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Mitsuo Maruyama

Researcher at Nagoya University

Publications -  42
Citations -  3135

Mitsuo Maruyama is an academic researcher from Nagoya University. The author has contributed to research in topics: Antigen & Germinal center. The author has an hindex of 17, co-authored 38 publications receiving 2960 citations. Previous affiliations of Mitsuo Maruyama include Dallas Museum of Art & Osaka University.

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Regulated expression of a gene encoding a nuclear factor, IRF-1, that specifically binds to IFN-β gene regulatory elements

TL;DR: It is shown here that the IRF-1 gene possesses virus-inducible promoter and is also involved in the regulation of other genes such as IFN-alpha and MHC class I genes.
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Structurally similar but functionally distinct factors, IRF-1 and IRF-2, bind to the same regulatory elements of IFN and IFN-inducible genes

TL;DR: The results suggest that transcription of the IFN and IFN-inducible genes is regulated by two similar trans-acting factors that apparently compete for the same cis-acting recognition sequences, but which have opposite effects.
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Evidence for aberrant activation of the interleukin-2 autocrine loop by HTLV-1-encoded p40x and T3/Ti complex triggering.

TL;DR: Evidence is provided that distinct DNA sequences within the 5'-flanking regions of the genes for interleukin-2 and its receptor are involved in human T-cell-specific activation of transcription by p40x, a product of human T cell leukemia virus type I (HTLV-1).
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The integrity of the conserved 'WS motif' common to IL-2 and other cytokine receptors is essential for ligand binding and signal transduction.

TL;DR: The results indicate the critical role of the two Trp residues in the proper folding of the IL‐2R beta extracellular domain and point to the general functional importance of the WS motif in the new cytokine receptor family.
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Elimination of p19 ARF -expressing cells enhances pulmonary function in mice

TL;DR: It is demonstrated that pulmonary function in 12-month-old mice was reversibly restored by the elimination of p19ARF-expressing cells, indicating that the aging-associated decline in lung function was, at least partly, attributed to p19arF and was recovered by eliminating p19 ARF- expressing cells.