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  1. Article ; Online: Distinct Radiation Responses in Virus-Positive and Virus-Negative Merkel Cell Carcinoma.

    Ahmed, Mona M / Rivas, Hembly G / Frost, Thomas C / DeCaprio, James A

    The Journal of investigative dermatology

    2022  Volume 143, Issue 1, Page(s) 166–169.e5

    MeSH term(s) Humans ; Carcinoma, Merkel Cell/pathology ; Merkel cell polyomavirus ; Tumor Virus Infections/pathology ; Skin Neoplasms/pathology ; Polyomavirus Infections/pathology
    Language English
    Publishing date 2022-08-08
    Publishing country United States
    Document type Letter ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 80136-7
    ISSN 1523-1747 ; 0022-202X
    ISSN (online) 1523-1747
    ISSN 0022-202X
    DOI 10.1016/j.jid.2022.07.015
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui VI Zs.124: Show issues Location:
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  2. Article ; Online: Shutoff of Host Gene Expression in Influenza A Virus and Herpesviruses: Similar Mechanisms and Common Themes.

    Rivas, Hembly G / Schmaling, Summer K / Gaglia, Marta M

    Viruses

    2016  Volume 8, Issue 4, Page(s) 102

    Abstract: The ability to shut off host gene expression is a shared feature of many viral infections, and it is thought to promote viral replication by freeing host cell machinery and blocking immune responses. Despite the molecular differences between viruses, an ... ...

    Abstract The ability to shut off host gene expression is a shared feature of many viral infections, and it is thought to promote viral replication by freeing host cell machinery and blocking immune responses. Despite the molecular differences between viruses, an emerging theme in the study of host shutoff is that divergent viruses use similar mechanisms to enact host shutoff. Moreover, even viruses that encode few proteins often have multiple mechanisms to affect host gene expression, and we are only starting to understand how these mechanisms are integrated. In this review we discuss the multiplicity of host shutoff mechanisms used by the orthomyxovirus influenza A virus and members of the alpha- and gamma-herpesvirus subfamilies. We highlight the surprising similarities in their mechanisms of host shutoff and discuss how the different mechanisms they use may play a coordinated role in gene regulation.
    MeSH term(s) Animals ; Gene Expression Regulation ; Herpesviridae/physiology ; Herpesviridae Infections/genetics ; Herpesviridae Infections/metabolism ; Herpesviridae Infections/virology ; Host-Pathogen Interactions/genetics ; Humans ; Influenza A virus/physiology ; Influenza, Human/genetics ; Influenza, Human/metabolism ; Influenza, Human/virology ; Proteolysis ; RNA Splicing ; RNA Stability ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Transcription, Genetic ; Virus Replication
    Chemical Substances RNA, Messenger
    Keywords covid19
    Language English
    Publishing date 2016-04-16
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2516098-9
    ISSN 1999-4915 ; 1999-4915
    ISSN (online) 1999-4915
    ISSN 1999-4915
    DOI 10.3390/v8040102
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Disrupting the DREAM complex enables proliferation of adult human pancreatic β cells.

    Wang, Peng / Karakose, Esra / Argmann, Carmen / Wang, Huan / Balev, Metodi / Brody, Rachel I / Rivas, Hembly G / Liu, Xinyue / Wood, Olivia / Liu, Hongtao / Choleva, Lauryn / Hasson, Dan / Bernstein, Emily / Paulo, Joao A / Scott, Donald K / Lambertini, Luca / DeCaprio, James A / Stewart, Andrew F

    The Journal of clinical investigation

    2022  Volume 132, Issue 15

    Abstract: Resistance to regeneration of insulin-producing pancreatic β cells is a fundamental challenge for type 1 and type 2 diabetes. Recently, small molecule inhibitors of the kinase DYRK1A have proven effective in inducing adult human β cells to proliferate, ... ...

