is commonly associated with an increased susceptibility to infection, which has been traditionally explained by impaired adaptive immunity. Here, we show that exposure to rapalogs increased susceptibility to SARS-CoV-2 infection in tissue culture and in immunologically naive rodents by antagonizing the cell-intrinsic immune response. We identified 1 rapalog (ridaforolimus) that was less potent in this regard and demonstrated that rapalogs promote spike-mediated entry into cells, by triggering the degradation of the antiviral proteins IFITM2 and IFITM3 via an endolysosomal remodeling program called microautophagy. Rapalogs that increased virus entry inhibited mTOR-mediated phosphorylation of the transcription factor TFEB, which facilitated its nuclear translocation and triggered microautophagy. In rodent models of infection, injection of rapamycin prior to and after virus exposure resulted in elevated SARS-CoV-2 replication and exacerbated viral disease, while ridaforolimus had milder effects. Overall, our findings indicate that preexisting use of certain rapalogs may elevate host susceptibility to SARS-CoV-2 infection and disease by activating lysosome-mediated suppression of intrinsic immunity.
    Keywords COVID-19 ; Medicine ; R
    Subject code 570
    Language English
    Publishing date 2022-12-01T00:00:00Z
    Publisher American Society for Clinical Investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Phosphor-IWS1-dependent U2AF2 splicing regulates trafficking of CAR-E-positive intronless gene mRNAs and sensitivity to viral infection

    Georgios I. Laliotis / Adam D. Kenney / Evangelia Chavdoula / Arturo Orlacchio / Abdul Kaba / Alessandro La Ferlita / Vollter Anastas / Christos Tsatsanis / Joal D. Beane / Lalit Sehgal / Vincenzo Coppola / Jacob S. Yount / Philip N. Tsichlis

    Communications Biology, Vol 4, Iss 1, Pp 1-

    2021  Volume 17

    Abstract: Laliotis et al. examine the role of the AKT3-phoshorylated RNA processing factor IWS1 and the IWS1 phosphorylation-dependent alternative splicing of U2AF2 in lung adenocarcinoma cells. The alternatively spliced variant of U2AF2 regulates the nuclear ... ...

    Abstract Laliotis et al. examine the role of the AKT3-phoshorylated RNA processing factor IWS1 and the IWS1 phosphorylation-dependent alternative splicing of U2AF2 in lung adenocarcinoma cells. The alternatively spliced variant of U2AF2 regulates the nuclear export of CAR-Epositive intronless mRNAs, including those encoding Type I interferons.
    Keywords Biology (General) ; QH301-705.5
    Language English
    Publishing date 2021-10-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Viral transport media for COVID-19 testing

    Matthew J. Mears / Michael J. Wallace / Jacob S. Yount / Lorri A. Fowler / Penny S. Jones / Peter J. Mohler / Loren E. Wold

    MethodsX, Vol 8, Iss , Pp 101433- (2021)

    2021  

    Abstract: Precautionary measures of physical isolation, social distancing, and masks have all aided in controlling the spread of COVID-19. However, detection of the virus is crucial to implement isolation of infected individuals. This paper presents the innovative ...

    Abstract Precautionary measures of physical isolation, social distancing, and masks have all aided in controlling the spread of COVID-19. However, detection of the virus is crucial to implement isolation of infected individuals. This paper presents the innovative repurposing of lab materials, workspace, and personnel in response to the COVID-19-induced shutdown and consequential shortage of commercially made virus transport media (VTM). This method for VTM production highlights the ability of standard research labs to fulfill the needs of those affected by the pandemic and potential recurrence of outbreaks. Further, the collaboration of the various entities at The Ohio State University Wexner Medical Center (OSUWMC) allowed for efficient production and distribution of VTM tubes to facilitate mass COVID-19 testing. We propose that implementation of this process by university research labs would enable quicker interventions, potentially better outcomes, and prevention of further spread of disease.
    Keywords Viral transport media ; COVID-19 ; Supply chain ; Pandemic ; Science ; Q
    Subject code 380
    Language English
    Publishing date 2021-01-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: E3 Ubiquitin Ligase NEDD4 Promotes Influenza Virus Infection by Decreasing Levels of the Antiviral Protein IFITM3.

