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  1. AU="Eing, Lorenz"
  2. AU="Geoffroy, Pierre A"
  3. AU="Chapuis, J"
  4. AU="Berta, László"
  5. AU="Barzilay, Regina"
  6. AU="Schmidt, Michael Rahbek"
  7. AU=Tack J
  8. AU="Oh, Hye Min"
  9. AU=Gaffen Sarah L AU=Gaffen Sarah L
  10. AU="Schmitt, Christine"
  11. AU="McKay, Jackie"
  12. AU="Bellissimo, Catherine A"
  13. AU="Desai, Urja"
  14. AU="Chini, Maria Giovanna"
  15. AU="Xiao, Difei"
  16. AU="Ryan, Chris"
  17. AU="Omar Bazighifan"
  18. AU="Corominas Galbany, Jordi"
  19. AU=Fox Norma E
  20. AU="Hamilton, Shelia M"
  21. AU="Nichols, J Wylie"
  22. AU="Pesce R."
  23. AU="Gambitta, P"
  24. AU="Imran, Aqeel"
  25. AU="Sharma, Yashoda"
  26. AU="Kosai, Jordyn"
  27. AU="Aroca Ferri, María"
  28. AU="Laba, Stephanie"
  29. AU="Kim, Ye-Sel"

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  1. Artikel: The glycolytic enzyme ALDOA and the exon junction complex protein RBM8A are regulators of ribosomal biogenesis.

    Schwarz, Jessica Denise / Lukassen, Sören / Bhandare, Pranjali / Eing, Lorenz / Snaebjörnsson, Marteinn Thor / García, Yiliam Cruz / Kisker, Jan Philipp / Schulze, Almut / Wolf, Elmar

    Frontiers in cell and developmental biology

    2022  Band 10, Seite(n) 954358

    Abstract: Cellular growth is a fundamental process of life and must be precisely controlled in multicellular organisms. Growth is crucially controlled by the number of functional ribosomes available in cells. The production of new ribosomes depends critically on ... ...

    Abstract Cellular growth is a fundamental process of life and must be precisely controlled in multicellular organisms. Growth is crucially controlled by the number of functional ribosomes available in cells. The production of new ribosomes depends critically on the activity of RNA polymerase (RNAP) II in addition to the activity of RNAP I and III, which produce ribosomal RNAs. Indeed, the expression of both, ribosomal proteins and proteins required for ribosome assembly (ribosomal biogenesis factors), is considered rate-limiting for ribosome synthesis. Here, we used genetic screening to identify novel transcriptional regulators of cell growth genes by fusing promoters from a ribosomal protein gene (
    Sprache Englisch
    Erscheinungsdatum 2022-09-14
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2022.954358
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: PROTAC-mediated degradation reveals a non-catalytic function of AURORA-A kinase.

    Adhikari, Bikash / Bozilovic, Jelena / Diebold, Mathias / Schwarz, Jessica Denise / Hofstetter, Julia / Schröder, Martin / Wanior, Marek / Narain, Ashwin / Vogt, Markus / Dudvarski Stankovic, Nevenka / Baluapuri, Apoorva / Schönemann, Lars / Eing, Lorenz / Bhandare, Pranjali / Kuster, Bernhard / Schlosser, Andreas / Heinzlmeir, Stephanie / Sotriffer, Christoph / Knapp, Stefan /
    Wolf, Elmar

    Nature chemical biology

    2020  Band 16, Heft 11, Seite(n) 1179–1188

    Abstract: The mitotic kinase AURORA-A is essential for cell cycle progression and is considered a priority cancer target. Although the catalytic activity of AURORA-A is essential for its mitotic function, recent reports indicate an additional non-catalytic ... ...

