Application Methods: Western Blotting
Background: Dysbindin, or dystrobrevin-binding protein 1, is a coiled-coil-containing protein expressed in muscle and brain that was identified as a binding partner of dystrobrevin (1). Dysbindin upregulates expression of the pre-synaptic proteins SNAP25 and synapsin I, thereby increasing glutamate release and promoting neuronal viability through Akt signaling. In particular, Akt phosphorylation is suppressed with downregulation of dysbindin and increased with upregulation of dysbindin (2). A nonsense mutation of dysbindin causes Hermansky-Pudlak disease, an autosomal recessive disorder characterized by lysosomal storage defects and prolonged bleeding. (2). Genetic variation in the gene encoding dysbindin is strongly associated with schizophrenia and protein levels are reduced in the prefrontal cortex, midbrain and hippocampus of brains from patients with schizophrenia (3,4).
Application Methods: Immunoprecipitation, Western Blotting
Background: Kinesin-like protein KIF1B is a member of the kinesin 3 family of C-kinesins that are characterized by a kinesin-motor domain in the carboxy-terminal region. As part of the general mechanism of kinesin-mediated cellular transport, C-kinesins are known to drive microtubule plus and minus end motilities (1-3). KIF1B is implicated in the transport of synaptic proteins to the cell periphery in neuronal cell axons by interaction with Rab3 guanine nucleotide exchange factor (3). Mitochondria are also often transported in axons by KIF1B (3-4).