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The identification of a neuronal T-type channel is reported, using a cloning strategy. An expressed sequence tag (EST) was expressed, which was then used to clone a full-length complementary DNA from rate brain. The human gene was mapped to chromosome 17q22 and the mouse gene to chromosome 11. It is concluded that the channel is a low-voltage-activated T-type calcium channel.

Abstract Background Semaphorins act as chemotactic cues for cell movement via their transmembrane receptors, plexins. Somatic missense mutations in the plexinB1 gene coupled with overexpression of the protein frequently occur in prostate tumours, indicating a role for plexinB1 in the pathogenesis of prostate cancer. Results Two specific mutations found in prostate cancer enhance RhoD binding and one other mutation results in loss of inhibition of Rac-dependent Pak1 phosphorylation and lamellipodia formation and in impairment of trafficking of plexinB1 to the membrane. None of the three characterised mutations affect PDZRhoGEF binding, RhoA activity, the interaction of plexinB1with the oncogenes ErbB2 or c-Met or ErbB2 phosphorylation. The mutations have the net effect of increasing cell motility by blocking plexinB1-mediated inhibition of Rac while enhancing the interaction with RhoD, an anti-migratory factor. Conclusions PlexinB1 mutations block plexinB1-mediated signalling pathways that inhibit cell motility.