Disease relevance of Map3k7

• The Yersinia enterocolitica effector YopP inhibits host cell signalling by inactivating the protein kinase TAK1 in the IL-1 signalling pathway [1].

High impact information on Map3k7

• The transforming-growth-factor-beta-activated kinase TAK1 is a member of the mitogen-activated protein kinase kinase kinase family, which couples extracellular stimuli to gene transcription [2].
• Here, we demonstrate that another protein kinase, TGFbeta-activated kinase (TAK)1, is essential for IKK activation in response to BCR stimulation [3].
• In addition, PMA/ionophore-mediated ubiquitination of NF-kappaB essential modulator (NEMO)/IkappaB kinase gamma (IKKgamma) and phosphorylation of TGF-beta-activated kinase 1 (TAK1) were nearly abolished in Ubc13-deficient thymocytes [4].
• Selection for a Snf+ growth phenotype yielded cDNA plasmids expressing LKB1, Ca2+/calmodulin-dependent protein kinase kinase, and transforming growth factor-beta-activated kinase (TAK1), a member of the mitogen-activated protein kinase kinase kinase family [5].
• Transforming growth factor-beta-activated kinase 1 is essential for differentiation and the prevention of apoptosis in epidermis [6].

Biological context of Map3k7

• Expression of TAK1, a mediator of TGF-beta and BMP signaling, during mouse embryonic development [7].
• Activation of NF-kappa B in virus-infected macrophages is dependent on mitochondrial oxidative stress and intracellular calcium: downstream involvement of the kinases TGF-beta-activated kinase 1, mitogen-activated kinase/extracellular signal-regulated kinase kinase 1, and I kappa B kinase [8].
• Our results demonstrate that JunB gene activation by TAK1 is mediated by the CCAAT-binding factor NF-Y [9].

Anatomical context of Map3k7

• At mid-gestation, TAK1 expression becomes more restricted, with high levels seen specifically during development of diverse organs and tissues including the nervous system, testis, kidney, liver and gut [7].

Regulatory relationships of Map3k7

• The CCAAT-binding transcription factor, nuclear factor Y (NF-Y), activated the JunB promoter and a dominant negative NF-YA construct inhibited TAK1 activation of JunB [9].
• TAK1 regulates ROS partially through c-Jun, which is important for preventing ROS-induced skin inflammation [10].
• Both TbetaRI-mediated TAK1 phosphorylation and TGF-beta1-induced TAK1 phosphorylation do not require kinase activity of TbetaRI [11].

Other interactions of Map3k7

• Additionally, TAK1 expression is seen in the developing lung and pancreas [7].
• Real-time PCR analysis confirmed that expression of the hypothalamic IL-1 pathway (IL-1beta, IL-1 type 1 and 2 receptors, and PPM1b/PP2C-beta, a molecule that has been implicated in the inhibition of transforming growth factor-beta-activated kinase-1-mediated IL-1 action) is altered after 2 days, but not 1 wk, of high-fat feeding [12].

Analytical, diagnostic and therapeutic context of Map3k7

• Using immunohistochemistry (IHC), we demonstrate that TAK1 is expressed ubiquitously during early development [7].

References