| protein
| repeat-1 response elements (RE) and RIP-140 ( |
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TNF receptor-associated factor 6, E3 ubiquitin protein ligase, TRAF6 ( |
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IKKalpha and IKKbeta ( |
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Smad6 ( |
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NIK and IKK2 ( |
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PP2Cbeta-1 ( |
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hepatocyte growth factor-regulated tyrosine kinase substrate, HGS ( |
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Raf kinase inhibitor protein, RKIP ( |
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XIAP, NAIP, and JNK1 ( |
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ILPIP and XIAP ( |
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TRAF6,TAB1, TAB2 ( |
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PP2Cepsilon ( |
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Smad7 ( |
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TLR3-TRAF6-TAK1-TAB2-PKR complex ( |
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TAK1-binding protein-3, TAB3 ( |
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Sef ( |
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Signal transducer and activator of transcription 3, STAT3 ( |
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TNF-alpha receptor complex and MEKK3 ( |
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CARMA1 ( |
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Suppressor of cytokine signaling (SOCS)-3, SOCS-3 ( |
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TAB1 is constitutively associated with MAP3K7 through its C-terminal region |
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ubiquitin-conjugating enzyme complex consisting of UBE2N and UBE2V1 catalyses Lys 63-linked polyubiquitination, which activates the MAP3K7 kinase complex |
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USP4 is a deubiquitinase for MAP3K7 |
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TRIM8 interacted with MAP3K7, a serine/threonine kinase essential for TNF- and IL1B–induced NFKB activation |
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FYB regulating T cell receptor-mediated activation of integrins via association with the SKAP1 adapter and the NFKB1 pathway through interactions with both the CARD11 adapter and MAP3K7 |
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KRAS stimulates BMP7 secretion and BMP signaling, leading to MAP3K7 activation and enhancement of Wnt-dependent transcription |
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is indispensable to TNFSF11-induced osteoclastogenesis |
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DUSP14 interacted with MAP3K7 and this interaction was enhanced by TNF or IL1 stimulation |
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RPS6KB1 negatively regulates TLR-mediated signals by inhibiting MAP3K7 activity |
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TAB2 is a sensor of stress conditions in the liver and functions to protect the liver by activating the MAP3K7 pathway |
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NLK functions as a pivotal negative regulator in TNF-induced activation of NFKB1 via disrupting the interaction of MAP3K7 with IKBKB |
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ECSIT interacted with each protein and regulated MAP3K7 activity, leading to the activation of NFKB1 |
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MAP3K7 regulates necroptotic signaling as well as CASP8-mediated apoptotic signaling through both NFKB1-dependent and -independent mechanisms |
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essential role for the adaptor protein TRADD in CASP8 activation and necrosome formation triggered by MAP3K7 inhibition |
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TNFAIP8L2 interacts with MAP3K7, a crucial regulatory molecule of inflammatory and immune signals, and consequently acts as a powerful negative regulator of MAP3K7 |
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TRIM8 plays a deleterious role in pressure overload-induced cardiac hypertrophy by accelerating the activation of MAP3K7-dependent signaling pathways |
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IRAK4 activity regulates likely MAP3K7 and IKBKB activation, leading to the nuclear translocation of IRF5 and induction of inflammatory cytokines in human monocytes |
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mechanistically, USP19 interacted with MAP3K7 in a TNF or IL1B-dependent manner |
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GRAMD4 interacted with MAP3K7 to promote its protein degradation, thus, resulting in the inactivation of MAPK (Mitogen-activated protein kinase) and NFKB1 pathways |
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| TAK1-deficient mous embryonic fibroblasts demonstrated loss of responses to interleukin 1beta and tumor necrosis factor ( | |
antigen-induced immune responses were considerably impaired in mice with B cell-specific TAK1 deficiency ( |
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deletion of TAK1 in mouse T cells prevented the maturation of single-positive thymocytes displaying CD4 or CD8, leading to reduction of T cells in the peripheral tissues ( |
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TAK1 deficiency in keratinocytes led to increased apoptosis in response to anoikis and TNF-& |
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945; treatment and was associated with elevated ROS level ( |
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epithelial-specific TAB1 and TAB2 double- but not TAB1 or TAB2 single-knockout mice phenocopied epithelial-specific TAK1 knockout mice |
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Ablation of both TAB1 and TAB2 diminished the activity of TAK1 in vivo and causes accumulation of ROS in the epithelial tissues |
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homozygous Tak1-deficient mice died early in embryonic development, at day 9.5 |
