徳島大学 教育・研究者情報データベース(EDB)

1. 徳島大学.大学院ヘルスバイオサイエンス研究部.生体システム栄養科学部門.摂食機能制御学講座(2004年4月1日〜2015年3月31日)
2. 徳島大学.歯学部.口腔保健学科.口腔保健基礎学講座(2007年4月1日〜)

1. 吉田 賀弥([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.口腔保健学系.口腔保健支援学]/[徳島大学.歯学部.口腔保健学科.口腔保健支援学講座])

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2. 岡村 裕彦

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3. (英) Amorim Rabelo Bruna

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4. 日野出 大輔([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.口腔保健学系.口腔保健衛生学]/[徳島大学.歯学部.口腔保健学科.口腔保健基礎学講座])

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5. 吉田 秀夫

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6. 羽地 達次

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(英) PKR-mediated degradation of STAT1 regulates osteoblast differentiation

(英) The double-stranded RNA-dependent protein kinase (PKR) plays a critical role in various biological responses including antiviral defense, cell differentiation, apoptosis, and tumorigenesis. In this study, we investigated whether PKR could affect the post-translational modifications of STAT1 protein and whether these modifications regulate osteoblast differentiation. We demonstrated that PKR was necessary for the ubiquitination of STAT1 protein. The expressions of bone-related genes such as type I collagen, integrin binding sialoprotein, osteopontin, and osterix were suppressed in osteoblasts lacking PKR activity. In contrast, the expressions of interleukin-6 and matrix metalloproteinases 8 and 13 increased in PKR-mutated osteoblasts. The expression and degradation of STAT1 protein were regulated by PKR in a SLIM-dependent pathway. Inhibition of SLIM by RNA interference resulted in the decreased activity of Runx2 in osteoblasts. Stimulation of interleukin-6 expression and suppression of alkaline phosphatase activity were regulated through by SLIM-dependent pathway. However, expressions of bone-related genes and MMPs were regulated by SLIM-independent pathway. Our present results suggest that the aberrant accumulation of STAT1 protein induced by loss of PKR regulate osteoblast differentiation through both SLIM/STAT1-dependent and -independent pathways.

1. (英) Adaptor Proteins, Signal Transducing
2. (英) Alkaline Phosphatase
3. (英) Animals
4. (英) Antigens, Differentiation
5. (英) Cell Differentiation
6. (英) Cell Line
7. (英) Interleukin-6
8. (英) LIM Domain Proteins
9. (英) Metalloproteases
10. (英) Mice
11. (英) Osteoblasts
12. (英) RNA, Messenger
13. (英) STAT1 Transcription Factor
14. (英) Ubiquitin-Protein Ligases
15. (英) Ubiquitination
16. (英) eIF-2 Kinase

1. (英) Article.Affiliation: Department of Fundamental Oral Health Science, Institute of Health Biosciences, The University of Tokushima Graduate School, Kuramoto, Tokushima 770-8504, Japan. kaya@dent.tokushima-u.ac.jp

2. (英) Article.PublicationTypeList.PublicationType: Journal Article

3. (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't