    Abstract The mitotic kinase AURORA-A is essential for cell cycle progression and is considered a priority cancer target. Although the catalytic activity of AURORA-A is essential for its mitotic function, recent reports indicate an additional non-catalytic function, which is difficult to target by conventional small molecules. We therefore developed a series of chemical degraders (PROTACs) by connecting a clinical kinase inhibitor of AURORA-A to E3 ligase-binding molecules (for example, thalidomide). One degrader induced rapid, durable and highly specific degradation of AURORA-A. In addition, we found that the degrader complex was stabilized by cooperative binding between AURORA-A and CEREBLON. Degrader-mediated AURORA-A depletion caused an S-phase defect, which is not the cell cycle effect observed upon kinase inhibition, supporting an important non-catalytic function of AURORA-A during DNA replication. AURORA-A degradation induced rampant apoptosis in cancer cell lines and thus represents a versatile starting point for developing new therapeutics to counter AURORA-A function in cancer.
    Mesh-Begriff(e) Adaptor Proteins, Signal Transducing/metabolism ; Antineoplastic Agents/chemistry ; Apoptosis/drug effects ; Aurora Kinase A/antagonists & inhibitors ; Aurora Kinase A/genetics ; Benzazepines/chemistry ; Catalytic Domain ; Cell Cycle/drug effects ; Cell Line, Tumor ; DNA Replication/drug effects ; Drug Design ; Female ; Humans ; Male ; Molecular Targeted Therapy ; Polyethylene Glycols/chemistry ; Protein Binding ; Protein Conformation ; Protein Kinase Inhibitors/chemistry ; Proteolysis/drug effects ; Thalidomide/chemistry ; Ubiquitin-Protein Ligases/metabolism
    Chemische Substanzen Adaptor Proteins, Signal Transducing ; Antineoplastic Agents ; Benzazepines ; CRBN protein, human ; MLN8054 ; Protein Kinase Inhibitors ; Polyethylene Glycols (3WJQ0SDW1A) ; Thalidomide (4Z8R6ORS6L) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; AURKA protein, human (EC 2.7.11.1) ; Aurora Kinase A (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2020-09-28
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2202962-X
    ISSN 1552-4469 ; 1552-4450
    ISSN (online) 1552-4469
    ISSN 1552-4450
    DOI 10.1038/s41589-020-00652-y
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

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  3. Artikel ; Online: Migration pattern, actin cytoskeleton organization and response to PI3K-, mTOR-, and Hsp90-inhibition of glioblastoma cells with different invasive capacities.

    Memmel, Simon / Sisario, Dmitri / Zöller, Caren / Fiedler, Vanessa / Katzer, Astrid / Heiden, Robin / Becker, Nicholas / Eing, Lorenz / Ferreira, Fábio L R / Zimmermann, Heiko / Sauer, Markus / Flentje, Michael / Sukhorukov, Vladimir L / Djuzenova, Cholpon S

    Oncotarget

    2017  Band 8, Heft 28, Seite(n) 45298–45310

    Abstract: High invasiveness and resistance to chemo- and radiotherapy of glioblastoma multiforme (GBM) make it the most lethal brain tumor. Therefore, new treatment strategies for preventing migration and invasion of GBM cells are needed. Using two different ... ...

    Abstract High invasiveness and resistance to chemo- and radiotherapy of glioblastoma multiforme (GBM) make it the most lethal brain tumor. Therefore, new treatment strategies for preventing migration and invasion of GBM cells are needed. Using two different migration assays, Western blotting, conventional and super-resolution (dSTORM) fluorescence microscopy we examine the effects of the dual PI3K/mTOR-inhibitor PI-103 alone and in combination with the Hsp90 inhibitor NVP-AUY922 and/or irradiation on the migration, expression of marker proteins, focal adhesions and F-actin cytoskeleton in two GBM cell lines (DK-MG and SNB19) markedly differing in their invasive capacity. Both lines were found to be strikingly different in morphology and migration behavior. The less invasive DK-MG cells maintained a polarized morphology and migrated in a directionally persistent manner, whereas the highly invasive SNB19 cells showed a multipolar morphology and migrated randomly. Interestingly, a single dose of 2 Gy accelerated wound closure in both cell lines without affecting their migration measured by single-cell tracking. PI-103 inhibited migration of DK-MG (p53 wt, PTEN wt) but not of SNB19 (p53 mut, PTEN mut) cells probably due to aberrant reactivation of the PI3K pathway in SNB19 cells treated with PI-103. In contrast, NVP-AUY922 exerted strong anti-migratory effects in both cell lines. Inhibition of cell migration was associated with massive morphological changes and reorganization of the actin cytoskeleton. Our results showed a cell line-specific response to PI3K/mTOR inhibition in terms of GBM cell motility. We conclude that anti-migratory agents warrant further preclinical investigation as potential therapeutics for treatment of GBM.
    Sprache Englisch
    Erscheinungsdatum 2017-07-11
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.16847
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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