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Showing 1–13 of 13 results
Advanced filters: Author: Angeleen Fleming Clear advanced filters

  • A compound screen using zebrafish identified carbonic anhydrase (CA) as a modulator of tau toxicity. CA inhibition abrogates lysosomal acidification and causes tau secretion by lysosomal exocytosis without having a prion effect. This mechanism lowers intracellular tau and is neuroprotective in zebrafish and mouse models of tauopathy.

    • Ana Lopez
    • Farah H. Siddiqi
    • David C. Rubinsztein
    ResearchOpen Access
    Nature Chemical Biology
    Volume: 21, P: 577-587

  • The protein PICALM/CALM is implicated in Alzheimer’s disease (AD) pathology, but it is unclear how. In this study, the authors show that CALM regulates clearance of the protein tau, which is also implicated in AD pathology, by facilitating endocytosis-dependent autophagy.

    • Kevin Moreau
    • Angeleen Fleming
    • David C. Rubinsztein
    ResearchOpen Access
    Nature Communications
    Volume: 5, P: 1-20

  • An siRNA screen for genes that suppress mutant huntingtin toxicity in both mammalian cells and Drosophila identifies glutaminyl cyclase (QPCT). Newly generated small-molecule inhibitors further identify QPCT as a druggable target for Huntington′s disease.

    • Maria Jimenez-Sanchez
    • Wun Lam
    • David C Rubinsztein
    Research
    Nature Chemical Biology
    Volume: 11, P: 347-354

  • Zhu et al. show that loss of WIPI4, as seen in β-propeller protein-associated neurodegeneration, causes ferroptosis independently of autophagy due to an imbalance in phosphatidylethanolamine levels.

    • Ye Zhu
    • Motoki Fujimaki
    • David C. Rubinsztein
    ResearchOpen Access
    Nature Cell Biology
    Volume: 26, P: 542-551

  • A key challenge is to find/re-purpose approved drugs that could be used in humans to induce autophagy-associated clearance of neurodegenerative proteins. Here, authors demonstrate that felodipine, an anti-hypertensive drug, can induce autophagy and clear a variety of aggregated neurodegenerative disease-associated proteins in mouse brains at plasma concentrations similar to those that would be seen in humans taking the drug.

    • Farah H. Siddiqi
    • Fiona M. Menzies
    • David C. Rubinsztein
    ResearchOpen Access
    Nature Communications
    Volume: 10, P: 1-14

  • The molecular mechanisms behind how autophagy may impact on developmental pathways and cell fate decisions are unclear. Here Wu et al.identify Notch receptors being taken up into ATG16L1-positive autophagosomes and, using a mouse mutant model, show that changes in autophagy can impact on stem cell fate.

    • Xiaoting Wu
    • Angeleen Fleming
    • David C. Rubinsztein
    ResearchOpen Access
    Nature Communications
    Volume: 7, P: 1-17

  • Dysfunction of autophagy — an intracellular degradation pathway for cytosolic material — has been implicated in the pathogenesis of various neurodegenerative diseases. Rubinsztein and colleagues review recent progress in this area, focusing on macroautophagy, and discuss how this process may be manipulated to protect against neurodegeneration.

    • Fiona M. Menzies
    • Angeleen Fleming
    • David C. Rubinsztein
    Reviews
    Nature Reviews Neuroscience
    Volume: 16, P: 345-357

  • Autophagy has emerged as a drug target for various diseases including cancer and neurodegeneration. Small molecules that affect components of the autophagic machinery and signaling pathways have led to new insights into autophagic mechanisms and also serve as lead compounds for therapeutic application.

    • Angeleen Fleming
    • Takeshi Noda
    • David C Rubinsztein
    Reviews
    Nature Chemical Biology
    Volume: 7, P: 9-17