Axonal transport of mitochondria to synapses depends on milton, a novel Drosophila protein.
By R. Stowers, L. J. Megeath, J. Górska-Andrzejak, Ian A. Meinertzhagen, Thomas Schwarz. Neuron, 2002
642 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/18cbcd97db4700a869013b1807a563d544ff129b
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In Cell Biology
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In Molecular Biology
- D. C. Chan
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Citations in the corpus
- Mechanisms of mesenchymal stem/stromal cell function (2016, background): “The resulting adaptor–motor protein complex shuttles mitochondria along microtubules and was demonstrated to be critical for neuronal transport of mitochondria to axons, dendrites, and synapses [129–131].”
- Docking of axonal mitochondria by syntaphilin controls their mobility and affects short-term facilitation. (2008, positive): “…force behind retrograde movement, the kinesin family of motors and their adaptors Milton and syntabulin are responsible for anterograde transport of axonal mitochondria (Stowers et al., 2002; Górska-Andrzejak et al., 2003; Hollenbeck and Saxton, 2005; Cai et al., 2005; Glater et al., 2006).”
- Matters Arising A Slowed Classical Pathway Rather Than Kiss-and-Run Mediates Endocytosis at Synapses Lacking Synaptojanin and Endophilin (2005, positive): “Two mutants in synaptojanin (synjLY and synjYN) were independently isolated from a forward genetic screen on chromosome 2R using the EGUF-hid method and identifying defects in photoreceptor transmission (Stowers et al., 2002; Stowers and Schwarz, 1999) (see Figure S1 in the Supplemental Data availab”
- Molecular motors in neurons: transport mechanisms and roles in brain function, development, and disease. (2010, positive): “The Milton-Miro complexwas identifiedasanadaptor betweenKIF5and themitochondria (Stowers et al., 2002; Fransson et al., 2003; Guo et al., 2005).”
- Miro1 Is a Calcium Sensor for Glutamate Receptor-Dependent Localization of Mitochondria at Synapses (2009, positive): “In Drosophila, dMiro forms a transport complex with the kinesin adaptor Milton (Glater et al., 2006; Stowers et al., 2002), and in dMiro mutants, mitochondria are not transported into neuronal processes but remain clustered in the neuronal somata (Guo et al., 2005).”
- The axonal transport of mitochondria (2005, background): “These conflicting details of how Khc, Klc, Miro and Milton-related proteins interact with one another could be due to evolutionary divergence of mechanisms as evidenced by the substantial sequence differences between Milton J o u rn a l o f C e ll S c ie n c e and Grif-1.”
- Metabolic regulation of mitochondrial dynamics (2016, background): “The motor proteins are connected to the mitochondrial surface through receptor and adaptor proteins, whose functions were first revealed in Drosophila melanogaster neurons (Stowers et al., 2002; Guo et al., 2005).”
- Kinesin superfamily motor proteins and intracellular transport (2009, background): “The recent discovery of the adaptors Milton and Miro, which bridge KIF5 motors and mitochondria, has shed some light on this phenomeno”
- The importance of dendritic mitochondria in the morphogenesis and plasticity of spines and synapses. (2004, positive): “importance of presynaptic mitochondria for synaptic An enhancement of mitochondrial density and activity transmission ( Stowers et al., 2002 ).”
- Disruption of axonal transport by loss of huntingtin or expression of pathogenic polyQ proteins in Drosophila. (2003, neutral): “port of mitochondria (Stowers et al., 2002).”
- Mitochondrial Fusion Protects against Neurodegeneration in the Cerebellum (2007, positive): “Genetic studies in flies suggest that neurons require abundant mitochondria at nerve termini to maintain synaptic transmission and proper ultrastructure (Guo et al., 2005; Stowers et al., 2002; Verstreken et al., 2005).”
- Decoding Alzheimer's disease from perturbed cerebral glucose metabolism: implications for diagnostic and therapeutic strategies. (2013, background): “The Tg2576 transgenic mice exhibited oxidative damage prior to Ab aggregation (Melov, 2004; Stowers et al., 2002; Wang et al., 2008).”
- The Mechanism of Kinesin Regulation by Ca++ for Control of Mitochondrial Motility (2009, neutral): “…regulate the anterograde motility of mitochondria. pRK5Myc-Miro1E208K,E328K (Miro KK ), (Fransson et al., 2006); Drosophila milton, pCMV-milton A (Stowers et al., 2002); rat KHC, KHC-Myc, KHC1- 682-Myc, (Verhey et al., 1998),KHC-ECFP and KHC-mCit (Cai et al., 2007); pCMV-GFP (gift of Dr. Z.…”
- Mitochondrial dysfunction as a cause of optic neuropathies. (2004, background): “A newly discovered protein named Milton may act as an adaptor complex, which links the kinesin motor to mitochondria and has been found to be essential for the proper localization of mitochondria to the axon and synaptic terminal in Drosophila (Stowers et al., 2002).”