Transactivation of the EGF receptor and a PI3 kinase-ATF-1 pathway is involved in the upregulation of NOX1, a catalytic subunit of NADPH oxidase

Autor: Chihiro Yabe-Nishimura, Toru Nishinaka, Masato Katsuyama, ChunYuan Fan
Rok vydání: 2005
Předmět:
Dinoprost
Biochemistry
Tropomyosin receptor kinase C
Phosphatidylinositol 3-Kinases
Transactivation
Structural Biology
NADH
NADPH Oxidoreductases
Phosphorylation
Phosphoinositide-3 Kinase Inhibitors
Mitogen-Activated Protein Kinase 1
Mitogen-Activated Protein Kinase 3
biology
Chemistry
Phosphoinositide 3 kinase
Up-Regulation
Cell biology
DNA-Binding Proteins
ErbB Receptors
Prostaglandin F2α
NOX1
NADPH Oxidase 1
cardiovascular system
Signal transduction
hormones
hormone substitutes
and hormone antagonists
Signal Transduction
Transcriptional Activation
Biophysics
Catalysis
Cell Line
Genetics
Animals
RNA
Messenger
Protein kinase A
Protein Kinase Inhibitors
Molecular Biology
Protein kinase B
Activating Transcription Factor 1
Mitogen-Activated Protein Kinase Kinases
Phosphoinositide 3-kinase
NADPH oxidase
Epidermal growth factor receptor
Akt/PKB signaling pathway
Cell Biology
Matrix Metalloproteinases
Rats
Protein Subunits
biology.protein
Cancer research
Transcription Factors
Zdroj: FEBS Letters. 579:1301-1305
ISSN: 0014-5793
DOI: 10.1016/j.febslet.2005.01.021
Popis: We previously reported that hypertrophy of vascular smooth muscle cells caused by prostaglandin (PG) F2alpha is mediated by the induction of NOX1, a catalytic subunit of NADPH oxidase that generates superoxide. The signal transduction pathway(s) involved in this process, however, remained unresolved. PGF2alpha enhanced the phosphorylation of the epidermal growth factor (EGF) receptor, and a selective inhibitor of EGF receptor kinase, tyrphostin AG1478, significantly suppressed PGF2alpha-induced NOX1 expression. AG1478 also blunted the PGF2alpha-induced phosphorylation of extracellular signal-regulated protein kinase (ERK)1/2 and Akt. Phosphoinositide 3 (PI3) kinase inhibitors not only reduced PGF2alpha-induced NOX1 expression, but also suppressed the phosphorylation of ATF-1, a transcription factor previously shown to play a key role in the induction of NOX1. Accordingly, the transactivation of the EGF receptor and the activation of ERK1/2, PI3 kinase, and ATF-1 constitute the signaling pathways involved in the upregulation of NOX1.
Databáze: OpenAIRE
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