Academic literature on the topic 'Autophagic lysosome reformation (ALR)'

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Journal articles on the topic "Autophagic lysosome reformation (ALR)"

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Zhang, Lu, Yu Fang, Xuan Cheng та ін. "TRPML1 Participates in the Progression of Alzheimer’s Disease by Regulating the PPARγ/AMPK/Mtor Signalling Pathway". Cellular Physiology and Biochemistry 43, № 6 (2017): 2446–56. http://dx.doi.org/10.1159/000484449.

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Background: TRPML1 is reported to be involved in the pathogenesis of Alzheimer’s disease (AD) by regulating autophagy; however, the underlying mechanism is not completely clear. Methods: We developed an APP/PS1 transgenic animal model that presents with AD. TRPML1 was also overexpressed in these mice. Protein expression levels were determined by Western blot. Morris water maze (MWM) and recognition tasks were performed to characterize cognitive ability. TUNEL assays were analysed for the detection of neuronal apoptosis. Primary neurons were isolated and treated with the vehicle, Aβ1-42 or Aβ1-
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Chen, Yang, and Li Yu. "Autophagic lysosome reformation." Experimental Cell Research 319, no. 2 (2013): 142–46. http://dx.doi.org/10.1016/j.yexcr.2012.09.004.

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Chen, Yang, and Li Yu. "Recent progress in autophagic lysosome reformation." Traffic 18, no. 6 (2017): 358–61. http://dx.doi.org/10.1111/tra.12484.

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Toifl, Stefanie, Sebastian Didusch, Karin Ehrenreiter, Enrico Desideri, Coralie Dorard, and Manuela Baccarini. "RAF1 kinase contributes to autophagic lysosome reformation." Cell Reports 44, no. 4 (2025): 115490. https://doi.org/10.1016/j.celrep.2025.115490.

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Gan, Qiwen, Xin Wang, Qian Zhang, et al. "The amino acid transporter SLC-36.1 cooperates with PtdIns3P 5-kinase to control phagocytic lysosome reformation." Journal of Cell Biology 218, no. 8 (2019): 2619–37. http://dx.doi.org/10.1083/jcb.201901074.

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Phagocytic removal of apoptotic cells involves formation, maturation, and digestion of cell corpse–containing phagosomes. The retrieval of lysosomal components following phagolysosomal digestion of cell corpses remains poorly understood. Here we reveal that the amino acid transporter SLC-36.1 is essential for lysosome reformation during cell corpse clearance in Caenorhabditis elegans embryos. Loss of slc-36.1 leads to formation of phagolysosomal vacuoles arising from cell corpse–containing phagosomes. In the absence of slc-36.1, phagosome maturation is not affected, but the retrieval of lysoso
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Rong, Yueguang, Mei Liu, Liang Ma, et al. "Clathrin and phosphatidylinositol-4,5-bisphosphate regulate autophagic lysosome reformation." Nature Cell Biology 14, no. 9 (2012): 924–34. http://dx.doi.org/10.1038/ncb2557.

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Chang, Jaerak, Seongju Lee, and Craig Blackstone. "Spastic paraplegia proteins spastizin and spatacsin mediate autophagic lysosome reformation." Journal of Clinical Investigation 124, no. 12 (2014): 5249–62. http://dx.doi.org/10.1172/jci77598.

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Rong, Y., C. K. McPhee, S. Deng, et al. "Spinster is required for autophagic lysosome reformation and mTOR reactivation following starvation." Proceedings of the National Academy of Sciences 108, no. 19 (2011): 7826–31. http://dx.doi.org/10.1073/pnas.1013800108.

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Magalhaes, Joana, Matthew E. Gegg, Anna Migdalska-Richards, Mary K. Doherty, Phillip D. Whitfield, and Anthony H. V. Schapira. "Autophagic lysosome reformation dysfunction in glucocerebrosidase deficient cells: relevance to Parkinson disease." Human Molecular Genetics 25, no. 16 (2016): 3432–45. http://dx.doi.org/10.1093/hmg/ddw185.

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Liu, Xu, and Daniel J. Klionsky. "Regulation of autophagic lysosome reformation by kinesin 1, clathrin and phosphatidylinositol-4,5-bisphosphate." Autophagy 14, no. 1 (2017): 1–2. http://dx.doi.org/10.1080/15548627.2017.1386821.

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Dissertations / Theses on the topic "Autophagic lysosome reformation (ALR)"

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Pietri, David. "Structure and function of the C9ORF72-SMCR8-WDR41 complex and its implication for Amyotrophic Lateral Sclerosis (ALS)." Electronic Thesis or Diss., Strasbourg, 2023. http://www.theses.fr/2023STRAJ087.

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La sclérose latérale amyotrophique (SLA ou maladie de Charcot) est la troisième maladie neurodégénérative la plus répandue. La principale cause génétique de la SLA est une expansion de répétitions GGGGCC dans le gène C9ORF72, dont la protéine forme un complexe avec les protéines SMCR8 et WDR41. Afin de mieux comprendre ses fonctions moléculaires, résoudre sa structure était un objectif principal de ma thèse. En parallèle, nous avons découvert que C9ORF72 régule un mécanisme nouvellement décrit de biogenèse de nouveaux lysosomes nommé reformation autophagique des lysosomes (ALR). Ce processus a
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Book chapters on the topic "Autophagic lysosome reformation (ALR)"

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Chen, Yang, Qian Peter Su, and Li Yu. "Studying Autophagic Lysosome Reformation in Cells and by an In Vitro Reconstitution System." In Methods in Molecular Biology. Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8873-0_9.

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Mahapatra, Kewal Kumar, and Sujit Kumar Bhutia. "Autophagic lysosome reformation: The beginning from the end." In Autophagy Processes and Mechanisms. Elsevier, 2024. http://dx.doi.org/10.1016/b978-0-323-90142-0.00009-8.

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