口腔組織構造生物学

がん細胞における細胞融合を制御する分子メカニズムの解析

【主な論文】

1. Mitochondrial protein E2F3d, a distinctive E2F3 product, mediates hypoxia-induced mitophagy in cancer cells. 

Keigo Araki*, Keiko Kawauchi, Wataru Sugimoto, Daisuke Tsuda, Hiroya Oda, Ryosuke Yoshida, Kiyoshi Ohtani    *Correspondence author

Communications Biology, 2019 January 3; 3(2): 1–12

 

2. Differential requirement for dimerization partner DP between E2F-dependent activation of tumor suppressor and growth-related genes.

Hideyuki Komori, Yasuko Goto, Kenta Kurayoshi, Eiko Ozono, Ritsuko Iwanaga, Andrew P. Bradford, Keigo Araki, Kiyoshi Ohtani

Scientific Reports, 2018 May 31; 8(1): 8438

 

3. The interaction mode of the acidic region of the cell cycle transcription factor DP1 with TFIIH.

Masahiko Okuda, Keigo Araki, Kiyoshi Ohtani, Yoshifumi Nishimura

Journal of Molecular Biology, 2016 December 4; 428(24 Pt B): 4993–5006

 

4. Cytoplasmic translocation of the retinoblastoma protein disrupts sarcomeric organization.

Keigo Araki*, Keiko Kawauchi, Hiroaki Hirata, Mie Yamamoto, Yoichi Taya*   *Correspondence author

Elife, 2013 December 3; 2: e01228

 

5. Loss of p53 enhances catalytic activity of IKKbeta through O-linked beta-N-acetyl glucosamine modification.

Keiko Kawauchi, Keigo Araki, Kei Tobiume, Nobuyuki Tanaka

Proc. Natl. Acad. Sci. U S A, 2009 March 3; 106(9): 3431–3436

 

6. IKK/NF-kappaB signaling pathway inhibits cell cycle progression via a novel Rb-independent suppression system for E2F transcription factors.

Keigo Araki, Keiko Kawauchi, Nobuyuki Tanaka

Oncogene, 2008 September 25; 27(43): 5696–5705

 

7. Activated p53 induces NF-kappaB DNA-binding but suppresses its transcriptional activation.

Keiko Kawauchi, Keigo Araki, Kei Tobiume, Nobuyuki Tanaka

Biochem. Biophys. Res. Commun., 2008 July 18; 372(1): 137–141

 

8. p53 regulates glucose metabolism through an IKK-NF-kappaB pathway and inhibits cell transformation.

Keiko Kawauchi, Keigo Araki, Kei Tobiume, Nobuyuki Tanaka

Nature Cell Biology, 2008 May; 10(5): 611–618

 

9. Distinct recruitment of E2F family members to specific E2F-binding sites mediates activation and repression of the E2F1 promoter.

Keigo Araki, Yusuke Nakajima, Kazuhiro Eto, Masa-Aki Ikeda

Oncogene, 2003 October 23; 22(48): 7632–7641

 

10. E2FBP1/DRIL1, an AT-rich interaction domain-family transcription factor, is regulated by p53.

Kaiwen Ma, Keigo Araki, Solachuddin J.A. Ichwan, Tamaki Suganuma, Mimi Tamamori-Adachi, Masa-Aki Ikeda

Molecular Cancer Research, 2003 April; 1(6): 438–444

 

 

【総説】

1. p53 regulates cytoskeleton remodeling to suppress tumor progression.

Keigo Araki, Takahiro Ebata, Alvin Kunyao Guo, Kei Tobiume, Steven John Wolf, Keiko Kawauchi

Cellular and Molecular Life Sciences, 2015 November; 72(21): 4077–4094

 

 

【著書】

(英文)

1. Distinct E2F-Mediated Transcriptional Mechanisms in Cell Proliferation, Endoreplication and Apoptosis

Hideyuki Komori, Ritsuko Iwanaga, Andrew P. Bradford, Keigo Araki and Kiyoshi Ohtani

“Gene Regulation” (Edited by Payam Behzadi) 

Chapter 4: 1–18, InTech Open Access Publisher, 2019

 

2. The Key Role of E2F in Tumor Suppression through Specific Regulation of Tumor Suppressor Genes in Response to Oncogenic Changes

Kenta Kurayoshi, Eiko Ozono, Ritsuko Iwanaga, Andrew P. Bradford, Hideyuki Komori, Keigo Araki and Kiyoshi Ohtani

   “Gene Expression and Regulation in Mammalian Cells” (Edited by Fumiaki Uchiumi) 

Chapter 7: 143–162, InTech Open Access Publisher, 2018

 

(和文)

1. がん細胞におけるE2Fファミリーの新たな役割

―新規メンバーE2F3dによるミトコンドリア品質管理機構―

荒木啓吾、大谷清

Journal of Japanese Biochemical Society, 2019年12月25日; 91(6): 781-784

 

2. 癌の発生と細胞周期の制御             

荒木啓吾

口腔病学会雑誌、2003年9月30日、第70巻第3号、195ページ        

 

日本分子生物学会