Gigaxonin is associated with the Golgi and dimerises via its BTB domain

V C Cullen, J Brownlees, S Banner, B H Anderton, P N Leigh, C E Shaw, C C J Miller

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)


Mutations in the gigaxonin gene cause giant axonal neuropathy. The amino-terminus of gigaxonin contains a BTB domain but no binding partners for this domain have so far been identified. Here, we demonstrate that the gigaxonin BTB domain forms homodimers. Other BTB-bearing proteins have also been shown to dimerise via their BTB domains with the dinners then capable of interacting with other ligands. Thus, the gigaxonin BTB domain may function in a similar manner. We also demonstrate that gigaxonin is expressed in a wide variety of neuronal cell types where a significant proportion exists in cell bodies. Confocal microscope studies of gigaxonin-transfected COS-7 cells and cultured neurones revealed that a proportion of gigaxonin localises to the Golgi and endoplasmic reticulum.
Original languageEnglish
Pages (from-to)873 - 876
Number of pages4
Issue number5
Publication statusPublished - 9 Apr 2004


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