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Masato Inazu

Researcher at Tokyo Medical University

Publications -  70
Citations -  1843

Masato Inazu is an academic researcher from Tokyo Medical University. The author has contributed to research in topics: Choline & Choline transporter. The author has an hindex of 24, co-authored 66 publications receiving 1599 citations.

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Molecular and Functional Analysis of Choline Transporters and Antitumor Effects of Choline Transporter-Like Protein 1 Inhibitors in Human Pancreatic Cancer Cells.

TL;DR: Results suggest that the uptake of extracellular choline in MIA PaCa-2 cells is mediated by CTL1, a target molecule for the treatment of pancreatic cancer, and its inhibitors Amb4269951 and Amb4269675 are novel lead compounds.
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Molecular and Functional Characterization of Choline Transporter-Like Proteins in Esophageal Cancer Cells and Potential Therapeutic Targets.

TL;DR: It is concluded that extracellular choline is mainly transported via a CTL1- and CTL2-mediated choline transport system, which is both Na+-independent and pH-dependent and provides a potential new target for esophageal cancer therapy.
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Macrolide Antibiotics Exhibit Cytotoxic Effect under Amino Acid-Depleted Culture Condition by Blocking Autophagy Flux in Head and Neck Squamous Cell Carcinoma Cell Lines.

TL;DR: Whether macrolides exhibit cytotoxic effect under an amino acid-starving condition in head and neck squamous cancer cell lines such as CAL 27 and Detroit 562 as models of solid tumors with an upregulated autophagy in the central region owing to hypovascularity is examined to suggest the possibility of using macrolide antibiotics for “tumor- starving therapy”.
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Molecular and functional characterization of choline transporter in the human trophoblastic cell line JEG-3 cells.

TL;DR: The present results suggest that choline is mainly transported via a high-affinity choline transport system (CTL1) and a low-Affinity ch Caroline transport system(CTL2) in human trophoblastic JEG-3 cells, which play an important role in the growth of the fetus.
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Macrolide Antibiotics Block Autophagy Flux and Sensitize to Bortezomib Via Endoplasmic Reticulum-Stress-Mediated CHOP Induction in Myeloma Cells

TL;DR: This work investigated whether simultaneous inhibition of protein degradation systems such as the ubiquitin-proteasome system by BZ and the autophagy-lysosomes system by a macrolide antibiotic enhances ER-stress-mediated apoptosis in MM cells.