کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10766905 | 1050686 | 2008 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Tuberous sclerosis complex 2 loss-of-function mutation regulates reactive oxygen species production through Rac1 activation
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
The products of the TSC1 (hamartin) and TCS2 (tuberin) tumor suppressor genes negatively regulate cell growth by inhibiting mTOR signaling. Recent research has led to the postulation that tuberin and/or hamartin are involved in tumor migration, presumably through Rho activation. Here we show that LEF-8 cells, which contain a Y1571 missense mutation in tuberin, express higher Rac1 activity than tuberin negative and positive cells. We also provide evidence of obvious lamellipodia formation in LEF-8 cells. Since the production of TSC2Y1571H cannot form a hetero-complex with hamartin, we further analyzed another mutant, TSC2R611Q, which also lacks the ability to form a complex with hamartin. Introducing both forms of mutated TSC2 into COS-1 cells increased Rac1 activity as well as cell motility. We also found these two mutants interacted with Rac1. We further demonstrated that the introduction of mutated TSC2 into COS-1 cells can generate higher reactive oxygen species (ROS). These results indicate that loss-of-function mutated tuberin can activate Rac1 and thereby increase ROS production.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 368, Issue 1, 28 March 2008, Pages 132-137
Journal: Biochemical and Biophysical Research Communications - Volume 368, Issue 1, 28 March 2008, Pages 132-137
نویسندگان
Tsukasa Suzuki, Swadesh K. Das, Hirohumi Inoue, Machiko Kazami, Okio Hino, Toshiyuki Kobayashi, Raymond S. Yeung, Ken-Ichi Kobayashi, Tadahiro Tadokoro, Yuji Yamamoto,