Evaluation of expression and function of the H+/myo-inositol transporter HMIT | BMC Molecular and Cell Biology | Springer Nature Link
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.
Evaluation of expression and function of the H + / myo -inositol transporter HMIT Research article Open access Published: 16 July 2009 Volume 10 , article number 54 ( 2009 ) Cite this article You have full access to this open access article Download PDF Save article View saved research BMC Cell Biology Aims and scope Submit manuscript Evaluation of expression and function of the H + / myo -inositol transporter HMIT Download PDF Abstract Background The phosphoinositide (PIns) signalling pathway regulates a series of neuronal processes, such as neurotransmitter release, that are thought to be al
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