Abstract:
:Stimulation of monocytes/macrophages with lipopolysaccharide (LPS) results in activation of nuclear factor-kappaB (NF-kappaB), which plays crucial roles in regulating expression of many genes involved in the subsequent inflammatory responses. Here, we investigated roles of transforming growth factor-beta activated kinase 1 (TGF-TAK1), a mitogen-activated protein kinase kinase kinase (MAPKKK), in the LPS-induced signaling cascade. A kinase-negative mutant of TAK1 inhibited the LPS-induced NF-kappaB activation both in a macrophage-like cell line, RAW 264.7, and in human embryonic kidney 293 cells expressing toll-like receptor 2 or 4. Furthermore, we demonstrated that endogenous TAK1 is phosphorylated upon simulation of RAW 264.7 cells with LPS. These results indicate that TAK1 functions as a critical mediator in the LPS-induced signaling pathway.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Irie T,Muta T,Takeshige Kdoi
10.1016/s0014-5793(00)01146-7keywords:
subject
Has Abstractpub_date
2000-02-11 00:00:00pages
160-4issue
2-3eissn
0014-5793issn
1873-3468pii
S0014-5793(00)01146-7journal_volume
467pub_type
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