کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10758297 | 1050406 | 2013 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Tubulin polymerization promoting protein 1 (TPPP1) increases β-catenin expression through inhibition of HDAC6 activity in U2OS osteosarcoma cells
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کلمات کلیدی
GSK3βCK1Rho-associated coiled-coil kinaseHDAC6ROCK1β-TrCPβ-catenin - بتا-کاتنینDeacetylation - دفع آلودگیMicrotubule - ریزلوله یا میکروتوبولPhosphorylation - فسفریلاسیونMitogen - میتوژنHistone deacetylase 6 - هیستون دیازتیلاز 6β-transducin repeat-containing protein - پروتئین حاوی تکرار β-transducinGlycogen synthase kinase 3β - گلیکوزین سنتاز کیناز 3βRock - یا راک
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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![عکس صفحه اول مقاله: Tubulin polymerization promoting protein 1 (TPPP1) increases β-catenin expression through inhibition of HDAC6 activity in U2OS osteosarcoma cells Tubulin polymerization promoting protein 1 (TPPP1) increases β-catenin expression through inhibition of HDAC6 activity in U2OS osteosarcoma cells](/preview/png/10758297.png)
چکیده انگلیسی
The Rho-associated coiled-coil kinase (ROCK) family of proteins, including ROCK1 and ROCK2, are key regulators of actin and intermediate filament morphology. The newly discovered ROCK substrate Tubulin polymerization promoting protein 1 (TPPP1) promotes microtubule polymerization and inhibits the activity of Histone deacetylase 6 (HDAC6). The effect of TPPP1 on HDAC6 activity is inhibited by ROCK signaling. Moreover, it was recently demonstrated that ROCK activity increases the cellular expression of the oncogene β-catenin, which is a HDAC6 substrate. In this study, we investigated the interplay between ROCK-TPPP1-HDAC6 signaling and β-catenin expression. We demonstrate that β-catenin expression is increased with ROCK signaling activation and is reduced with increased TPPP1 expression in U2OS cells. Further investigation revealed that ROCK-mediated TPPP1 phosphorylation, which prevents its binding to HDAC6, negates TPPP1-mediated reduction in β-catenin expression. We also show that increased HDAC6 activity resulting from ROCK signaling activation reduced β-catenin acetylation at Lys-49, which was also accompanied by its decreased phosphorylation by Caesin kinase 1 (CK1) and Glycogen synthase kinase 3β (GSK3β), thus preventing its proteasomal degradation. Overall, our results suggest that ROCK regulates β-catenin stability in cells via preventing TPPP1-mediated inhibition of HDAC6 activity, to reduce its acetylation and degradation via phosphorylation by CK1 and GSK3β.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 436, Issue 4, 12 July 2013, Pages 571-577
Journal: Biochemical and Biophysical Research Communications - Volume 436, Issue 4, 12 July 2013, Pages 571-577
نویسندگان
Alice V. Schofield, Cristina Gamell, Ora Bernard,