Abstract
Kalirin (KAL) is a Rho GEF that is involved in regulation of dendritic morphology. A missense mutation (KAL-PT) has been associated with schizophrenia. KAL coordinates RhoA activation downstream of p75 when p75 interacts with Nogo receptor (NGR). This NGR/p75/KAL complex acts to restrict dendritic morphogenesis. I have found that KAL-PT increases RhoA activity when expressed in vitro and impairs dendritic morphogenesis. We hypothesize that enhanced activation of the NGR/p75/KAL pathway downregulates the expression of microtubule transport proteins and subsequently impairs dendritic morphogenesis across development.
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