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

Di Daniel, Elena and Mok, Selina M.H. and Mead, Emma and Mutinelli, Chiara and Zambello, Erika and Caberlotto, Laura and Pell, Theresa J. and Langmead, Christopher J. and Shah, Ajit J. and Duddy, Graham and Kew, James N. C. and Maycox, Peter R. (2009) Evaluation of expression and function of the H+/myo-inositol transporter HMIT;. BMC Cell Biology, 10 (54). ISSN 1471-2121

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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.

Item Type: Article
Research Areas: A. > School of Science and Technology > Natural Sciences
Item ID: 22785
Depositing User: Ajit Shah
Date Deposited: 01 Nov 2017 10:09
Last Modified: 14 Mar 2018 08:26
URI: http://eprints.mdx.ac.uk/id/eprint/22785

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