Provided herein are uses of genes for HOG, Ras and cAMP
signal transduction pathways to treat fungal infection. To regulate the HOG pathway of
Cryptococcus neoformans, roles of SSK1, TCO2, SSK2, PBS2, HOG1, ENA1 and NHA1 genes were investigated to find that a
biosynthesis level of
ergosterol is increased when these genes are inhibited. When the genes are inhibited, a large amount of
ergosterol is distributed on a fungal
cell membrane. Accordingly, since there are many working points of an
ergosterol-binding
antifungal agent, an efficiency of the ergosterol-binding
antifungal agent can be considerably improved. To regulate the Ras and cAMP pathways of
Cryptococcus neoformans, roles of RAS1, RAS2, CDC24, GPA1, CAC1, ACA1, PKA1, HSP12 and HSP122 genes were investigated to find that a sensitivity to a
polyene- or
azole-based
drug is increased when these genes are inhibited. Therefore, an
antifungal pharmaceutical composition including an inhibitor against the
gene or
protein encoded by the same can be used as an excellent combined antifungal agent which can reduce a conventional amount of an antifungal agent used and increase an efficiency.