期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 108, 期 26, 页码 10550-10555出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1011665108
关键词
disulfide; receptor tyrosine kinase; DCF; DCP-Bio1
资金
- American Heart Association [SDG 0730069N]
- National Institutes of Health [R01 CA136810, R33 CA126659]
- Korean Ministry of Education, Science and Technology [FPR08-A1-020]
- National Core Research Center through the Center for Cell Signaling Research and Drug Discovery Research [R15-2006-020]
Isoform-specific signaling of Akt, a major signaling hub and a prominent therapeutic target, remained poorly defined until recently. Subcellular distribution, tissue-specific expression, substrate specificity, and posttranslational modifications are believed to underlie isoform-specific signaling of Akt. The studies reported here show inhibition of Akt2 activity under physiologically relevant conditions of oxidation created by PDGF-induced reactive oxygen species. Combined MS and functional assays identified Cys124 located in the linker region between the N-terminal pleckstrin homology domain and the catalytic kinase domain as one of the unique regulatory redox sites in Akt2 with functional consequence on PDGF-stimulated glucose uptake. A model is proposed describing the consequence of increased endogenous oxidation induced by extracellular cues such as PDGF on Akt2 activity.
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