| First Author | Tang X | Year | 2011 |
| Journal | PLoS One | Volume | 6 |
| Issue | 9 | Pages | e25083 |
| PubMed ID | 21980379 | Mgi Jnum | J:244629 |
| Mgi Id | MGI:5913408 | Doi | 10.1371/journal.pone.0025083 |
| Citation | Tang X, et al. (2011) Novel regulation of CCL2 gene expression by murine LITAF and STAT6B. PLoS One 6(9):e25083 |
| abstractText | Inflammation is a multifaceted process: beneficial as a defense mechanism but also detrimental depending on its severity and duration. At the site of injury, inflammatory cells are activated by a cascade of mediators, one of which is LITAF, a transcription regulator known to upregulate TNF-alpha. We previously showed that human LITAF forms a complex with human STAT6B, which translocates into the nucleus to upregulate cytokine transcription. To dissect the molecular implications of this complex, a murine model was developed and interactions between mouse STAT6B (mSTAT6B) and mouse LITAF (mLITAF) were analyzed. Both mLITAF and mSTAT6B expression were MyD88- and TLR ligand-dependent. Furthermore, mLITAF was found to mediate LPS-induced CCL2 gene transcription with the cooperation of mSTAT6B leading to CCL2 protein expression. In LITAF-deficient mice, mLITAF-mediated CCL2 production in macrophages was significantly reduced compared to the wild-type control animals. Mice knockdown for mSTAT6B by 6BsiRNA1 tail vein injection resulted in a decrease in serum TNF-alpha and CCL2 production. mLITAF/mSTAT6B complex is proposed to play a role in LPS-induced CCL2 expression and possibly other cytokines. |
