AI Article Synopsis
- N-acetylglucosamine kinase (NAGK) shows high expression levels in neurons, with lower levels in astrocytes and oligodendrocytes, as confirmed through various immunohistochemical techniques.
- Overexpressing NAGK in rat hippocampal neurons enhances dendritic complexity by increasing the number of primary dendrites and branches.
- Knockdown of NAGK leads to dendrite degeneration, but this effect can be reversed with co-expression of NAGK, indicating its important role in neuronal health and function.
Article Abstract
N-acetylglucosamine kinase (GlcNAc kinase or NAGK; EC 2.7.1.59) is a N-acetylhexosamine kinase that belong to the sugar kinase/heat shock protein 70/actin superfamily. In this study, we investigated both the expression and function of NAGK in neurons. Immunohistochemistry of rat brain sections showed that NAGK was expressed at high levels in neurons but at low levels in astrocytes. Immunocytochemistry of rat hippocampal dissociate cultures confirmed these findings and showed that NAGK was also expressed at low levels in oligodendrocytes. Furthermore, several NAGK clusters were observed in the nucleoplasm of both neuron and glia. The overexpression of EGFP- or RFP (DsRed2)-tagged NAGK in rat hippocampal neurons (DIV 5-9) increased the complexity of dendritic architecture by increasing the numbers of primary dendrites and dendritic branches. In contrast, knockdown of NAGK by shRNA resulted in dendrite degeneration, and this was prevented by the co-expression of RFP-tagged NAGK. These results suggest that the upregulation of dendritic complexity is a non-canonical function of NAGK.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3969046 | PMC |
| http://dx.doi.org/10.14348/molcells.2014.2354 | DOI Listing |
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