    Nicholas M Chesarino / Temet M McMichael / Jacob S Yount

    PLoS Pathogens, Vol 11, Iss 8, p e

    2015  Volume 1005095

    Abstract: Interferon (IFN)-induced transmembrane protein 3 (IFITM3) is a cell-intrinsic factor that limits influenza virus infections. We previously showed that IFITM3 degradation is increased by its ubiquitination, though the ubiquitin ligase responsible for this ...

    Abstract Interferon (IFN)-induced transmembrane protein 3 (IFITM3) is a cell-intrinsic factor that limits influenza virus infections. We previously showed that IFITM3 degradation is increased by its ubiquitination, though the ubiquitin ligase responsible for this modification remained elusive. Here, we demonstrate that the E3 ubiquitin ligase NEDD4 ubiquitinates IFITM3 in cells and in vitro. This IFITM3 ubiquitination is dependent upon the presence of a PPxY motif within IFITM3 and the WW domain-containing region of NEDD4. In NEDD4 knockout mouse embryonic fibroblasts, we observed defective IFITM3 ubiquitination and accumulation of high levels of basal IFITM3 as compared to wild type cells. Heightened IFITM3 levels significantly protected NEDD4 knockout cells from infection by influenza A and B viruses. Similarly, knockdown of NEDD4 in human lung cells resulted in an increase in steady state IFITM3 and a decrease in influenza virus infection, demonstrating a conservation of this NEDD4-dependent IFITM3 regulatory mechanism in mouse and human cells. Consistent with the known association of NEDD4 with lysosomes, we demonstrate for the first time that steady state turnover of IFITM3 occurs through the lysosomal degradation pathway. Overall, this work identifies the enzyme NEDD4 as a new therapeutic target for the prevention of influenza virus infections, and introduces a new paradigm for up-regulating cellular levels of IFITM3 independently of IFN or infection.
    Keywords Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2015-08-01T00:00:00Z
    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 ; Online: Retraction Note

    Georgios I. Laliotis / Adam D. Kenney / Evangelia Chavdoula / Arturo Orlacchio / Abdul Kaba / Alessandro La Ferlita / Vollter Anastas / Christos Tsatsanis / Joal D. Beane / Lalit Sehgal / Vincenzo Coppola / Jacob S. Yount / Philip N. Tsichlis

    Communications Biology, Vol 4, Iss 1, Pp 1-

    Phosphor-IWS1-dependent U2AF2 splicing regulates trafficking of CAR-E-positive intronless gene mRNAs and sensitivity to viral infection

    2021  Volume 1

    Keywords Biology (General) ; QH301-705.5
    Language English
    Publishing date 2021-12-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: MG53 suppresses interferon-β and inflammation via regulation of ryanodine receptor-mediated intracellular calcium signaling

    Matthew Sermersheim / Adam D. Kenney / Pei-Hui Lin / Temet M. McMichael / Chuanxi Cai / Kristyn Gumpper / T. M. Ayodele Adesanya / Haichang Li / Xinyu Zhou / Ki-Ho Park / Jacob S. Yount / Jianjie Ma

    Nature Communications, Vol 11, Iss 1, Pp 1-

    2020  Volume 12

    Abstract: TRIM proteins are known to play critical roles in the context of viral infection. Here the authors establish MG53 (TRIM72) suppresses IFN and inflammation by modulation of ryanodine receptor related intracellular calcium induction. ...

