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  1. AU="John Tam"
  2. AU="Yi, Rong"
  3. AU="Bhandary, R P"
  4. AU="Merkebu, Jerusalem"
  5. AU="Han, Junhyek"
  6. AU="Muneoka, Yusuke"
  7. AU="Griggs, Lisa"
  8. AU="Klauck, Sabine M"
  9. AU="Turton, James A"
  10. AU="Patel, Abhijit A"
  11. AU="Shankowsky, Heather A"
  12. AU="Płóciennik, Przemysław"
  13. AU="Marchesi, Pietro"
  14. AU="Kim Je Hyoung"
  15. AU="Huber, Ingrid"
  16. AU="Hasuko, K."
  17. AU="Yao, Weigen"
  18. AU="Huang, Xiao-Fan"
  19. AU=Zuo Chuantian
  20. AU="Varchetta, Veronica"
  21. AU="Zhang, Lingye"
  22. AU="Venko, Katja"
  23. AU="Kasthuri, Thirupathi"
  24. AU="Pirtskhalava, Tamar"
  25. AU="Saridakis, E N"
  26. AU="Vithana, Eranga N"
  27. AU="Suárez-Lledó, M"
  28. AU="Olivo-Marston, Susan"
  29. AU="Denise P Momesso"
  30. AU="Obrecht-Sturm, Denise"

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  1. Artikel: Small Molecules Take A Big Step Against Clostridium difficile

    Beilhartz, Greg L / John Tam / Roman A. Melnyk

    Trends in microbiology. 2015 Dec., v. 23

    2015  

    Abstract: Effective treatment of Clostridium difficile infections demands a shift away from antibiotics towards toxin-neutralizing agents. Work by Bender et al., using a drug that attenuates toxin action in vivo without affecting bacterial survival, demonstrates ... ...

    Abstract Effective treatment of Clostridium difficile infections demands a shift away from antibiotics towards toxin-neutralizing agents. Work by Bender et al., using a drug that attenuates toxin action in vivo without affecting bacterial survival, demonstrates the exciting potential of small molecules as a new modality in the fight against C. difficile.
    Schlagwörter antibiotics ; Clostridium difficile ; drugs
    Sprache Englisch
    Erscheinungsverlauf 2015-12
    Umfang p. 746-748.
    Erscheinungsort Elsevier Ltd
    Dokumenttyp Artikel
    ZDB-ID 1158963-2
    ISSN 1878-4380 ; 0966-842X
    ISSN (online) 1878-4380
    ISSN 0966-842X
    DOI 10.1016/j.tim.2015.10.009
    Datenquelle NAL Katalog (AGRICOLA)

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    Verfügbar in ZB MED Bonn

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  2. Artikel ; Online: Host-targeted niclosamide inhibits C. difficile virulence and prevents disease in mice without disrupting the gut microbiota

    John Tam / Therwa Hamza / Bing Ma / Kevin Chen / Greg L. Beilhartz / Jacques Ravel / Hanping Feng / Roman A. Melnyk

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Band 11

    Abstract: Clostridium difficile causes diarrhea and colitis by producing up to three different protein toxins. Here, Tam et al. show that an anthelmintic drug, niclosamide, inhibits the pathogenesis of all three toxins by targeting a host process required for ... ...

    Abstract Clostridium difficile causes diarrhea and colitis by producing up to three different protein toxins. Here, Tam et al. show that an anthelmintic drug, niclosamide, inhibits the pathogenesis of all three toxins by targeting a host process required for toxin entry into host cells, without disrupting the gut microbiota.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2018-12-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Host-targeted niclosamide inhibits C. difficile virulence and prevents disease in mice without disrupting the gut microbiota

    John Tam / Therwa Hamza / Bing Ma / Kevin Chen / Greg L. Beilhartz / Jacques Ravel / Hanping Feng / Roman A. Melnyk

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Band 11

    Abstract: Clostridium difficile causes diarrhea and colitis by producing up to three different protein toxins. Here, Tam et al. show that an anthelmintic drug, niclosamide, inhibits the pathogenesis of all three toxins by targeting a host process required for ... ...

    Abstract Clostridium difficile causes diarrhea and colitis by producing up to three different protein toxins. Here, Tam et al. show that an anthelmintic drug, niclosamide, inhibits the pathogenesis of all three toxins by targeting a host process required for toxin entry into host cells, without disrupting the gut microbiota.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2018-12-01T00:00:00Z
    Verlag Nature Publishing Group
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Role of chaperone mediated autophagy (CMA) in the degradation of misfolded N-CoR protein in non-small cell lung cancer (NSCLC) cells.

    Azhar Bin Ali / Dawn Sijin Nin / John Tam / Matiullah Khan

    PLoS ONE, Vol 6, Iss 9, p e

    2011  Band 25268

    Abstract: Nuclear receptor co-repressor (N-CoR) plays important role in transcriptional control mediated by several tumor suppressor proteins. Recently, we reported a role of misfolded-conformation dependent loss (MCDL) of N-CoR in the activation of oncogenic ... ...

    Abstract Nuclear receptor co-repressor (N-CoR) plays important role in transcriptional control mediated by several tumor suppressor proteins. Recently, we reported a role of misfolded-conformation dependent loss (MCDL) of N-CoR in the activation of oncogenic survival pathway in acute promyelocytic leukemia (APL). Since N-CoR plays important role in cellular homeostasis in various tissues, therefore, we hypothesized that an APL like MCDL of N-CoR might also be involved in other malignancy. Indeed, our initial screening of N-CoR status in various leukemia and solid tumor cells revealed an APL like MCDL of N-CoR in primary and secondary tumor cells derived from non-small cell lung cancer (NSCLC). The NSCLC cell specific N-CoR loss could be blocked by Kaletra, a clinical grade protease inhibitor and by genistein, an inhibitor of N-CoR misfolding previously characterized by us. The misfolded N-CoR presented in NSCLC cells was linked to the amplification of ER stress and was subjected to degradation by NSCLC cell specific aberrant protease activity. In NSCLC cells, misfolded N-CoR was found to be associated with Hsc70, a molecular chaperone involved in chaperone mediated autophagy (CMA). Genetic and chemical inhibition of Lamp2A, a rate limiting factor of CMA, significantly blocked the loss of N-CoR in NSCLC cells, suggesting a crucial role of CMA in N-CoR degradation. These findings identify an important role of CMA-induced degradation of misfolded N-CoR in the neutralization of ER stress and suggest a possible role of misfolded N-CoR protein in the activation of oncogenic survival pathway in NSCLC cells.
    Schlagwörter Medicine ; R ; Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2011-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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