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  1. Article ; Online: Cytometry profiling of

    Raju Paul, Susan / Scholzen, Anja / Reeves, Patrick M / Shepard, Robert / Hess, Joshua M / Dzeng, Richard K / Korek, Skylar / Garritsen, Anja / Poznansky, Mark C / Sluder, Ann E

    Frontiers in immunology

    2023  Volume 14, Page(s) 1249581

    Abstract: Introduction: Q fever, caused by the intracellular bacterium : Methods: Individuals exposed during the 2007-2010 Dutch Q fever outbreak were grouped in 2015, based on a : Results: Cytokine release analysis showed significantly elevated IL-2 ... ...

    Abstract Introduction: Q fever, caused by the intracellular bacterium
    Methods: Individuals exposed during the 2007-2010 Dutch Q fever outbreak were grouped in 2015, based on a
    Results: Cytokine release analysis showed significantly elevated IL-2 responses in all seropositive individuals and elevated IL-1β responses in those recovered from symptomatic infection. Comparative flow cytometry analysis revealed significantly increased IFNγ, TNFα and IL-2 recall responses by CD4 T cells and higher IL-6 production by monocytes from symptomatic, IGRA-positive/seropositive individuals compared to controls. Mass cytometry profiling and unsupervised clustering analysis confirmed recall responses in seropositive individuals by two activated CD4 T cell subsets, one characterized by a strong Th1 cytokine profile (IFNγ
    Discussion: These data highlight that there are long-term increased responses to
    MeSH term(s) Humans ; Coxiella burnetii ; Q Fever ; Tumor Necrosis Factor-alpha ; Interleukin-2 ; Interleukin-6 ; Cytokines ; Immunity, Innate
    Chemical Substances Tumor Necrosis Factor-alpha ; Interleukin-2 ; Interleukin-6 ; Cytokines
    Language English
    Publishing date 2023-10-11
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1249581
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Natural Exposure- and Vaccination-Induced Profiles of

    Raju Paul, Susan / Scholzen, Anja / Mukhtar, Ghazel / Wilkinson, Stephanie / Hobson, Peter / Dzeng, Richard K / Evans, Jennifer / Robson, Jennifer / Cobbold, Rowland / Graves, Stephen / Poznansky, Mark C / Garritsen, Anja / Sluder, Ann E

    Frontiers in immunology

    2022  Volume 13, Page(s) 886698

    Abstract: Q fever is a zoonotic disease caused by the highly infectious Gram-negative coccobacillus, ...

    Abstract Q fever is a zoonotic disease caused by the highly infectious Gram-negative coccobacillus,
    MeSH term(s) Australia ; Chemokine CXCL10 ; Coxiella burnetii ; Cytokines ; Humans ; Interleukin-2 ; Interleukin-6 ; Q Fever ; Retrospective Studies ; Tumor Necrosis Factor-alpha ; Vaccination/adverse effects
    Chemical Substances Chemokine CXCL10 ; Cytokines ; Interleukin-2 ; Interleukin-6 ; Tumor Necrosis Factor-alpha
    Language English
    Publishing date 2022-06-23
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.886698
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Repertoires of SARS-CoV-2 epitopes targeted by antibodies vary according to severity of COVID-19.

    Gregory, David J / Vannier, Augustin / Duey, Akiro H / Roady, Tyler J / Dzeng, Richard K / Pavlovic, Maia N / Chapin, Michael H / Mukherjee, Sonia / Wilmot, Hannah / Chronos, Nic / Charles, Richelle C / Ryan, Edward T / LaRocque, Regina C / Miller, Tyler E / Garcia-Beltran, Wilfredo F / Thierauf, Julia C / Iafrate, A John / Mullenbrock, Steven / Stump, Mark D /
    Wetzel, Randall K / Polakiewicz, Roberto D / Naranbhai, Vivek / Poznansky, Mark C

    Virulence

    2022  Volume 13, Issue 1, Page(s) 890–902

    Abstract: Antibodies to SARS-CoV-2 are central to recovery and immunity from COVID-19. However, the relationship between disease severity and the repertoire of antibodies against specific SARS-CoV-2 epitopes an individual develops following exposure remains ... ...

