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Hiroyuki Inuzuka

Researcher at Beth Israel Deaconess Medical Center

Publications -  121
Citations -  7607

Hiroyuki Inuzuka is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: Ubiquitin ligase & Kinase. The author has an hindex of 44, co-authored 107 publications receiving 6509 citations. Previous affiliations of Hiroyuki Inuzuka include Kagawa University & Emory University.

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SCF FBW7 regulates cellular apoptosis by targeting MCL1 for ubiquitylation and destruction

TL;DR: It is shown that the E3 ubiquitin ligase SCFFBW7 (a SKP1–cullin-1–F-box complex that contains FBW7 as the F-box protein) governs cellular apoptosis by targeting MCL1, a pro-survival BCL2 family member, for ubiquitylation and destruction in a manner that depends on phosphorylation by glycogen synthase kinase 3.
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Roles of F-box proteins in cancer

TL;DR: Additional genetic and mechanistic studies will help to define the role of each F-box protein in tumorigenesis, thereby paving the road for the rational design of F- box protein-targeted anticancer therapies.
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Cell-cycle-regulated activation of Akt kinase by phosphorylation at its carboxyl terminus

TL;DR: The results of this study show Akt S477/T479 phosphorylation to be an essential layer of the Akt activation mechanism to regulate its physiological functions, thereby providing a new mechanistic link between aberrant cell cycle progression and Akt hyperactivation in cancer.
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STO-609, a Specific Inhibitor of the Ca2+/Calmodulin-dependent Protein Kinase Kinase

TL;DR: Results indicate that STO-609 is a selective and cell-permeable inhibitor of CaM-KK and that it may be a useful tool for evaluating the physiological significance of the CaM/calmodulin-dependent protein kinase kinase pathway in vivo as well as in vitro.
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mTOR drives its own activation via SCF(βTrCP)-dependent degradation of the mTOR inhibitor DEPTOR.

TL;DR: This work describes an mTOR-dependent phosphorylation-driven pathway for DEPTOR destruction via SCF(βTrCP) and reveals a positive feedback loop involving mTOR and CKI-dependent turnover of its inhibitor, DEPTor, suggesting that misregulation of the DEptOR destruction pathway might contribute to aberrant activation of mTOR in disease.