Bibliografie tematiche / Autophagic lysosome reformation (ALR)

Letteratura scientifica selezionata sul tema "Autophagic lysosome reformation (ALR)"

Autore: Grafiati
Pubblicato: 7 luglio 2024
Ultima modifica: 7 luglio 2024

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Articoli di riviste sul tema "Autophagic lysosome reformation (ALR)":

1

Zhang, Lu, Yu Fang, Xuan Cheng, Yajun Lian, Hongliang Xu, Zhaoshu Zeng e Hongcan Zhu. "TRPML1 Participates in the Progression of Alzheimer’s Disease by Regulating the PPARγ/AMPK/Mtor Signalling Pathway". Cellular Physiology and Biochemistry 43, n. 6 (2017): 2446–56. http://dx.doi.org/10.1159/000484449.

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Abstract (sommario):
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 Aβ1-42 + mTOR activator, as well as infected with the recombinant adenovirus TRPML1 overexpression vector in vitro. Cell viability was measured by the MTS assay, and lysosomal Ca2+ was also measured. Results: In the APP/PS1 transgenic mice, TRPML1 was downregulated, the PPARγ/AMPK signalling pathway was activated, the mTOR/S6K signalling pathway was suppressed, and autophagic lysosome reformation (ALR)-related proteins were upregulated. TRPML1 overexpression or treatment with PPARγ and AMPK inhibitors or an mTOR activator reduced the expression levels of ALR-related proteins, rescued the memory and recognition impairments and attenuated neuronal apoptosis in mice with the APP/PS1 transgenes. In vitro experiments showed that TRPML1 overexpression or treatment with the mTOR activator propranolol attenuated the Aβ1-42-suppressed cell viability and the Aβ1-42-decreased lysosomal [Ca2+] ion concentration in primary neurons. TRPML1 overexpression or treatment with the mTOR activator propranolol also attenuated the Aβ1-42-inhibited mTOR/S6K signalling pathway and the Aβ1-42-induced ALR-related protein expression levels. Conclusion: TRPML1 is involved in the pathogenesis of AD by regulating autophagy at least in part through the PPARγ/AMPK/mTOR signallingpathway.
2

Chen, Yang, e Li Yu. "Autophagic lysosome reformation". Experimental Cell Research 319, n. 2 (gennaio 2013): 142–46. http://dx.doi.org/10.1016/j.yexcr.2012.09.004.

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3

Chen, Yang, e Li Yu. "Recent progress in autophagic lysosome reformation". Traffic 18, n. 6 (5 maggio 2017): 358–61. http://dx.doi.org/10.1111/tra.12484.

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4

Gan, Qiwen, Xin Wang, Qian Zhang, Qiuyuan Yin, Youli Jian, Yubing Liu, Nan Xuan et al. "The amino acid transporter SLC-36.1 cooperates with PtdIns3P 5-kinase to control phagocytic lysosome reformation". Journal of Cell Biology 218, n. 8 (24 giugno 2019): 2619–37. http://dx.doi.org/10.1083/jcb.201901074.

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Abstract (sommario):
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 lysosomal components is inhibited. Moreover, loss of PPK-3, the C. elegans homologue of the PtdIns3P 5-kinase PIKfyve, similarly causes accumulation of phagolysosomal vacuoles that are defective in phagocytic lysosome reformation. SLC-36.1 and PPK-3 function in the same genetic pathway, and they directly interact with one another. In addition, loss of slc-36.1 and ppk-3 causes strong defects in autophagic lysosome reformation in adult animals. Our findings thus suggest that the PPK-3–SLC-36.1 axis plays a central role in both phagocytic and autophagic lysosome formation.
5

Rong, Yueguang, Mei Liu, Liang Ma, Wanqing Du, Hanshuo Zhang, Yuan Tian, Zhen Cao et al. "Clathrin and phosphatidylinositol-4,5-bisphosphate regulate autophagic lysosome reformation". Nature Cell Biology 14, n. 9 (12 agosto 2012): 924–34. http://dx.doi.org/10.1038/ncb2557.

