• Medientyp: E-Artikel
  • Titel: MEK Kinase 1 Gene Disruption Alters Cell Migration and c-Jun NH2-Terminal Kinase Regulation but Does Not Cause a Measurable Defect in NF-κ B Activation
  • Beteiligte: Yujiri, Toshiaki; Ware, Margaret; Widmann, Christian; Oyer, Ryan; Russell, David; Chan, Edward; Zaitsu, Yuzuru; Clarke, Penny; Tyler, Kenneth; Oka, Yoshitomo; Fanger, Gary R.; Henson, Peter; Johnson, Gary L.
  • Erschienen: National Academy of Sciences of the United States of America, 2000
  • Erschienen in: Proceedings of the National Academy of Sciences of the United States of America
  • Sprache: Englisch
  • ISSN: 0027-8424
  • Schlagwörter: Biological Sciences
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  • Beschreibung: <p>MEK kinase 1 (MEKK1) is a 196-kDa mitogen-activated protein kinase (MAPK) kinase kinase that, in addition to regulating the c-Jun NH<sub>2</sub>-terminal kinase (JNK) pathway, is involved in the control of cell motility. MEKK1R-/- mice are defective in eyelid closure, a TGFα -directed process involving the migration of epithelial cells. MEKK1 expression in epithelial cells stimulates lamellipodia formation, a process required for cell movement. In addition, mouse embryo fibroblasts derived from MEKK1<sup>-/-</sup>mice are inhibited in their migration relative to MEKK1<sup>+/+</sup>fibroblasts. MEKK1 is required for JNK but not NF-κ B activation in response to virus infection, microtubule disruption, and stimulation of embryonic stem cells with lysophosphatidic acid. MEKK1 is not required for TNFα or IL-1 regulation of JNK or NF-κ B activation in macrophages or fibroblasts. Thus, MEKK1 senses microtubule integrity, contributes to the regulation of fibroblast and epithelial cell migration, and is required for activation of JNK but not NF-κ B in response to selected stress stimuli.</p>
  • Zugangsstatus: Freier Zugang