    Abstract Resistance to regeneration of insulin-producing pancreatic β cells is a fundamental challenge for type 1 and type 2 diabetes. Recently, small molecule inhibitors of the kinase DYRK1A have proven effective in inducing adult human β cells to proliferate, but their detailed mechanism of action is incompletely understood. We interrogated our human insulinoma and β cell transcriptomic databases seeking to understand why β cells in insulinomas proliferate, while normal β cells do not. This search reveals the DREAM complex as a central regulator of quiescence in human β cells. The DREAM complex consists of a module of transcriptionally repressive proteins that assemble in response to DYRK1A kinase activity, thereby inducing and maintaining cellular quiescence. In the absence of DYRK1A, DREAM subunits reassemble into the pro-proliferative MMB complex. Here, we demonstrate that small molecule DYRK1A inhibitors induce human β cells to replicate by converting the repressive DREAM complex to its pro-proliferative MMB conformation.
    MeSH term(s) Adult ; Cell Proliferation ; Diabetes Mellitus, Type 2 ; Humans ; Insulin-Secreting Cells/metabolism ; Insulinoma/genetics ; Pancreatic Neoplasms ; Protein Serine-Threonine Kinases/genetics ; Protein-Tyrosine Kinases/metabolism
    Chemical Substances Protein-Tyrosine Kinases (EC 2.7.10.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2022-06-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI157086
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.184: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: MMB-FOXM1-driven premature mitosis is required for CHK1 inhibitor sensitivity.

    Branigan, Timothy B / Kozono, David / Schade, Amy E / Deraska, Peter / Rivas, Hembly G / Sambel, Larissa / Reavis, Hunter D / Shapiro, Geoffrey I / D'Andrea, Alan D / DeCaprio, James A

    Cell reports

    2021  Volume 34, Issue 9, Page(s) 108808

    Abstract: To identify genes whose loss confers resistance to CHK1 inhibitors, we perform genome-wide CRISPR-Cas9 screens in non-small-cell lung cancer (NSCLC) cell lines treated with the CHK1 inhibitor prexasertib (CHK1i). Five of the top six hits of the screens, ... ...

    Abstract To identify genes whose loss confers resistance to CHK1 inhibitors, we perform genome-wide CRISPR-Cas9 screens in non-small-cell lung cancer (NSCLC) cell lines treated with the CHK1 inhibitor prexasertib (CHK1i). Five of the top six hits of the screens, MYBL2 (B-MYB), LIN54, FOXM1, cyclin A2 (CCNA2), and CDC25B, are cell-cycle-regulated genes that contribute to entry into mitosis. Knockout of MMB-FOXM1 complex components LIN54 and FOXM1 reduce CHK1i-induced DNA replication stress markers and premature mitosis during Late S phase. Activation of a feedback loop between the MMB-FOXM1 complex and CDK1 is required for CHK1i-induced premature mitosis in Late S phase and subsequent replication catastrophe, indicating that dysregulation of the S to M transition is necessary for CHK1 inhibitor sensitivity. These findings provide mechanistic insights into small molecule inhibitors currently studied in clinical trials and provide rationale for combination therapies.
    MeSH term(s) A549 Cells ; Antineoplastic Agents/pharmacology ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/enzymology ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/pathology ; Cell Cycle Checkpoints/drug effects ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Checkpoint Kinase 1/antagonists & inhibitors ; Checkpoint Kinase 1/genetics ; Checkpoint Kinase 1/metabolism ; Forkhead Box Protein M1/genetics ; Forkhead Box Protein M1/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/enzymology ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Mitosis/drug effects ; Multiprotein Complexes ; Protein Kinase Inhibitors/pharmacology ; Pyrazines/pharmacology ; Pyrazoles/pharmacology ; Signal Transduction ; Trans-Activators/genetics ; Trans-Activators/metabolism
    Chemical Substances Antineoplastic Agents ; Cell Cycle Proteins ; FOXM1 protein, human ; Forkhead Box Protein M1 ; Lin54 protein, human ; MYBL2 protein, human ; Multiprotein Complexes ; Protein Kinase Inhibitors ; Pyrazines ; Pyrazoles ; Trans-Activators ; prexasertib ; CHEK1 protein, human (EC 2.7.11.1) ; Checkpoint Kinase 1 (EC 2.7.11.1)
    Language English
    Publishing date 2021-03-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2021.108808
    Database MEDical Literature Analysis and Retrieval System OnLINE

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