Antagonism of p66shc by melanoma inhibitory activity
العنوان: | Antagonism of p66shc by melanoma inhibitory activity |
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المؤلفون: | Tohru Yamamori, Kaikobad Irani, Kenji Kasuno, Asma Naqvi, Jeremy DeRicco, Sun Yang, Ilwola Mattagajasingh, Lakshmi Santhanam, A.-K. Bosserhoff, Frank L. Meyskens |
المصدر: | Kasuno, K; Naqvi, A; DeRicco, J; Yamamori, T; Santhanam, L; Mattagajasingh, I; et al.(2007). Antagonism of p66shc by melanoma inhibitory activity. Cell Death and Differentiation, 14(8), 1414-1421. doi: 10.1038/sj.cdd.4402131. UC Irvine: Retrieved from: http://www.escholarship.org/uc/item/4855x9w7Test |
بيانات النشر: | Springer Science and Business Media LLC, 2007. |
سنة النشر: | 2007 |
مصطلحات موضوعية: | Src Homology 2 Domain-Containing, Transforming Protein 1, endocrine system diseases, Apoptosis, Endogeny, Biology, Serine, Mice, Downregulation and upregulation, Cell Line, Tumor, Chlorocebus aethiops, Animals, Humans, Phosphorylation, Melanoma, Molecular Biology, Adaptor Proteins, Signal Transducing, Extracellular Matrix Proteins, Binding Sites, Melanoma inhibitory activity, Hydrogen Peroxide, Cell Biology, Molecular biology, digestive system diseases, Neoplasm Proteins, Oxidative Stress, Shc Signaling Adaptor Proteins, Biochemistry, Cell culture, COS Cells, Protein Binding, Proto-oncogene tyrosine-protein kinase Src |
الوصف: | The p66shc protein governs oxidant stress and mammalian lifespan. Here, we identify melanoma inhibitory activity (MIA), a protein secreted by melanoma cells, as a novel binding partner and antagonist of p66shc. The N-terminal collagen homology-2 (CH2) domain of p66shc binds to the Src Homology-3 (SH3)-like domain of MIA in vitro. In cells, ectopically expressed MIA and p66shc colocalize and co-precipitate. MIA also co-precipitates with the CH2 domain of p66shc in vivo. MIA expression in vivo suppresses p66shc-stimulated increase in endogenous hydrogen peroxide (H(2)O(2)), and inhibits basal and H(2)O(2)-induced phosphorylation of p66shc on serine 36 and H(2)O(2)-induced death. In human melanoma cells expressing MIA, endogenous MIA and p66shc co-precipitate. Downregulation of MIA in melanoma cells increases basal and ultraviolet radiation (UVR)-induced phosphorylation of p66shc on serine 36, augments endogenous H(2)O(2) levels, and increases their susceptibility to UVR-induced death. These findings show that MIA binds to p66shc, and suggest that this interaction antagonizes phosphorylation and function of p66shc. |
وصف الملف: | application/pdf |
تدمد: | 1476-5403 1350-9047 |
الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8b97a3acff1c70b20770980de198b230Test https://doi.org/10.1038/sj.cdd.4402131Test |
حقوق: | OPEN |
رقم الانضمام: | edsair.doi.dedup.....8b97a3acff1c70b20770980de198b230 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 14765403 13509047 |
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