Progressive transcriptional changes in metabolic genes and altered fatbody homeostasis in Drosophila model of Huntington’s disease
Author:
Publisher
Springer Science and Business Media LLC
Subject
Cellular and Molecular Neuroscience,Neurology (clinical),Biochemistry
Link
https://link.springer.com/content/pdf/10.1007/s11011-022-01078-2.pdf
Reference29 articles.
1. Aditi K, Shakarad MN, Agrawal N (2016) Altered lipid metabolism in Drosophila model of Huntington’s disease. Sci Rep 6:31411. https://doi.org/10.1038/srep31411
2. Aziz NA, van der Burg JM, Landwehrmeyer GB, Brundin P, Stijnen T, EHDI Study Group, &, Roos RA (2008) Weight loss in Huntington disease increases with higher CAG repeat number. Neurology 71:1506–1513. https://doi.org/10.1212/01.wnl.0000334276.09729.0e
3. Baker KD, Thummel CS (2007) Diabetic larvae and obese flies-emerging studies of metabolism in Drosophila. Cell Metabol 6:257–266. https://doi.org/10.1016/j.cmet.2007.09.002
4. Baltzer C, Tiefenböck SK, Marti M, Frei C (2009) Nutrition controls mitochondrial biogenesis in the Drosophila adipose tissue through Delg and Cyclin D/Cdk4. PLoS ONE 4(9):e6935. https://doi.org/10.1371/journal.pone.0006935
5. Baumbach J, Hummel P, Bickmeyer I, Kowalczyk KM, Frank M, Knorr K, Hildebrandt A, Riedel D, Jäckle H, Kühnlein RP (2014) A Drosophila in vivo screen identifies store-operated calcium entry as a key regulator of adiposity. Cell Metab 19:331–343. https://doi.org/10.1016/j.cmet.2013.12.004
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