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Masahiko Kuroda

Researcher at Tokyo Medical University

Publications -  255
Citations -  15032

Masahiko Kuroda is an academic researcher from Tokyo Medical University. The author has contributed to research in topics: Cancer & Medicine. The author has an hindex of 50, co-authored 232 publications receiving 13576 citations. Previous affiliations of Masahiko Kuroda include Tokyo Medical and Dental University & Kyoto University.

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Function of the chemokine receptor CXCR4 in haematopoiesis and in cerebellar development

TL;DR: This is the first demonstration of the involvement of a G-protein-coupled chemokine receptor in neuronal cell migration and patterning in the central nervous system and may be important for designing strategies to block HIV entry into cells and for understanding mechanisms of pathogenesis in AIDS dementia.
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CHOP is implicated in programmed cell death in response to impaired function of the endoplasmic reticulum

TL;DR: Compared with the wild type, mouse embryonic fibroblasts derived from chop -/- animals exhibited significantly less programmed cell death when challenged with agents that perturb ER function, and the proximal tubule epithelium of chop -/+ animals exhibited fourfold lower levels of TUNEL-positive cells, and significantly less evidence for subsequent regeneration.
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Systemically Injected Exosomes Targeted to EGFR Deliver Antitumor MicroRNA to Breast Cancer Cells

TL;DR: It is shown that exosomes can efficiently deliver microRNA (miRNA) to epidermal growth factor receptor (EGFR)-expressing breast cancer cells, and the results suggest that exOSomes can be used therapeutically to target EGFR-expressing cancerous tissues with nucleic acid drugs.
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Cloning of mammalian Ire1 reveals diversity in the ER stress responses.

TL;DR: The cloning of a murine homolog of yeast IRE1, an essential upstream component of the ER stress‐ response in yeast, is reported on, indicating that a single upstream component, Ire1, plays a role in multiple facets of theER stress‐response in mammalian cells.
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Leukemia cell to endothelial cell communication via exosomal miRNAs.

TL;DR: The exosome, derived from K562 cells with enforced miR-92a expression, did not affect the growth of HUVECs but did enhance endothelial cell migration and tube formation, supporting the idea that exosomal miRNAs have an important role in neoplasia-to-endothelial cell communication.