Shootin 1 (ST1)

Shootin1 upregulated during polarization of rat hippocampal neurons in culture. Expression fluctuated among multiple neurites and eventually Shootin1 accumulated asymmetrically in a single neurite, which led to axon induction and neuron polarization. Disturbing the asymmetric organization of Shootin1 with excess Shootin1 disrupted polarization, whereas repressing Shootin1 expression inhibited polarization. Overexpression and RNA interference studies suggested that Shootin1 was required for spatially localized phosphoinositide 3-kinase (see PIK3CG) activity.

Shootin1 showed anterograde transport to the growth cones and diffused back to the soma, and inhibition of this transport prevented its asymmetric accumulation in neurons.