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The E3 Ligase TTC3 Facilitates Ubiquitination and Degradation of Phosphorylated Akt

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Title: The E3 Ligase TTC3 Facilitates Ubiquitination and Degradation of Phosphorylated Akt
Authors: Suizu, Futoshi Browse this author →KAKEN DB
Hiramuki, Yosuke Browse this author
Okumura, Fumihiko Browse this author
Matsuda, Mami Browse this author
Okumura, Akiko J. Browse this author
Hirata, Noriyuki Browse this author
Narita, Masumi Browse this author
Kohno, Takashi Browse this author
Yokota, Jun Browse this author
Bohgaki, Miyuki Browse this author
Obuse, Chikashi Browse this author
Hatakeyama, Shigetsugu Browse this author →KAKEN DB
Obata, Toshiyuki Browse this author
Noguchi, Masayuki Browse this author →KAKEN DB
Keywords: Akt
ubiquitin ligase
signal transduction
Issue Date: Dec-2009
Publisher: Elsevier
Journal Title: Developmental Cell
Volume: 17
Issue: 6
Start Page: 800
End Page: 810
Publisher DOI: 10.1016/j.devcel.2009.09.007
PMID: 20059950
Abstract: The serine threonine kinase Akt is a core survival factor that underlies a variety of human diseases. Although regulatory phosphorylation and dephosphorylation have been well documented, the other post-translational mechanisms that modulate Akt activity remain unclear. We show herein that TTC3 (tetratricopeptide repeat domain 3) is an E3 ligase that interacts with Akt. TTC3 contains a canonical RING-finger motif, a pair of TPR (tetratricopeptide) motifs, a putative Akt phosphorylation site, and nuclear localization signals, and is encoded by a gene within the Down Syndrome (DS) Critical Region on chromosome 21. TTC3 is an Akt-specific specific E3 ligase that binds to phosphorylated Akt and facilitates its ubiquitination and degradation within the nucleus. Moreover, DS cells exhibit elevated TTC3 expression, reduced phosphorylated Akt, and accumulation in the G2M phase, which can be reversed by TTC3 siRNA or Myr-Akt. Thus, interaction between TTC3 and Akt may contribute to the clinical symptoms of DS.
Type: article (author version)
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 野口 昌幸

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