    Abstract Antibodies to SARS-CoV-2 are central to recovery and immunity from COVID-19. However, the relationship between disease severity and the repertoire of antibodies against specific SARS-CoV-2 epitopes an individual develops following exposure remains incompletely understood. Here, we studied seroprevalence of antibodies to specific SARS-CoV-2 and other betacoronavirus antigens in a well-annotated, community sample of convalescent and never-infected individuals obtained in August 2020. One hundred and twenty-four participants were classified into five groups: previously exposed but without evidence of infection, having no known exposure or evidence of infection, seroconverted without symptoms, previously diagnosed with symptomatic COVID-19, and recovered after hospitalization with COVID-19. Prevalence of IgGs specific to the following antigens was compared between the five groups: recombinant SARS-CoV-2 and betacoronavirus spike and nucleocapsid protein domains, peptides from a tiled array of 22-mers corresponding to the entire spike and nucleocapsid proteins, and peptides corresponding to predicted immunogenic regions from other proteins of SARS-CoV-2. Antibody abundance generally correlated positively with severity of prior illness. A number of specific immunogenic peptides and some that may be associated with milder illness or protection from symptomatic infection were identified. No convincing association was observed between antibodies to Receptor Binding Domain(s) (RBDs) of less pathogenic betacoronaviruses HKU1 or OC43 and COVID-19 severity. However, apparent cross-reaction with SARS-CoV RBD was evident and some predominantly asymptomatic individuals had antibodies to both MERS-CoV and SARS-CoV RBDs. Findings from this pilot study may inform development of diagnostics, vaccines, and therapeutic antibodies, and provide insight into viral pathogenic mechanisms.
    MeSH term(s) Antibodies, Neutralizing ; Antibodies, Viral ; COVID-19 ; Epitopes ; Humans ; Pilot Projects ; SARS-CoV-2 ; Seroepidemiologic Studies ; Spike Glycoprotein, Coronavirus
    Chemical Substances Antibodies, Neutralizing ; Antibodies, Viral ; Epitopes ; Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2
    Language English
    Publishing date 2022-05-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 2657572-3
    ISSN 2150-5608 ; 2150-5594
    ISSN (online) 2150-5608
    ISSN 2150-5594
    DOI 10.1080/21505594.2022.2073025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Phosphorylated MED1 links transcription recycling and cancer growth.

    Chen, Zhong / Ye, Zhenqing / Soccio, Raymond E / Nakadai, Tomoyoshi / Hankey, William / Zhao, Yue / Huang, Furong / Yuan, Fuwen / Wang, Hongyan / Cui, Zhifen / Sunkel, Benjamin / Wu, Dayong / Dzeng, Richard K / Thomas-Ahner, Jennifer M / Huang, Tim H M / Clinton, Steven K / Huang, Jiaoti / Lazar, Mitchell A / Jin, Victor X /
    Roeder, Robert G / Wang, Qianben

    Nucleic acids research

    2022  Volume 50, Issue 8, Page(s) 4450–4463

    Abstract: Mediator activates RNA polymerase II (Pol II) function during transcription, but it remains unclear whether Mediator is able to travel with Pol II and regulate Pol II transcription beyond the initiation and early elongation steps. By using in vitro and ... ...

