التفاصيل البيبلوغرافية
| العنوان: |
GSK3beta regulates Bcl2L12 and Bcl2L12A anti‐apoptosis signaling in glioblastoma and is inhibited by LiCl |
| المؤلفون: |
Hong, Yi-Ren, Lin, Ching-Chih, Chou, Chia-Hua, Howng, Shen-Long |
| المصدر: |
The FASEB Journal ; volume 26, issue S1 ; ISSN 0892-6638 1530-6860 |
| بيانات النشر: |
Wiley |
| سنة النشر: |
2012 |
| المجموعة: |
Wiley Online Library (Open Access Articles via Crossref) |
| الوصف: |
Bcl2L12 has been reported to be involved in post‐mitochondrial apoptotic events in glioblastoma, but the role of Bcl2L12A, a splicing variant of Bcl2L12, remains unknown. In this study, our data demonstrated that GSK3beta interacts with Bcl2L12, but not Bcl2L12A, which C‐terminal lacks a binding region. We found that a Bcl2L12153‐191 fragment located outside of the C‐terminus BH2 motif is responsible for GSK3beta binding. In vitro kinase and lamda‐phosphatase assays showed that GSK3beta phosphorylates Bcl2L12 at S156, while this site is absent on Bcl2L12A. Transiently expressed GFP‐fused proteins, including Bcl2L12, Bcl2L12(S156A) and Bcl2L12A, in U87MG cells. Staurosporine (STS) treatment demonstrated that both Bcl2L12 and Bcl2L12A may have anti‐apoptotic properties. In contrast, no anti‐apoptotic ability was seen in Bcl2L12(S156A). When STS was administered in combination with LiCl, the Bcl2L12‐expressing U87MG cells underwent apoptosis. This effect could be reversed by LiCl. In short, we established a model to demonstrate that GSK3beta interacts and phosphorylates Bcl2L12 and might also affect Bcl2L12A to modulate of the apoptosis signaling pathway in glioblastoma. These findings suggest that LiCl may be a prospective therapeutic agent against GBM |
| نوع الوثيقة: |
article in journal/newspaper |
| اللغة: |
English |
| DOI: |
10.1096/fasebj.26.1_supplement.797.7 |
| الاتاحة: |
http://dx.doi.org/10.1096/fasebj.26.1_supplement.797.7 |
| Rights: |
http://onlinelibrary.wiley.com/termsAndConditions#vor |
| رقم الانضمام: |
edsbas.FE243116 |
| قاعدة البيانات: |
BASE |