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  1. AU="Perrine Gaub"
  2. AU="Pier-Alexandre Tardif"
  3. AU="Aksu, Tuana" AU="Aksu, Tuana"
  4. AU="Mukherjee, Mousumi"
  5. AU=Qualliotine Jesse R
  6. AU="Lookzadeh, Somayeh"
  7. AU=Cartwright Bethany R.
  8. AU="Kappenberger, Alina-Sophie"
  9. AU=Luukinen H
  10. AU="Przybylski, Bartłomiej"
  11. AU="Lisda Amalia" AU="Lisda Amalia"
  12. AU="Ahmed S.M. Al-Janabi"
  13. AU="Yamaguchi, Hiromi"
  14. AU="Boyatzis, Chris J"

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  1. Artikel ; Online: Peroxisome disruption alters lipid metabolism and potentiates antitumor response with MAPK-targeted therapy in melanoma

    Fan Huang / Feiyang Cai / Michael S. Dahabieh / Kshemaka Gunawardena / Ali Talebi / Jonas Dehairs / Farah El-Turk / Jae Yeon Park / Mengqi Li / Christophe Goncalves / Natascha Gagnon / Jie Su / Judith H. LaPierre / Perrine Gaub / Jean-Sébastien Joyal / John J. Mitchell / Johannes V. Swinnen / Wilson H. Miller Jr. / Sonia V. del Rincón

    The Journal of Clinical Investigation, Vol 133, Iss

    2023  Band 20

    Abstract: Melanomas reprogram their metabolism to rapidly adapt to therapy-induced stress conditions, allowing them to persist and ultimately develop resistance. We report that a subpopulation of melanoma cells tolerate MAPK pathway inhibitors (MAPKis) through a ... ...

    Abstract Melanomas reprogram their metabolism to rapidly adapt to therapy-induced stress conditions, allowing them to persist and ultimately develop resistance. We report that a subpopulation of melanoma cells tolerate MAPK pathway inhibitors (MAPKis) through a concerted metabolic reprogramming mediated by peroxisomes and UDP-glucose ceramide glycosyltransferase (UGCG). Compromising peroxisome biogenesis, by repressing PEX3 expression, potentiated the proapoptotic effects of MAPKis via an induction of ceramides, an effect limited by UGCG-mediated ceramide metabolism. Cotargeting PEX3 and UGCG selectively eliminated a subset of metabolically active, drug-tolerant CD36+ melanoma persister cells, thereby sensitizing melanoma to MAPKis and delaying resistance. Increased levels of peroxisomal genes and UGCG were found in patient-derived MAPKi-relapsed melanomas, and simultaneously inhibiting PEX3 and UGCG restored MAPKi sensitivity in multiple models of therapy resistance. Finally, combination therapy consisting of a newly identified inhibitor of the PEX3-PEX19 interaction, a UGCG inhibitor, and MAPKis demonstrated potent antitumor activity in preclinical melanoma models, thus representing a promising approach for melanoma treatment.
    Schlagwörter Oncology ; Medicine ; R
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2023-10-01T00:00:00Z
    Verlag American Society for Clinical Investigation
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: HBpF-proBDNF

    Perrine Gaub / Andrès de Léon / Julien Gibon / Vincent Soubannier / Geneviève Dorval / Philippe Séguéla / Philip A Barker

    PLoS ONE, Vol 11, Iss 3, p e

    A New Tool for the Analysis of Pro-Brain Derived Neurotrophic Factor Receptor Signaling and Cell Biology.

    2016  Band 0150601

    Abstract: Neurotrophins activate intracellular signaling pathways necessary for neuronal survival, growth and apoptosis. The most abundant neurotrophin in the adult brain, brain-derived neurotrophic factor (BDNF), is first synthesized as a proBDNF precursor and ... ...

    Abstract Neurotrophins activate intracellular signaling pathways necessary for neuronal survival, growth and apoptosis. The most abundant neurotrophin in the adult brain, brain-derived neurotrophic factor (BDNF), is first synthesized as a proBDNF precursor and recent studies have demonstrated that proBDNF can be secreted and that it functions as a ligand for a receptor complex containing p75NTR and sortilin. Activation of proBDNF receptors mediates growth cone collapse, reduces synaptic activity, and facilitates developmental apoptosis of motoneurons but the precise signaling cascades have been difficult to discern. To address this, we have engineered, expressed and purified HBpF-proBDNF, an expression construct containing a 6X-HIS tag, a biotin acceptor peptide (BAP) sequence, a PreScission™ Protease cleavage site and a FLAG-tag attached to the N-terminal part of murine proBDNF. Intact HBpF-proBDNF has activities indistinguishable from its wild-type counterpart and can be used to purify proBDNF signaling complexes or to monitor proBDNF endocytosis and retrograde transport. HBpF-proBDNF will be useful for characterizing proBDNF signaling complexes and for deciphering the role of proBDNF in neuronal development, synapse function and neurodegenerative disease.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 572
    Sprache Englisch
    Erscheinungsdatum 2016-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

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    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

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