| First Author | Lee SM | Year | 2015 |
| Journal | Cell Immunol | Volume | 296 |
| Issue | 2 | Pages | 115-21 |
| PubMed ID | 25929183 | Mgi Jnum | J:229763 |
| Mgi Id | MGI:5754437 | Doi | 10.1016/j.cellimm.2015.04.004 |
| Citation | Lee SM, et al. (2015) Myristoylated alanine-rich C kinase substrate (MARCKS) regulates the expression of proinflammatory cytokines in macrophages through activation of p38/JNK MAPK and NF-kappaB. Cell Immunol 296(2):115-21 |
| abstractText | MARCKS, a substrate of protein kinase C, is involved in various processes associated with cytoskeletal movement. Although the expression of MARCKS is highly induced in macrophages, its role in macrophage function has not been studied in detail. Notably, the suppression of MARCKS expression in macrophage cell lines blocked LPS-induced expression of TNF-alpha at the transcriptional level. Treatment of macrophages with MARCKS N-terminus sequence (MANS) and effector domain (ED) peptides, which mimic functional domains and block the phosphorylation of MARCKS, suppressed the LPS-induced expression of TNF-alpha through suppression of p38 and JNK MAPKs and NF-kappaB. Treatment of mice with MANS peptide reduced serum TNF-alpha and IL-6 levels and resulted in 40% survival of mice after the administration of a lethal dose of LPS. These data demonstrate that MARCKS is involved in the regulation of proinflammatory cytokine expression in macrophages and that MARCKS-derived peptides can be used to suppress inflammatory responses. |
