R. Grace Zhai

Molecular mechanisms of CNS synaptogenesis.

Unitary assembly of presynaptic active zones from Piccolo-Bassoon transport vesicles.

Mapping Drosophila mutations with molecularly defined P element insertions.

Synaptojanin is recruited by endophilin to promote synaptic vesicle uncoating.

The architecture of the active zone in the presynaptic nerve terminal.

Hauling t-SNAREs on the microtubule highway.

Mutations in Drosophila sec15 reveal a function in neuronal targeting for a subset of exocyst components.

The v-ATPase V0 subunit a1 is required for a late step in synaptic vesicle exocytosis in Drosophila.

Activity-independent prespecification of synaptic partners in the visual map of Drosophila.

Drosophila NMNAT maintains neural integrity independent of its NAD synthesis activity.

NAD synthase NMNAT acts as a chaperone to protect against neurodegeneration.

Nicotinamide/nicotinic acid mononucleotide adenylyltransferase, new insights into an ancient enzyme.

BMAA neurotoxicity in Drosophila.

Dealing with misfolded proteins: examining the neuroprotective role of molecular chaperones in neurodegeneration.

Nicotinamide mononucleotide adenylyltransferase is a stress response protein regulated by the heat shock factor/hypoxia-inducible factor 1alpha pathway.

Nmnat exerts neuroprotective effects in dendrites and axons.

NMNAT suppresses tau-induced neurodegeneration by promoting clearance of hyperphosphorylated tau oligomers in a Drosophila model of tauopathy.

CREB-activity and nmnat2 transcription are down-regulated prior to neurodegeneration, while NMNAT2 over-expression is neuroprotective, in a mouse model of human tauopathy.

Protein Aggregates Are Recruited to Aggresome by Histone Deacetylase 6 via Unanchored Ubiquitin C Termini.

β-N-Methylamino-L-alanine Induces Neurological Deficits and Shortened Life Span in Drosophila.

Nicotinamide mononucleotide adenylyltransferase maintains active zone structure by stabilizing Bruchpilot.

Alternative splicing of Drosophila Nmnat functions as a switch to enhance neuroprotection under stress.

Attenuation of polyglutamine-induced toxicity by enhancement of mitochondrial OXPHOS in yeast and fly models of aging.

NMNAT: It's an NAD synthase… It's a chaperone… It's a neuroprotector.

Spermine synthase deficiency causes lysosomal dysfunction and oxidative stress in models of Snyder-Robinson syndrome.

Publisher Correction: Spermine synthase deficiency causes lysosomal dysfunction and oxidative stress in models of Snyder-Robinson syndrome.

Nmnat mitigates sensory dysfunction in a model of paclitaxel-induced peripheral neuropathy.