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Tetsu M.C. Yung

Researcher at Tokyo Institute of Technology

Publications -  10
Citations -  569

Tetsu M.C. Yung is an academic researcher from Tokyo Institute of Technology. The author has contributed to research in topics: Poly ADP ribose polymerase & DNA repair. The author has an hindex of 9, co-authored 10 publications receiving 527 citations. Previous affiliations of Tetsu M.C. Yung include Laval University.

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NELF interacts with CBC and participates in 3' end processing of replication-dependent histone mRNAs.

TL;DR: It is shown that NELF interacts with the nuclear cap binding complex (CBC), a multifunctional factor that plays important roles in several mRNA processing steps, and the two factors together participate in the 3' end processing of replication-dependent histone mRNAs.
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A cellular defense pathway regulating transcription through poly(ADP-ribosyl)ation in response to DNA damage

TL;DR: It is found that automodification of poly(ADP-ribose) polymerase in response to DNA damage resulted in the up-regulation of transcription, presumably because automodified poly( ADP)-ribose molecules were released from transcripts, thereby relieving the block on transcription.
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Poly(ADP-ribosyl)ation as a DNA damage-induced post-translational modification regulating poly(ADP-ribose) polymerase-1-topoisomerase I interaction.

TL;DR: It is demonstrated that PARP-1 co-localizes with Topo I throughout the cell cycle and results suggest that a function for the automodification reaction is to regulate the interaction between PARp-1 and topoisomerase I, and consequently, the Topa I activity, in response to DNA damage.
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Systemic distribution and tissue localizations of human 17beta-hydroxysteroid dehydrogenase type 12.

TL;DR: The results support previous reports and solidify the possibility that 17beta-HSD type 12 may play critical roles in the physiological processes, such as fatty acid synthesis, in addition to the steroid metabolism.
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Functional competition between poly(ADP-ribose) polymerase and its 24-kDa apoptotic fragment in DNA repair and transcription.

TL;DR: The ability of the 24-kDa fragment to inhibit DNA repair, ADP-ribose polymer formation, and damage-dependent up-regulation of transcription may contribute to the apoptotic shift from cell survival to cell death mode.