Table 3.
Treatment/model | Signaling pathway | References | |
---|---|---|---|
Immunocytes | |||
T cells | -CD28-activated | -Vav1 R-methylation and translocation into the nucleus | [44,45] |
CD4+ T cells (but not CD8+ T cells) | -SAHase inhibition | -Reduced Vav R-methylation -Reduced Akt, Erk 1/2, NF-κB phosphorylation |
[36] |
Protein methyltransferase | |||
PRMT-1 | -Arginine methyltransferase | -Binding to IFNAR1 -Inhibition of antiproliferative effects of IFN-β by blocking PRMT-1 -STAT1 R-methylation by PRMT1? |
[38] [39–42] |
SETD6 | -Lysine methyltransferase | -Monomethylation of RelA at Lysine 310 -Basal condition: RelAK310me1 bound to H3K9me2 by recognition of the GLP domain of SETD6 -Pro-inflammatory stimulus: PKCζ-mediated phosphorylation of RelAK310me1 blocks GLP-RelAK310me1 recognition→chromatin relaxation and RelA target genes expression |
[43] |
Autoimmunity | |||
Lupus | -Transgenic mouse that inducibly expresses a dominant-negative MEK in T cells -Hydralazine/ Erk inhibitor-treated murine T cells -Human T cells from SLE patient |
-Decreased Erk 1/2 pathway signaling -Impaired PKCδ -Decreases DNA methylation -Modification of gene expression rendering T cells autoreactive |
[95–97] |