| First Author | Sato S | Year | 2005 |
| Journal | Nat Immunol | Volume | 6 |
| Issue | 11 | Pages | 1087-95 |
| PubMed ID | 16186825 | Mgi Jnum | J:112597 |
| Mgi Id | MGI:3662818 | Doi | 10.1038/ni1255 |
| Citation | Sato S, et al. (2005) Essential function for the kinase TAK1 in innate and adaptive immune responses. Nat Immunol 6(11):1087-95 |
| abstractText | Transforming growth factor-beta-activated kinase 1 (TAK1) has been linked to interleukin 1 receptor and tumor necrosis factor receptor signaling. Here we generated mouse strains with conditional expression of a Map3k7 allele encoding part of TAK1. TAK1-deficient embryonic fibroblasts demonstrated loss of responses to interleukin 1beta and tumor necrosis factor. Studies of mice with B cell-specific TAK1 deficiency showed that TAK1 was indispensable for cellular responses to Toll-like receptor ligands, CD40 and B cell receptor crosslinking. In addition, antigen-induced immune responses were considerably impaired in mice with B cell-specific TAK1 deficiency. TAK1-deficient cells failed to activate transcription factor NF-kappaB and mitogen-activated protein kinases in response to interleukin 1beta, tumor necrosis factor and Toll-like receptor ligands. However, TAK1-deficient B cells were able to activate NF-kappaB but not the kinase Jnk in response to B cell receptor stimulation. These results collectively indicate that TAK1 is key in the cellular response to a variety of stimuli. |
