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Aaron DiAntonio

Researcher at Washington University in St. Louis

Publications -  151
Citations -  12883

Aaron DiAntonio is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Axon & Synaptic vesicle. The author has an hindex of 56, co-authored 138 publications receiving 10615 citations. Previous affiliations of Aaron DiAntonio include University of California, Berkeley & University of Washington.

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Genetic Analysis of Glutamate Receptors in Drosophila Reveals a Retrograde Signal Regulating Presynaptic Transmitter Release

TL;DR: A decrease in post Synaptic receptors leads to an increase in presynaptic transmitter release, indicating that postsynaptic activity controls a retrograde signal that regulates presynptic function.
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SARM1 activation triggers axon degeneration locally via NAD+ destruction

TL;DR: It is reported that SARM1 initiates a local destruction program involving rapid breakdown of nicotinamide adenine dinucleotide (NAD+) after injury and may explain the potent axon protection in Wallerian degeneration slow (Wlds) mutant mice.
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The SARM1 Toll/Interleukin-1 Receptor Domain Possesses Intrinsic NAD+ Cleavage Activity that Promotes Pathological Axonal Degeneration

TL;DR: It is demonstrated that the NADase activity of full-length SARM1 is required in axons to promote axonal NAD+ depletion and axonal degeneration after injury and represents a novel therapeutic target for axonopathies.
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Highwire regulates synaptic growth in Drosophila.

TL;DR: The formation, stabilization, and growth of synaptic connections are dynamic and highly regulated processes in Drosophila and in hiw mutants, the specificity of motor axon pathfinding and synapse formation appears normal, however, NMJ synapses grow exuberantly and are greatly expanded in both the number of boutons and the extent and length of branches.
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Ubiquitination-dependent mechanisms regulate synaptic growth and function

TL;DR: It is shown that ubiquitin-dependent mechanisms regulate synaptic development at the Drosophila neuromuscular junction (NMJ) and genetic interactions between fat facets and highwire suggest that synaptic development may be controlled by the balance between positive and negative regulators of ubiquitination.