Daniel L. Vogt

The paper develops murine and zebrafish Wac deletion models to study DeSanto-Shinawi Syndrome, finding craniofacial, behavioral, and neurodevelopmental phenotypes similar to the human condition.

This paper investigates the neurobehavioral impacts of the autism risk gene WAC in C. elegans and mice, finding altered neurotransmitter systems and gene expression patterns.

This study shows that transplanting GABAergic interneuron progenitors restores slow oscillation rhythms in Alzheimer's disease mouse models.

The paper shows that Kit Ligand and Kit receptor maintain synaptic inhibition in Purkinje Cells through their expression in specific neuronal populations.

The paper investigates how distinct hyperactive RAS/MAPK alleles affect cortical GABAergic interneurons, revealing shared molecular programs and a role for increased neural activity in altering interneuron subtypes.

This study investigates the role of ERK1/2 signaling in the development of MGE-derived glia and cortical inhibitory neurons, showing its necessity for glial number and activity-dependent responses in neurons.

The paper generates a murine Wac mutant model to study DeSanto-Shinawi Syndrome, finding relevant craniofacial, anatomical, behavioral, and seizure phenotypes.

The paper identifies and validates enhancers active in early postnatal mouse brain using a modified MPRA approach and rAAV delivery.

This study assesses how TSC1 missense variants affect cortical inhibitory interneurons, revealing some variants can partially restore function while others show specific deficits.

This study identifies transcriptomic and neuroanatomical changes in mouse embryos exposed to maternal immune activation, revealing altered neurodevelopmental timing and cortical development.

This study shows that Nf1 deletion causes loss of parvalbumin+ cortical interneurons and reduces Lhx6 expression, affecting their development.

This study shows that loss of Tsc1 leads to PV expression and fast-spiking properties in SST+ cortical interneurons, reversible by rapamycin.

The paper compares gene expression profiles of ASD and 22 cancer types, finding shared and opposing deregulations in specific cancers and common biological pathways.