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6

Chang, Jaerak, Seongju Lee e Craig Blackstone. "Spastic paraplegia proteins spastizin and spatacsin mediate autophagic lysosome reformation". Journal of Clinical Investigation 124, n. 12 (3 novembre 2014): 5249–62. http://dx.doi.org/10.1172/jci77598.

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7

Rong, Y., C. K. McPhee, S. Deng, L. Huang, L. Chen, M. Liu, K. Tracy, E. H. Baehrecke, L. Yu e M. J. Lenardo. "Spinster is required for autophagic lysosome reformation and mTOR reactivation following starvation". Proceedings of the National Academy of Sciences 108, n. 19 (25 aprile 2011): 7826–31. http://dx.doi.org/10.1073/pnas.1013800108.

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8

Magalhaes, Joana, Matthew E. Gegg, Anna Migdalska-Richards, Mary K. Doherty, Phillip D. Whitfield e Anthony H. V. Schapira. "Autophagic lysosome reformation dysfunction in glucocerebrosidase deficient cells: relevance to Parkinson disease". Human Molecular Genetics 25, n. 16 (4 luglio 2016): 3432–45. http://dx.doi.org/10.1093/hmg/ddw185.

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9

Liu, Xu, e Daniel J. Klionsky. "Regulation of autophagic lysosome reformation by kinesin 1, clathrin and phosphatidylinositol-4,5-bisphosphate". Autophagy 14, n. 1 (21 dicembre 2017): 1–2. http://dx.doi.org/10.1080/15548627.2017.1386821.

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10

Sharma, Prashant, Jenny Serra-Vinardell, Wendy J. Introne e May Christine V. Malicdan. "Role of lysosomal trafficking regulator in autophagic lysosome reformation in neurons: a disease perspective". Neural Regeneration Research 19, n. 5 (22 settembre 2023): 957–58. http://dx.doi.org/10.4103/1673-5374.385298.

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Ti possono interessare anche gli elenchi estesi di opere sul tema "Autophagic lysosome reformation (ALR)":
Articoli di riviste

Tesi sul tema "Autophagic lysosome reformation (ALR)":

1

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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Abstract (sommario):
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 largement été investigué dans cette thèse afin de mieux comprendre sa régulation, notamment pour la régénération des lysosomes en conditions basales et de privation d’acides aminés. Mon travail révèle un nouveau partenaire du complexe C9ORF72 et une nouvelle fonction de ce complexe dans la biogenèse des lysosomes. Ces résultats pourraient ainsi expliquer le dysfonctionnement des lysosomes et la neurodégénérescence observés dans la SLA, ce qui pourrait ainsi ouvrir de nouvelles voies thérapeutiques pour cette maladie dévastatrice
Amyotrophic lateral sclerosis (ALS or Charcot disease) is the third most common neurodegenerative disease. The main genetic cause of ALS is an expansion of GGGGCC repeats in the C9ORF72 gene which protein forms a complex with the SMCR8 and WDR41 proteins. To better understand its molecular functions, solving its structure was a main goal of my thesis. In parallel, we discovered that C9ORF72 regulates a newly described mechanism of biogenesis of newly-formed lysosomes, called autophagic lysosome reformation (ALR). This process has been extensively investigated during my thesis, in order to better understand its regulation, particularly for the regeneration of lysosomes in basal conditions and amino acid deprivation. My work reveals a new partner of the C9ORF72 complex as a novel function in lysosome biogenesis. These results could thus explain the dysfunction of lysosomes and neurodegeneration observed in ALS, which open new therapeutic ways for this devastating disease

Capitoli di libri sul tema "Autophagic lysosome reformation (ALR)":

1

Chen, Yang, Qian Peter Su e Li Yu. "Studying Autophagic Lysosome Reformation in Cells and by an In Vitro Reconstitution System". In Methods in Molecular Biology, 163–72. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8873-0_9.

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2

Mahapatra, Kewal Kumar, e Sujit Kumar Bhutia. "Autophagic lysosome reformation: The beginning from the end". In Autophagy Processes and Mechanisms, 153–62. Elsevier, 2024. http://dx.doi.org/10.1016/b978-0-323-90142-0.00009-8.

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