TABLE 2.
Potential therapeutic target in AD associated with protein post-translational modifications.
| Modifiers | Agents | Targets | Functions | References |
|---|---|---|---|---|
| MAPK inhibitors | vitamin K2 | JNK, ERK | Suppress skin inflammation; attenuate activated T-cell immunity | Zhang et al. (2021) |
| Galactose | ITLN1 | Interfere ERK phosphorylation; suppress TH2 immune responses | Yi et al. (2017) | |
| BTP2/SKF96365 | STIM1 | Suppress skin inflammation | Hong et al. (2015) | |
| SB202190 | p38 MAPK | Repair skin barrier | Kanemaru et al. (2017) | |
| SP600125 | JNK | Repair skin barrier | Cha et al. (2019a) | |
| AKT inhibitors | LY294002 | PI3K | Suppress T cell immune responses; inhibit serum IgE and skin inflammation; repair skin barrier | Xiao et al. (2017), Hu et al. (2021) |
| Rapamycin | mTOR | Suppress TH2 immune responses; repair skin barrier | Yang et al. (2014a) | |
| PKC inhibitor | 4,5-bis (4-fluoroanilino) | PKCβII | Inhibit l-plastin phosphorylation | Pazdrak et al. (2011) |
| HDAC inhibitor | Butyric acid | Most HDACs, except Class IIB and III | Reduce S. aureus colonization; decrease pro-inflammatory interleukins | Davie (2003), Traisaeng et al. (2019) |
| Phenylbutyrate | Most HDACs, except Class IIB and III | Inhibit local mast cells; activating Tregs | Chung and Pui (2011) | |
| Tubastatin A | HDAC 6 | Rescue barrier dysfunction; inhibit skin inflammation; activating Tregs | Kwon et al. (2021) | |
| Belinostat | Class I, II | Rescue barrier dysfunction | Liew et al. (2020), Quah et al. (2021) | |
| Trichostatin A | Class I, II | Suppress TH2 immune response | Kim et al. (2010), Banerjee et al. (2012), Shi et al. (2012) | |
| Glycan inhibitor | neuraminidase | sialic acid | Attenuate allergic response | Shade et al. (2020) |
Abbreviations: AD, atopic dermatitis; AKT, protein kinase B; ERK, extracellular signal-regulated protein kinase; HDAC, histone deacetylase; ITLN1, intelectin-1; JNK, c-Jun N-terminal kinases; mTOR, mammalian target of rapamycin; PI3K, phosphoinositide 3-kinase; PKCβII, protein kinase C βII; S. aureus, Staphylococcus aureus; STIM, stromal interaction molecule 1; TH2, T helper 2 cells; Treg, T regulatory cells; MAPK, mitogen-activated protein kinases.