دورية أكاديمية
TRAIL-induced caspase/p38 activation is responsible for the increased catalytic and invasive activities of Akt.
| العنوان: | TRAIL-induced caspase/p38 activation is responsible for the increased catalytic and invasive activities of Akt. |
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| المؤلفون: | Sun BK; Institute for Cancer Research, Yonsei Cancer Center, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea., Kim JH, Nguyen HN, Kim SY, Oh S, Lee YJ, Song JJ |
| المصدر: | International journal of oncology [Int J Oncol] 2011 Jan; Vol. 38 (1), pp. 249-56. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: D.A. Spandidos Country of Publication: Greece NLM ID: 9306042 Publication Model: Print Cited Medium: Internet ISSN: 1791-2423 (Electronic) Linking ISSN: 10196439 NLM ISO Abbreviation: Int J Oncol Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: <2003->: Athens, Greece : D.A. Spandidos Original Publication: Athens, Greece : Lychnia, |
| مواضيع طبية MeSH: | Caspases/*metabolism , Proto-Oncogene Proteins c-akt/*metabolism , TNF-Related Apoptosis-Inducing Ligand/*pharmacology , p38 Mitogen-Activated Protein Kinases/*metabolism, Humans ; Phosphorylation ; Signal Transduction ; p38 Mitogen-Activated Protein Kinases/genetics |
| مستخلص: | We previously observed that TRAIL induces acquired TRAIL resistance coinciding with increased Akt phosphorylation brought about by the Src-PI3K-Akt signaling pathways and mediated by c-Cbl. c-Cbl, a ubiquitously expressed cytoplasmic adaptor protein, is simultaneously involved in the rapid degradation of TRAIL receptors and Akt phosphorylation during TRAIL treatment. Here, we show that Akt phosphorylation is not exclusively responsible for acquired TRAIL resistance. Akt catalytic activation is known to increase during metabolic oxidative stress, but we show that TRAIL also dramatically induces the catalytic activation of Akt in TRAIL-sensitive cells, but not in TRAIL-resistant cells. This suggests that Akt catalytic activation during TRAIL-induced apoptosis is likely to play a compensatory role in the maintenance of cell homeostasis. In addition, activated p38 and phosphorylated HSP27 were found to act as downstream effector molecules of p38 during TRAIL treatment and were shown to be responsible for increased Akt catalytic and invasive activities. |
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| معلومات مُعتمدة: | R01 CA140554 United States CA NCI NIH HHS; R01 CA140554-02 United States CA NCI NIH HHS; CA140554 United States CA NCI NIH HHS |
| المشرفين على المادة: | 0 (TNF-Related Apoptosis-Inducing Ligand) EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases) EC 3.4.22.- (Caspases) |
| تواريخ الأحداث: | Date Created: 20101127 Date Completed: 20110524 Latest Revision: 20211020 |
| رمز التحديث: | 20231215 |
| مُعرف محوري في PubMed: | PMC3004145 |
| PMID: | 21109947 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1791-2423 |
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