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Minoru Matsui

Researcher at University of Tokyo

Publications -  19
Citations -  3809

Minoru Matsui is an academic researcher from University of Tokyo. The author has contributed to research in topics: Thioredoxin & Gene. The author has an hindex of 13, co-authored 19 publications receiving 3679 citations. Previous affiliations of Minoru Matsui include Kyoto University.

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AP-1 transcriptional activity is regulated by a direct association between thioredoxin and Ref-1

TL;DR: It is proved that TRX can associate directly with Ref-1 in the nucleus and the requirement of cysteine residues in the TRX catalytic center for the potentiation of AP-1 activity is demonstrated.
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Identification of Thioredoxin-binding Protein-2/Vitamin D3 Up-regulated Protein 1 as a Negative Regulator of Thioredoxin Function and Expression

TL;DR: The results suggested that TBP-2/VDUP1 serves as a negative regulator of the biological function and expression of TRX, an important redox regulatory mechanism in cellular processes, including differentiation of myeloid and macrophage lineages.
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Intestinal tumorigenesis in compound mutant mice of both dpc4 (smad4) and apc genes

TL;DR: The authors showed that mutations in the DPC4 (SMAD4) gene play a significant role in the malignant progression of colorectal tumors in mice. But, their experiments were performed on Apc Δ 716 knockout mice, a model for human familial adenomatous polyposis.
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Early embryonic lethality caused by targeted disruption of the mouse thioredoxin gene

TL;DR: The phenotype of mice carrying a targeted disruption of the thioredoxin gene (Txn) is described and results indicate that Txn expression is essential for early differentiation and morphogenesis of the mouse embryo.
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Multiple functional defects in peripheral autonomic organs in mice lacking muscarinic acetylcholine receptor gene for the M3 subtype

Abstract: Muscarinic acetylcholine receptors consist of five distinct subtypes and have been important targets for drug development. In the periphery, muscarinic acetylcholine receptors mediate cholinergic signals to autonomic organs, but specific physiological functions of each subtype remain poorly elucidated. Here, we have constructed and analyzed mutant mice lacking the M3 receptor and have demonstrated that this subtype plays key roles in salivary secretion, pupillary constriction, and bladder detrusor contractions. However, M3-mediated signals in digestive and reproductive organs are dispensable, likely because of redundant mechanisms through other muscarinic acetylcholine receptor subtypes or other mediators. In addition, we have found prominent urinary retention only in the male, which indicates a considerable sex difference in the micturition mechanism. Accordingly, this mutant mouse should provide a useful animal model for investigation of human diseases that are affected in the peripheral cholinergic functions.