    Abstract Mediator activates RNA polymerase II (Pol II) function during transcription, but it remains unclear whether Mediator is able to travel with Pol II and regulate Pol II transcription beyond the initiation and early elongation steps. By using in vitro and in vivo transcription recycling assays, we find that human Mediator 1 (MED1), when phosphorylated at the mammal-specific threonine 1032 by cyclin-dependent kinase 9 (CDK9), dynamically moves along with Pol II throughout the transcribed genes to drive Pol II recycling after the initial round of transcription. Mechanistically, MED31 mediates the recycling of phosphorylated MED1 and Pol II, enhancing mRNA output during the transcription recycling process. Importantly, MED1 phosphorylation increases during prostate cancer progression to the lethal phase, and pharmacological inhibition of CDK9 decreases prostate tumor growth by decreasing MED1 phosphorylation and Pol II recycling. Our results reveal a novel role of MED1 in Pol II transcription and identify phosphorylated MED1 as a targetable driver of dysregulated Pol II recycling in cancer.
    MeSH term(s) Animals ; Humans ; Male ; Mammals/genetics ; Mediator Complex/metabolism ; Mediator Complex Subunit 1/genetics ; Neoplasms/genetics ; Phosphorylation ; RNA Polymerase II/metabolism ; Transcription, Genetic
    Chemical Substances MED1 protein, human ; MED31 protein, human ; Mediator Complex ; Mediator Complex Subunit 1 ; RNA Polymerase II (EC 2.7.7.-)
    Language English
    Publishing date 2022-04-29
    Publishing country England
    Document type Journal Article
    ZDB-ID 186809-3
    ISSN 1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
    ISSN (online) 1362-4962 ; 1362-4954
    ISSN 0301-5610 ; 0305-1048
    DOI 10.1093/nar/gkac246
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1067: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  5. Article ; Online: Small molecule growth inhibitors of human oncogenic gammaherpesvirus infected B-cells.

    Dzeng, Richard K / Jha, Hem Chandra / Lu, Jie / Saha, Abhik / Banerjee, Sagarika / Robertson, Erle S

    Molecular oncology

    2014  Volume 9, Issue 2, Page(s) 365–376

    Abstract: Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) are two human gammaherpesviruses associated with a broad spectrum of B-cell lymphomas, most acutely in immuno-compromised populations. However, there are no drugs which ... ...

    Abstract Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) are two human gammaherpesviruses associated with a broad spectrum of B-cell lymphomas, most acutely in immuno-compromised populations. However, there are no drugs which specifically target KSHV or EBV-associated lymphomas. To identify small molecules which selectively inhibit the growth of EBV or KSHV-associated B-cell lines, we performed a fluorescence based high-throughput screen on multiple stable GFP expressing virus-infected or uninfected B-cell lines. We identified 40 initial compounds with selective growth inhibition and subsequently determined the 50% growth inhibitory concentrations (GI50) for each drug. We further examined compounds with higher specificity to explore the underlying molecular mechanisms using transcription factor analysis, as well as a shRNA based knockdown strategy. Our data identified ten compounds with relatively high efficacy for growth inhibition. Two novel small molecules, NSC#10010 and NSC#65381 were potent growth inhibitors for gammaherpesvirus-associated B-lymphomas through activation of both the NF-κB and c-Myc-mediated signaling pathways. These drugs can serve as potential lead compounds to expand the current therapeutic window against EBV or KSHV-associated human B-cell malignancies.
    MeSH term(s) Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Antiviral Agents/chemistry ; Antiviral Agents/pharmacology ; B-Lymphocytes/metabolism ; B-Lymphocytes/pathology ; B-Lymphocytes/virology ; Cell Line, Tumor ; Epstein-Barr Virus Infections/drug therapy ; Epstein-Barr Virus Infections/genetics ; Epstein-Barr Virus Infections/metabolism ; Epstein-Barr Virus Infections/pathology ; Herpesvirus 4, Human/genetics ; Herpesvirus 4, Human/metabolism ; Herpesvirus 8, Human/genetics ; Herpesvirus 8, Human/metabolism ; Humans ; Lymphoma, B-Cell/drug therapy ; Lymphoma, B-Cell/genetics ; Lymphoma, B-Cell/metabolism ; Lymphoma, B-Cell/pathology ; Lymphoma, B-Cell/virology ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics
    Chemical Substances Antineoplastic Agents ; Antiviral Agents ; MYC protein, human ; NF-kappa B ; Proto-Oncogene Proteins c-myc
    Language English
    Publishing date 2014-09-26
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2415106-3
    ISSN 1878-0261 ; 1574-7891
    ISSN (online) 1878-0261
    ISSN 1574-7891
    DOI 10.1016/j.molonc.2014.09.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6637: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
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  6. Article ; Online: Targeting PPARγ in the epigenome rescues genetic metabolic defects in mice.

