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Gene Information
Gene symbol: MAP3K7
Gene name: mitogen-activated protein kinase kinase kinase 7
HGNC ID: 6859
Synonyms: MEKK7
Related Genes
| # | Gene Symbol | Number of hits |
| 1 | AKT1 | 1 hits |
| 2 | CAMKK2 | 1 hits |
| 3 | IL1B | 1 hits |
| 4 | KITLG | 1 hits |
| 5 | PRKAA1 | 1 hits |
| 6 | RPS27A | 1 hits |
| 7 | SOCS3 | 1 hits |
| 8 | TRAF6 | 1 hits |
Related Sentences
| # | PMID | Sentence |
| 1 | 21233843 | Herein, we show that transforming growth factor ?-activated kinase 1 (TAK1) directly regulates stem cell factor (SCF) expression, which activates the protein kinase B (PKB)? pro-survival pathway in a cell-autonomous manner to protect keratinocytes from ROS-mediated cell death. |
| 2 | 21233843 | Ectopic expression of TAK1 or treatment with exogenous recombinant SCF restored the increased ROS production and apoptotic cell death in TAK1-deficient keratinocytes. |
| 3 | 16543409 | We show here that SOCS-3 inhibits NFkappaB-dependent transcription induced by overexpression of the upstream IL-1 signaling molecules MyD88, IL-1R-activated kinase 1, TNF receptor-associated factor (TRAF)6, and TGFbeta-activated kinase (TAK)1, but not when the MAP3K MAPK/ERK kinase kinase-1 is used instead of TAK1, indicating that the target for SOCS-3 is the TRAF6/TAK1 signaling complex. |
| 4 | 16543409 | By coimmunoprecipitation, it was shown that SOCS-3 inhibited the association between TRAF6 and TAK1 and that SOCS-3 coimmunoprecipitated with TAK1 and TRAF6. |
| 5 | 16543409 | Furthermore, SOCS-3 inhibited the IL-1-induced catalytic activity of TAK1. |
| 6 | 16543409 | Because ubiquitination of TRAF6 is required for activation of TAK1, we analyzed the role of SOCS-3 on TRAF6 ubiquitination and found that SOCS-3 inhibited ubiquitin modification of TRAF6. |
| 7 | 16543409 | These results indicate that SOCS-3 inhibits IL-1 signal transduction by inhibiting ubiquitination of TRAF6, thus preventing association and activation of TAK1. |
| 8 | 18810325 | AMPKalpha, beta, and gamma), and their differential localization in response to stimulation in muscle; (2) the biochemical regulation of AMPK by AMP, protein phosphatases, and its three known upstream kinases, LKB1, Ca2+/calmodulin-dependent protein kinase kinase (CaMKK), and transforming growth factor-beta-activated kinase 1 (TAK1); (3) the pharmacological agents that are currently available for the activation and inhibition of AMPK; (4) the physiological stimuli that activate AMPK in muscle; and (5) the metabolic processes that AMPK regulates in skeletal muscle. |