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Drosophila model

Feany, MB and Bender, WW (2000) A Drosophila model of Parkinson s disease. Nature 404 394-398. [Pg.323]

HD In Drosophila models of Huntington s disease, the HDAC inhibitors SAHA and sodium butyrate arrest the progressive neuronal degeneration and lethality (Steffan et al, 2001). SAHA and sodium butyrate have also been demonstrated to extend survival, ameliorate motor deficits and delay characteristic neuropathology in the mouse Huntington s disease model, R6/2 (Ferrante et al, 2003 Hockly et al, 2003). In NaBu-treated animals, animals displayed enhanced acetylation status of histones and pro-survival transcription factors like Spl and reduction in several neuropatho-logical hallmarks like striatal neuronal atrophy (Ferrante et al, 2003). Consistent with the idea that HDAC inhibition relieves transcriptional repression and that protection is downstream of mutant htt, neither SAHA nor sodium butyrate decreased mutant htt expression or aggregates (Ferrante et al, 2003 Hockly et al, 2003). [Pg.282]

Vidal M, Cagan RL (2006) Drosophila models for cancer research. Curr Opin Genet Dev 16 10-16... [Pg.304]

Celotto, A. M., Frank, A. C., Seigle, J. L., and Palladino, M. J. (2006). Drosophila model of human inherited triosephosphate isomerase deficiency glycolytic enzymopathy. Genetics 174,1237-1246. [Pg.137]

Sang TK, Jackson GR (2005) Drosophila models of neurodegenerative disease. NeuroRx 2 ... [Pg.96]

Chen L, Feany MB (2005) Alpha-synuclein phosphorylation controls neurotoxicity and inclusion formation in a Drosophila model of Parkinson disease. Nat Neurosci 8 657-663... [Pg.734]

Several mutagenicity studies in Drosophila models have been either inconclusive or negative. Studies of meprobamate activity from cultured rat hippocampal neurons have described meprobamate enhanced GABA-evoked responses in a concentration-depen-dent manner. [Pg.1614]

In a Drosophila model of tauopathy in which abnormal human tau mediates neuronal dysfunction characterized by microtubule destabilization, axonal transport disruption, synaptic defects and behavioral impairments, the microtubule-stabilizing drug, NAPVSIPQ (NAP) (davunetide), prevents as well as reverses these phenotypes even after they have become established [341],... [Pg.421]

Quraishe S, Cowan CM, Mudher A (2013) NAP (davunetide) rescues neuronal dysfunction in a Drosophila model of tauopathy. Mol Psychiatry 18 834-842... [Pg.535]

Pallos J et al (2008) Inhibition of specific HDACs and sirtuins suppresses pathogenesis in a Drosophila model of Huntington s disease. Hum Mol Genet 17(23) 3767-3775... [Pg.47]

Ghosh S, Feany MB (2004) Comparison of pathways controlling toxicity in the eye and brain in Drosophila models of human neurodegenerative diseases. Hum Mol Genet 13(18) 2011—2018... [Pg.47]

Taylor JP et al (2003) Aberrant histone acetylation, altered transcription, and retinal degeneration in a Drosophila model of polyglutamine disease are rescued by CREB-binding protein. Genes Dev 17(12) 1463-1468... [Pg.50]

David Schneider and Mohammed Shahabuddin, Malaria parasite development in a Drosophila model. Science, 288 (2000), 2376-2379. [Pg.281]

Parkinson s disease is a common neurodegenerative syndrome characterized by loss of dopaminergic neurons in the substantia nigra, formation of filamentous intraneuronal inclusions (Lewy bodies) and an extrapyramidal movement disorder. Mutations in the a-synuclein gene are linked to familial Parkinson s disease, and a-synuclein accumulates in Lewy bodies and Lewy neurites. Normal and mutant forms of a-synuclein were expressed in Drosophila and produced adult-onset loss of dopaminergic neurons, filamentous intraneuronal inclusions containing a-synuclein and locomotor dysfunction. The Drosophila model thus recapitulates the essential features of the human disorder and makes possible a powerful genetic approach to Parkinson s disease. [Pg.165]

Gibson, A.C. (1982). Phylogenetic relationships of Pachycereeae. In Barker, J.S.F., Starmer, W.T. (eds.). Ecological Genetics and Evolution the Cactus-Yeast-Drosophila Model System, pp. 3-16. Sydney Academic Press. [Pg.167]

Reim, I. Frasch, M. (2010). Genetic and genomic dissection of cardiogenesis in the Drosophila model. Pediatr Cardiol 31, 325-334. [Pg.421]

Geniposides, 6 -0-tra/is-p-Coumaroylgeniposide (177) and 6 -0-acetylgeniposide (178) isolated from the fruits of Gardenia jasminoides showed significant improvement of short-term memory capacity on an Ab42 transgenic drosophila model assay at a concentration of 7.6 pM [184]. [Pg.3058]


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See also in sourсe #XX -- [ Pg.18 , Pg.153 ]




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