KIF1B{beta} mutations detected in hereditary neuropathy impair IGF1R transport and axon growth

In this study, we show that the receptor tyrosine kinase IGF1R is a new direct binding partner of KIF1Bβ, and its binding and transport is specifically impaired by the Y1087C mutation of KIF1Bβ, which we detected in hereditary neuropathic patients. The axonal outgrowth and IGF-I signaling of Kif1b–/– neurons were significantly impaired, consistent with decreased surface IGF1R expression. The complementary capacity of KIF1Bβ-Y1087C of these phenotypes was significantly impaired, but the binding capacity to synaptic vesicle precursors was not affected. These data have supported the relevance of KIF1Bβ in IGF1R transport, which may give new clue to the neuropathic pathogenesis.

Source: Journal of Cell Biology - October 1, 2018 Category: Cytology Authors: Xu, F., Takahashi, H., Tanaka, Y., Ichinose, S., Niwa, S., Wicklund, M. P., Hirokawa, N. Tags: Disease, Trafficking, Neuroscience Articles Source Type: research