Aaron D. Gitler

Hop is an unusual homeobox gene that modulates cardiac development.

Nf1 has an essential role in endothelial cells.

Regulating heart development: the role of Nf1.

Cardiac hypertrophy and histone deacetylase-dependent transcriptional repression mediated by the atypical homeodomain protein Hop.

Molecular markers of cardiac endocardial cushion development.

Tie2-Cre-induced inactivation of a conditional mutant Nf1 allele in mouse results in a myeloproliferative disorder that models juvenile myelomonocytic leukemia.

PlexinD1 and semaphorin signaling are required in endothelial cells for cardiovascular development.

Semaphorin-plexin signaling guides patterning of the developing vasculature.

Insertion of Cre into the Pax3 locus creates a new allele of Splotch and identifies unexpected Pax3 derivatives.

Alpha-synuclein blocks ER-Golgi traffic and Rab1 rescues neuron loss in Parkinson's models.

Kermit 2/XGIPC, an IGF1 receptor interacting protein, is required for IGF signaling in Xenopus eye development.

Prime time for alpha-synuclein.

A suite of Gateway cloning vectors for high-throughput genetic analysis in Saccharomyces cerevisiae.

Beer and bread to brains and beyond: can yeast cells teach us about neurodegenerative disease?

The Parkinson's disease protein alpha-synuclein disrupts cellular Rab homeostasis.

A yeast TDP-43 proteinopathy model: Exploring the molecular determinants of TDP-43 aggregation and cellular toxicity.

Discovery and characterization of three novel synuclein genes in zebrafish.

Evidence that alpha-synuclein does not inhibit phospholipase D.

Alpha-synuclein is part of a diverse and highly conserved interaction network that includes PARK9 and manganese toxicity.

Bridging high-throughput genetic and transcriptional data reveals cellular responses to alpha-synuclein toxicity.

Disease models and mechanisms in the classroom.

TDP-43 is intrinsically aggregation-prone, and amyotrophic lateral sclerosis-linked mutations accelerate aggregation and increase toxicity.

Prion-like disorders: blurring the divide between transmissibility and infectivity.

GTPase activity plays a key role in the pathobiology of LRRK2.

Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS.

TDP-43 toxicity in yeast.

Ataxin-2 intermediate-length polyglutamine expansions in European ALS patients.

PolyQ repeat expansions in ATXN2 associated with ALS are CAA interrupted repeats.

A yeast model for polyalanine-expansion aggregation and toxicity.

Molecular determinants and genetic modifiers of aggregation and toxicity for the ALS disease protein FUS/TLS.

Model organisms reveal insight into human neurodegenerative disease: ataxin-2 intermediate-length polyglutamine expansions are a risk factor for ALS.

RNA-binding proteins with prion-like domains in ALS and FTLD-U.

The modulation of Amyotrophic Lateral Sclerosis risk by ataxin-2 intermediate polyglutamine expansions is a specific effect.

Neuroscience. Another reason to exercise.

A yeast functional screen predicts new candidate ALS disease genes.

Local RNA translation at the synapse and in disease.