LIVIVO - Das Suchportal für Lebenswissenschaften

switch to English language
Zurück zur letzten Suche Suchhistorie
Erweiterte Suche

Ihre letzten Suchen

  1. AU="Kong, Rebekah"
  2. AU="Karen de Jager"
  3. AU=Peters A
  4. AU="Xiaofang Li"
  5. AU="Campbell, John D"
  6. AU="Emara, Yasmine"
  7. AU="Orbe, Paul"
  8. AU="Karel J van Erpecum"
  9. AU=Oltean Mihai
  10. AU="Relph, Katharine A"
  11. AU=Li Jifen AU=Li Jifen
  12. AU="Diamant, Eran"
  13. AU="Kyoung, Henry" AU="Kyoung, Henry"
  14. AU=al-Gazali L I
  15. AU="Maillet, Jean-Michel"
  16. AU="Enlong Liu"
  17. AU="Afria, Dikshant"
  18. AU="Duggal, M. S."
  19. AU="Narcisa G. Pricope"
  20. AU="Kunisada, Toshiyuki"
  21. AU="Barvkar, Vitthal"

Suchergebnis

Treffer 1 - 3 von insgesamt 3

Suchoptionen

  1. Artikel: Identifying Potent Nonsense-Mediated mRNA Decay Inhibitors with a Novel Screening System.

    Carrard, Julie / Ratajczak, Fiona / Elsens, Joséphine / Leroy, Catherine / Kong, Rebekah / Geoffroy, Lucie / Comte, Arnaud / Fournet, Guy / Joseph, Benoît / Li, Xiubin / Moebs-Sanchez, Sylvie / Lejeune, Fabrice

    Biomedicines

    2023  Band 11, Heft 10

    Abstract: Nonsense-mediated mRNA decay (NMD) is a quality control mechanism that degrades mRNAs carrying a premature termination codon. Its inhibition, alone or in combination with other approaches, could be exploited to develop therapies for genetic diseases ... ...

    Abstract Nonsense-mediated mRNA decay (NMD) is a quality control mechanism that degrades mRNAs carrying a premature termination codon. Its inhibition, alone or in combination with other approaches, could be exploited to develop therapies for genetic diseases caused by a nonsense mutation. This, however, requires molecules capable of inhibiting NMD effectively without inducing toxicity. We have built a new screening system and used it to identify and validate two new molecules that can inhibit NMD at least as effectively as cycloheximide, a reference NMD inhibitor molecule. These new NMD inhibitors show no cellular toxicity at tested concentrations and have a working concentration between 6.2 and 12.5 µM. We have further validated this NMD-inhibiting property in a physiopathological model of lung cancer in which the
    Sprache Englisch
    Erscheinungsdatum 2023-10-16
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines11102801
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

  2. Artikel ; Online: A role for AKT1 in nonsense-mediated mRNA decay.

    Palma, Martine / Leroy, Catherine / Salomé-Desnoulez, Sophie / Werkmeister, Elisabeth / Kong, Rebekah / Mongy, Marc / Le Hir, Hervé / Lejeune, Fabrice

    Nucleic acids research

    2021  Band 49, Heft 19, Seite(n) 11022–11037

    Abstract: Nonsense-mediated mRNA decay (NMD) is a highly regulated quality control mechanism through which mRNAs harboring a premature termination codon are degraded. It is also a regulatory pathway for some genes. This mechanism is subject to various levels of ... ...

