| First Author | Papoutsopoulou S | Year | 2006 |
| Journal | Nat Immunol | Volume | 7 |
| Issue | 6 | Pages | 606-15 |
| PubMed ID | 16633345 | Mgi Jnum | J:112395 |
| Mgi Id | MGI:3656197 | Doi | 10.1038/ni1334 |
| Citation | Papoutsopoulou S, et al. (2006) ABIN-2 is required for optimal activation of Erk MAP kinase in innate immune responses. Nat Immunol 7(6):606-15 |
| abstractText | The TPL-2 MEK kinase is essential for activation of the Erk MAP kinase pathway during innate immune responses. TPL-2 is found in complex with ABIN-2 (A20-binding inhibitor of NF-kappaB 2). Here, using antigen-presenting cells from ABIN-2-deficient mice, we show that ABIN-2 was required for optimal activation of Erk induced by receptors that signal via TPL-2, including Toll-like receptor 4 and tumor necrosis factor receptor 1 in macrophages, and CD40 in B cells. ABIN-2 was necessary for the maintenance of TPL-2 protein stability. In contrast, ABIN-2 deficiency did not affect agonist-induced regulation of transcription factor NF-kappaB. Stimulation of ABIN-2-deficient macrophages via Toll-like receptor 4 showed that different thresholds of Erk signaling were required for optimal induction of tumor necrosis factor and interleukin 1beta. Thus, ABIN-2 acts to positively regulate the Erk signaling potential by stabilizing TPL-2. |