    Abstract TRIM proteins are known to play critical roles in the context of viral infection. Here the authors establish MG53 (TRIM72) suppresses IFN and inflammation by modulation of ryanodine receptor related intracellular calcium induction.
    Keywords Science ; Q
    Language English
    Publishing date 2020-07-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Aiolos represses CD4+ T cell cytotoxic programming via reciprocal regulation of TFH transcription factors and IL-2 sensitivity

    Kaitlin A. Read / Devin M. Jones / Srijana Pokhrel / Emily D. S. Hales / Aditi Varkey / Jasmine A. Tuazon / Caprice D. Eisele / Omar Abdouni / Abbey Saadey / Melissa R. Leonard / Robert T. Warren / Michael D. Powell / Jeremy M. Boss / Emily A. Hemann / Jacob S. Yount / Gang Xin / Hazem E. Ghoneim / Chan-Wang J. Lio / Aharon G. Freud /
    Patrick L. Collins / Kenneth J. Oestreich

    Nature Communications, Vol 14, Iss 1, Pp 1-

    2023  Volume 18

    Abstract: The regulation and direction of CD4+ T cells into phenotypic and functional lineages is coordinated by a complex set of mechanisms. Here the authors show a role for Aiolos as a regulator of the CD4+ cytotoxic and T follicular helper lineages. ...

    Abstract The regulation and direction of CD4+ T cells into phenotypic and functional lineages is coordinated by a complex set of mechanisms. Here the authors show a role for Aiolos as a regulator of the CD4+ cytotoxic and T follicular helper lineages.
    Keywords Science ; Q
    Language English
    Publishing date 2023-03-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: Macaque interferon-induced transmembrane proteins limit replication of SHIV strains in an Envelope-dependent manner.

    Amit Sharma / Richard N McLaughlin / Ryan S Basom / Caroline Kikawa / Molly OhAinle / Jacob S Yount / Michael Emerman / Julie Overbaugh

    PLoS Pathogens, Vol 15, Iss 7, p e

    2019  Volume 1007925

    Abstract: HIV-1 does not persistently infect macaques due in part to restriction by several macaque host factors. This has been partially circumvented by generating chimeric SIV/HIV-1 viruses (SHIVs) that encode SIV antagonist of known restriction factors. However, ...

    Abstract HIV-1 does not persistently infect macaques due in part to restriction by several macaque host factors. This has been partially circumvented by generating chimeric SIV/HIV-1 viruses (SHIVs) that encode SIV antagonist of known restriction factors. However, most SHIVs replicate poorly in macaques unless they are further adapted in culture and/or macaques (adapted SHIVs). Therefore, development of SHIVs encoding HIV-1 sequences derived directly from infected humans without adaptation (unadapted SHIVs) has been challenging. In contrast to the adapted SHIVs, the unadapted SHIVs have lower replication kinetics in macaque lymphocytes and are sensitive to type-1 interferon (IFN). The HIV-1 Envelope (Env) in the chimeric virus determines both the reduced replication and the IFN-sensitivity differences. There is limited information on macaque restriction factors that specifically limit replication of the more biologically relevant, unadapted SHIV variants. In order to identify the IFN-induced host factor(s) that could contribute to the inhibition of SHIVs in macaque lymphocytes, we measured IFN-induced gene expression in immortalized pig-tailed macaque (Ptm) lymphocytes using RNA-Seq. We found 147 genes that were significantly upregulated upon IFN treatment in Ptm lymphocytes and 31/147 were identified as genes that encode transmembrane helices and thus are likely present in membranes where interaction with viral Env is plausible. Within this group of upregulated genes with putative membrane-localized proteins, we identified several interferon-induced transmembrane protein (IFITM) genes, including several previously uncharacterized Ptm IFITM3-related genes. An evolutionary genomic analysis of these genes suggests the genes are IFITM3 duplications not found in humans that are both within the IFITM locus and also dispersed elsewhere in the Ptm genome. We observed that Ptm IFITMs are generally packaged at higher levels in unadapted SHIVs when compared to adapted SHIVs. CRISPR/Cas9-mediated knockout of Ptm IFITMs showed that ...
    Keywords Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2019-07-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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