Evaluation of expression and function of the H+/myo-inositol transporter HMIT;

Article

Di Daniel, E., Mok, S., Mead, E., Mutinelli, C., Zambello, E., Caberlotto, L., Pell, T., Langmead, C., Shah, A., Duddy, G., Kew, J. and Maycox, P. 2009. Evaluation of expression and function of the H+/myo-inositol transporter HMIT; BMC Cell Biology. 10. https://doi.org/10.1186/1471-2121-10-54
TypeArticle
TitleEvaluation of expression and function of the H+/myo-inositol transporter HMIT;
AuthorsDi Daniel, E., Mok, S., Mead, E., Mutinelli, C., Zambello, E., Caberlotto, L., Pell, T., Langmead, C., Shah, A., Duddy, G., Kew, J. and Maycox, P.
Abstract

BACKGROUND:
The phosphoinositide (PIns) signalling pathway regulates a series of neuronal processes, such as neurotransmitter release, that are thought to be altered in mood disorders. Furthermore, mood-stabilising drugs have been shown to inhibit key enzymes that regulate PIns production and alter neuronal growth cone morphology in an inositol-reversible manner. Here, we describe analyses of expression and function of the recently identified H+/myo-inositol transporter (HMIT) investigated as a potential regulator of PIns signalling.
RESULTS:
We show that HMIT is primarily a neuronal transporter widely expressed in the rat and human brain, with particularly high levels in the hippocampus and cortex, as shown by immunohistochemistry. The transporter is localised at the Golgi apparatus in primary cultured neurones. No HMIT-mediated electrophysiological responses were detected in rat brain neurones or slices; in addition, inositol transport and homeostasis were unaffected in HMIT targeted null-mutant mice.
CONCLUSION:
Together, these data do not support a role for HMIT as a neuronal plasma membrane inositol transporter, as previously proposed. However, we observed that HMIT can transport inositol triphosphate, indicating unanticipated intracellular functions for this transporter that may be relevant to mood control.

PublisherBioMed Central
JournalBMC Cell Biology
ISSN1471-2121
Publication dates
Print16 Jul 2009
Publication process dates
Deposited01 Nov 2017
Accepted16 Jul 2009
Output statusPublished
Publisher's version
Copyright Statement

© 2009 Di Daniel et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Additional information

Article number = 54

Digital Object Identifier (DOI)https://doi.org/10.1186/1471-2121-10-54
LanguageEnglish
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