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Showing 1–8 of 8 results
Advanced filters: Author: Maurizio Renna Clear advanced filters

  • Here the authors develop an assay capable of selecting Sec61 inhibitors by exploiting the inactivation of firefly luciferase, once translocated into the endoplasmic reticulum (ER), and the possibility of diverting and “re-lighting” luciferase into the cytosol by a Sec61 inhibitor.

    • Fulvia Vitale
    • Gianluca Scerra
    • Massimo D’Agostino
    ResearchOpen Access
    Nature Communications
    Volume: 16, P: 1-14

  • At high cell density or when plated on soft matrix, YAP/TAZ are redistributed from the nucleus to the cytosol, becoming transcriptionally inactive. Here the authors show that at high cell density, autophagosome formation is impaired due to reduced YAP/TAZ-dependent transcription of actomyosin genes

    • Mariana Pavel
    • Maurizio Renna
    • David C. Rubinsztein
    ResearchOpen Access
    Nature Communications
    Volume: 9, P: 1-18

  • Autophagy regulates multiple pathways including YAP/TAZ of the Hippo pathway, but precise mechanisms are unclear as autophagy may either activate or inhibit YAP/TAZ. Here, the authors show that autophagy can either activate or regulate YAP/TAZ via dynamic negative feedback loops involving alpha-catenin.

    • Mariana Pavel
    • So Jung Park
    • David C. Rubinsztein
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-21

  • Starvation triggers autophagy by inhibiting mTOR signalling. Here, Moreau et al.identify an alternative, transcriptional activation pathway: starvation-induced JNK signalling upregulates Annexin A2 transcription, which in turn enhances actin-dependent transport of Atg9 vesicles from endosomes to autophagosomes.

    • Kevin Moreau
    • Ghita Ghislat
    • David C. Rubinsztein
    ResearchOpen Access
    Nature Communications
    Volume: 6, P: 1-12

  • The CCT complex, a key player in the chaperone machinery, has been implicated in Huntington’s disease. Pavelet al. show that CCT2/5/7 also play an essential role in autophagosome degradation, and that the aggregation of proteins upon CCT2/5/7 depletion is primarily a consequence of impaired autophagy.

    • Mariana Pavel
    • Sara Imarisio
    • David C. Rubinsztein
    ResearchOpen Access
    Nature Communications
    Volume: 7, P: 1-18

  • A recent study makes the surprising observation that autophagosomes can still form in the absence of the core conjugation machinery. Furthermore, while such autophagosomes can fuse with lysosomes, their degradation is delayed, and this is associated with delayed destruction of the inner autophagosomal double membrane, highlighting a new role for proteins thought to act exclusively in the formation of autophagosomes in late stages of the autophagic itinerary within autolysosomes.

    • Maurizio Renna
    • David C Rubinsztein
    Research Highlights
    Cell Research
    Volume: 27, P: 5-6