    Soccio, Raymond E / Li, Zhenghui / Chen, Eric R / Foong, Yee Hoon / Benson, Kiara K / Dispirito, Joanna R / Mullican, Shannon E / Emmett, Matthew J / Briggs, Erika R / Peed, Lindsey C / Dzeng, Richard K / Medina, Carlos J / Jolivert, Jennifer F / Kissig, Megan / Rajapurkar, Satyajit R / Damle, Manashree / Lim, Hee-Woong / Won, Kyoung-Jae / Seale, Patrick /
    Steger, David J / Lazar, Mitchell A

    The Journal of clinical investigation

    2017  Volume 127, Issue 4, Page(s) 1451–1462

    Abstract: Obesity causes insulin resistance, and PPARγ ligands such as rosiglitazone are insulin sensitizing, yet the mechanisms remain unclear. In C57BL/6 (B6) mice, obesity induced by a high-fat diet (HFD) has major effects on visceral epididymal adipose tissue ( ...

    Abstract Obesity causes insulin resistance, and PPARγ ligands such as rosiglitazone are insulin sensitizing, yet the mechanisms remain unclear. In C57BL/6 (B6) mice, obesity induced by a high-fat diet (HFD) has major effects on visceral epididymal adipose tissue (eWAT). Here, we report that HFD-induced obesity in B6 mice also altered the activity of gene regulatory elements and genome-wide occupancy of PPARγ. Rosiglitazone treatment restored insulin sensitivity in obese B6 mice, yet, surprisingly, had little effect on gene expression in eWAT. However, in subcutaneous inguinal fat (iWAT), rosiglitazone markedly induced molecular signatures of brown fat, including the key thermogenic gene Ucp1. Obesity-resistant 129S1/SvImJ mice (129 mice) displayed iWAT browning, even in the absence of rosiglitazone. The 129 Ucp1 locus had increased PPARγ binding and gene expression that were preserved in the iWAT of B6x129 F1-intercrossed mice, with an imbalance favoring the 129-derived alleles, demonstrating a cis-acting genetic difference. Thus, B6 mice have genetically defective Ucp1 expression in iWAT. However, when Ucp1 was activated by rosiglitazone, or by iWAT browning in cold-exposed or young mice, expression of the B6 version of Ucp1 was no longer defective relative to the 129 version, indicating epigenomic rescue. These results provide a framework for understanding how environmental influences like drugs can affect the epigenome and potentially rescue genetically determined disease phenotypes.
    MeSH term(s) Animals ; Diet, High-Fat/adverse effects ; Epigenesis, Genetic ; Hypoglycemic Agents/pharmacology ; Intra-Abdominal Fat/metabolism ; Male ; Mice, 129 Strain ; Mice, Inbred C57BL ; Obesity/metabolism ; PPAR gamma/physiology ; Protein Binding ; Regulatory Elements, Transcriptional ; Subcutaneous Fat, Abdominal/metabolism ; Thiazolidinediones/pharmacology ; Transcriptional Activation ; Transcriptome ; Uncoupling Protein 1/genetics ; Uncoupling Protein 1/metabolism
    Chemical Substances Hypoglycemic Agents ; PPAR gamma ; Thiazolidinediones ; Ucp1 protein, mouse ; Uncoupling Protein 1 ; rosiglitazone (05V02F2KDG)
    Language English
    Publishing date 2017-04-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI91211
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ua VI Zs.184: Show issues Location:
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