| Defects of full-length dystrophin trigger retinal neuron damage and synapse alterations by disrupting functional autophagy. | Defects of full-length dystrophin trigger retinal neuron damage and synapse alterations by disrupting functional autophagy.
Catalani E, Bongiorni S, Taddei AR, Mezzetti M, Silvestri F, Coazzoli M, Zecchini S, Giovarelli M, Perrotta C, De Palma C, Clementi E, Ceci M, Prantera G, Cervia D., Free PMC Article | 03/6/2021 |
| Oriented basement membrane fibrils provide a memory for F-actin planar polarization via the Dystrophin-Dystroglycan complex during tissue elongation. | Oriented basement membrane fibrils provide a memory for F-actin planar polarization via the Dystrophin-Dystroglycan complex during tissue elongation.
Cerqueira Campos F, Dennis C, Alégot H, Fritsch C, Isabella A, Pouchin P, Bardot O, Horne-Badovinac S, Mirouse V., Free PMC Article | 10/31/2020 |
| The evidence has been presented that the highly conserved Cdc42 Rho GTPase plays a key role in the postsynaptic Dystrophin/Dystrobrevin pathway for synaptic homeostasis. | Dystrobrevin is required postsynaptically for homeostatic potentiation at the Drosophila NMJ.
Jantrapirom S, Nimlamool W, Temviriyanukul P, Ahmadian S, Locke CJ, Davis GW, Yamaguchi M, Noordermeer JN, Fradkin LG, Potikanond S. | 02/8/2020 |
| Dys protein regulates tarsal joint formation in response to Notch activity during Drosophila leg development. | The bHLH-PAS transcription factor dysfusion regulates tarsal joint formation in response to Notch activity during drosophila leg development.
Córdoba S, Estella C., Free PMC Article | 04/30/2016 |
| The findings suggest that the signaling functions of Dystrophin protein are able to ameliorate dilated cardiomyopathy, and thus might help to improve heart muscle function in micro-Dystrophin-based gene therapy approaches. | Mechanical and non-mechanical functions of Dystrophin can prevent cardiac abnormalities in Drosophila.
Taghli-Lamallem O, Jagla K, Chamberlain JS, Bodmer R., Free PMC Article | 08/9/2014 |
| Nrk, mbl, capt and Cam genetically interact with dystrophin and/or dystroglycan in the process of axon path-finding in the eye. | New dystrophin/dystroglycan interactors control neuron behavior in Drosophila eye.
Marrone AK, Kucherenko MM, Rishko VM, Shcherbata HR., Free PMC Article | 07/28/2012 |
| only dystroglycan, but not dystrophin deficiency causes myodegeneration induced by energetic stress suggesting that dystroglycan might be a component of the low-energy pathway and act as a transducer of energetic stress in normal and dystrophic muscles | Stress and muscular dystrophy: a genetic screen for dystroglycan and dystrophin interactors in Drosophila identifies cellular stress response components.
Kucherenko MM, Marrone AK, Rishko VM, Magliarelli Hde F, Shcherbata HR. | 05/28/2011 |
| Dystrophin and the Rho GTPase crossveinless-c signaling pathway likely interact at the postsynaptic side of the NMJ to maintain synaptic homeostasis. | The RhoGAP crossveinless-c interacts with Dystrophin and is required for synaptic homeostasis at the Drosophila neuromuscular junction.
Pilgram GS, Potikanond S, van der Plas MC, Fradkin LG, Noordermeer JN., Free PMC Article | 02/26/2011 |
| Possibility that Dp186 modulates other non-Gbb/Wit-dependent retrograde signaling pathways required to maintain normal synaptic physiology. | The dystrophin Dp186 isoform regulates neurotransmitter release at a central synapse in Drosophila.
Fradkin LG, Baines RA, van der Plas MC, Noordermeer JN., Free PMC Article | 01/21/2010 |
| RNAi-mediated knockdown in the mesoderm shortens lifespan. Deletion of the large isoforms increases the heart rate by widening the cardiac tube and lowering fractional shortening, a phenotype reminiscent of dilated cardiomyopathy | Dystrophin deficiency in Drosophila reduces lifespan and causes a dilated cardiomyopathy phenotype.
Taghli-Lamallem O, Akasaka T, Hogg G, Nudel U, Yaffe D, Chamberlain JS, Ocorr K, Bodmer R., Free PMC Article | 01/21/2010 |
| The det locus encodes Drosophila dys, which acts with other components of the DAPC to influence intercellular signalling in developing wing veins. | The detached locus encodes Drosophila Dystrophin, which acts with other components of the Dystrophin Associated Protein Complex to influence intercellular signalling in developing wing veins.
Christoforou CP, Greer CE, Challoner BR, Charizanos D, Ray RP. | 01/21/2010 |
| Our results indicate the existence of at least two possibly separate roles of dystrophin in muscle, maintaining synaptic homeostasis and preserving the structural stability of the muscle. | Drosophila Dystrophin is required for integrity of the musculature.
van der Plas MC, Pilgram GS, de Jong AW, Bansraj MR, Fradkin LG, Noordermeer JN. | 01/21/2010 |
| Lack of the large dystrophin isoforms in the postsynaptic muscle cell leads to elevated evoked neurotransmitter release from presynaptic terminals. | Dystrophin is required for appropriate retrograde control of neurotransmitter release at the Drosophila neuromuscular junction.
van der Plas MC, Pilgram GS, Plomp JJ, de Jong A, Fradkin LG, Noordermeer JN., Free PMC Article | 01/21/2010 |
| 3 5' promoters and 3 internal promoters regulate expression of 3 full-length and 3 truncated products, respectively. The existence of this complex gene structure in such evolutionary remote organisms suggests that it has diverse important functions | The Drosophila homologue of the dystrophin gene - introns containing promoters are the major contributors to the large size of the gene.
Neuman S, Kovalio M, Yaffe D, Nudel U. | 01/21/2010 |