    Abstract Nonsense-mediated mRNA decay (NMD) is a highly regulated quality control mechanism through which mRNAs harboring a premature termination codon are degraded. It is also a regulatory pathway for some genes. This mechanism is subject to various levels of regulation, including phosphorylation. To date only one kinase, SMG1, has been described to participate in NMD, by targeting the central NMD factor UPF1. Here, screening of a kinase inhibitor library revealed as putative NMD inhibitors several molecules targeting the protein kinase AKT1. We present evidence demonstrating that AKT1, a central player in the PI3K/AKT/mTOR signaling pathway, plays an essential role in NMD, being recruited by the UPF3X protein to phosphorylate UPF1. As AKT1 is often overactivated in cancer cells and as this should result in increased NMD efficiency, the possibility that this increase might affect cancer processes and be targeted in cancer therapy is discussed.
    Mesh-Begriff(e) Cell Proliferation ; Codon, Nonsense ; Eukaryotic Initiation Factor-4E/genetics ; Eukaryotic Initiation Factor-4E/metabolism ; Gene Library ; Genes, Reporter ; HEK293 Cells ; HeLa Cells ; Humans ; Luciferases/genetics ; Luciferases/metabolism ; Nonsense Mediated mRNA Decay ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; RNA Helicases/genetics ; RNA Helicases/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism ; Trans-Activators/genetics ; Trans-Activators/metabolism
    Chemische Substanzen Codon, Nonsense ; Eukaryotic Initiation Factor-4E ; RNA, Messenger ; RNA-Binding Proteins ; Trans-Activators ; UPF3A protein, human ; Luciferases (EC 1.13.12.-) ; MTOR protein, human (EC 2.7.1.1) ; AKT1 protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; RNA Helicases (EC 3.6.4.13) ; UPF1 protein, human (EC 3.6.4.13)
    Sprache Englisch
    Erscheinungsdatum 2021-09-27
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    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/gkab882
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 1067: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

  3. Artikel ; Online: Use of 2,6-diaminopurine as a potent suppressor of UGA premature stop codons in cystic fibrosis.

    Leroy, Catherine / Spelier, Sacha / Essonghe, Nadège Charlene / Poix, Virginie / Kong, Rebekah / Gizzi, Patrick / Bourban, Claire / Amand, Séverine / Bailly, Christine / Guilbert, Romain / Hannebique, David / Persoons, Philippe / Arhant, Gwenaëlle / Prévotat, Anne / Reix, Philippe / Hubert, Dominique / Gérardin, Michèle / Chamaillard, Mathias / Prevarskaya, Natalia /
    Rebuffat, Sylvie / Shapovalov, George / Beekman, Jeffrey / Lejeune, Fabrice

    Molecular therapy : the journal of the American Society of Gene Therapy

    2023  Band 31, Heft 4, Seite(n) 970–985

    Abstract: Nonsense mutations are responsible for around 10% of cases of genetic diseases, including cystic fibrosis. 2,6-diaminopurine (DAP) has recently been shown to promote efficient readthrough of UGA premature stop codons. In this study, we show that DAP can ... ...

    Abstract Nonsense mutations are responsible for around 10% of cases of genetic diseases, including cystic fibrosis. 2,6-diaminopurine (DAP) has recently been shown to promote efficient readthrough of UGA premature stop codons. In this study, we show that DAP can correct a nonsense mutation in the Cftr gene in vivo in a new CF mouse model, in utero, and through breastfeeding, thanks, notably, to adequate pharmacokinetic properties. DAP turns out to be very stable in plasma and is distributed throughout the body. The ability of DAP to correct various endogenous UGA nonsense mutations in the CFTR gene and to restore its function in mice, in organoids derived from murine or patient cells, and in cells from patients with cystic fibrosis reveals the potential of such readthrough-stimulating molecules in developing a therapeutic approach. The fact that correction by DAP of certain nonsense mutations reaches a clinically relevant level, as judged from previous studies, makes the use of this compound all the more attractive.
    Mesh-Begriff(e) Mice ; Animals ; Codon, Nonsense ; Cystic Fibrosis/drug therapy ; Cystic Fibrosis/genetics ; Codon, Terminator/genetics ; Cystic Fibrosis Transmembrane Conductance Regulator/genetics
    Chemische Substanzen Codon, Nonsense ; Codon, Terminator ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; 2,6-diaminopurine (49P95BAU4Z)
    Sprache Englisch
    Erscheinungsdatum 2023-01-14
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2010592-7
    ISSN 1525-0024 ; 1525-0016
    ISSN (online) 1525-0024
    ISSN 1525-0016
    DOI 10.1016/j.ymthe.2023.01.014
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 5640: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

Zum Seitenanfang