Component of the N-acetylglucosamine catabolic cascade that phosphorylates N-acetylglucosamine (GlcNAc), and allows the unique ability to utilise GlcNAc as carbon source. Converts GlcNAc to GlcNAc-6-P. Also able to phosphorylate glucose, glucosamine (GlcN), and mannose. Galactose, fructose, N-acetylmannosamine (ManNAc), mannosamine (ManN), galactosamine (GalN), and N-acetylgalactosamine (GalNAc) are not phosphorylated by HXK1. GlcNAc metabolism is closely associated with virulence and morphogenesis, and is involved in the cell wall synthesis. Acts both as a repressor and an activator of genes involved in maintaining cellular homeostasis. Contributes to white-opaque morphological transition and plays a role as a filamentation repressor. ATP + N-acetyl-D-glucosamine = ADP + H(+) + N-acetyl-D-glucosamine 6-phosphate ATP + D-mannose = ADP + D-mannose 6-phosphate + H(+) ATP + D-glucose = ADP + D-glucose 6-phosphate + H(+) ATP + D-glucosamine = ADP + D-glucosamine 6-phosphate + H(+) Carbohydrate metabolism; hexose metabolism. Carbohydrate degradation; glycolysis; D-glyceraldehyde 3-phosphate and glycerone phosphate from D-glucose: step 1/4. Interacts with histone deacetylase SIR2 under filamentation-inducing conditions. Localized in cytoplasm and nucleus in a filamentation-inducing medium whereas in 2% GlcNAc, where catabolism is more prominent, a major fraction is seen to be present in cytoplasm. Localizes to mitochondria in non-fermentative carbon sources like ethanol. Expression is induced by N-acetylglucosamine (GlcNAc), by the alpha pheromone, and in filamentation-inducing media. Greatly retards the growth of cells using GlcNAc as the sole carbon source, increases resistance against farnesol, and attenuates the virulence in a mouse systemic infection model. Leads to derepression of opaque specific gene expression, as well as to constitutive filamentous growth and hyperfilamentation in filamentation-inducing conditions. Belongs to the hexokinase family.