| First Author | Kim HR | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Issue | 1 | Pages | 8731 |
| PubMed ID | 28821818 | Mgi Jnum | J:256571 |
| Mgi Id | MGI:6108704 | Doi | 10.1038/s41598-017-09144-x |
| Citation | Kim HR, et al. (2017) An Essential Role for TAGLN2 in Phagocytosis of Lipopolysaccharide-activated Macrophages. Sci Rep 7(1):8731 |
| abstractText | Activated macrophages have a greater ability of phagocytosis against pathogens that is mediated by large-scale actin rearrangement. However, molecular machineries that conduct this task have not been fully identified. Here, we demonstrate an unanticipated role of TAGLN2, a 22-kDa actin-binding protein, in Toll-like receptor (TLR)-stimulated phagocytosis. TAGLN2 was greatly induced in macrophages in response to lipopolysaccharide (LPS), a ligand for TLR4, partly via the NF-kappaB pathway. TAGLN2-deficient macrophages (TAGLN2 (-/-)) showed defective phagocytic functions of IgM- and IgG-coated sheep red blood cells as well as bacteria. Cell signaling pathways involved in actin rearrangement-PI3 kinase/AKT and Ras-ERK-were also down-regulated in LPS-stimulated TAGLN2-deficient macrophages. Moreover, TAGLN2 (-/-) mice showed higher mortality after bacterial infection than wild-type littermates. Thus, our results revealed a novel function of TAGLN2 as a molecular armament required for host defense. |
