Learn More
Image overlay of fluorescently labeled cultured mouse hippocampal neurons transfected with green fluorescent protein and Ca v 1.3 Ca 2ϩ channels (background; green and red), or densin-GFP (foreground; blue), which colocalizes with PSD-95 (red) in dendritic spines (white). Together with Ca 2ϩ / calmodulin-dependent protein kinase II, densin mediates a novel(More)
To identify Huntington's Disease therapeutics, we conducted high-content small molecule and RNAi suppressor screens using a Drosophila primary neural culture Huntingtin model. Drosophila primary neurons offer a sensitive readout for neurotoxicty, as their neurites develop dysmorphic features in the presence of mutant polyglutamine-expanded Huntingtin(More)
Cell-based high content screening (HCS) is becoming an important and increasingly favored approach in therapeutic drug discovery and functional genomics. In HCS, changes in cellular morphology and biomarker distributions provide an information-rich profile of cellular responses to experimental treatments such as small molecules or gene knockdown probes. One(More)
Huntington's Disease is an adult-onset dominant heritable disorder characterized by progressive psychiatric disruption, cognitive deficits, and loss of motor coordination. It is caused by expansion of a polyglutamine tract within the N-terminal domain of the Huntingtin protein. The mutation confers a toxic gain-of-function phenotype, resulting in(More)
The monopolar spindle-one-binder (Mob) family of kinase-interacting proteins regulate cell cycle and cell morphology, and their dysfunction has been linked to cancer. Models for Mob function are primarily based on studies of Mob1 and Mob2 family members in yeast. In contrast, the function of the highly conserved metazoan Phocein/Mob3 subfamily is unknown.(More)
  • 1