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Naoto Hirano

Researcher at University of Tokyo

Publications -  36
Citations -  2767

Naoto Hirano is an academic researcher from University of Tokyo. The author has contributed to research in topics: Medicine & Gene. The author has an hindex of 20, co-authored 29 publications receiving 2694 citations. Previous affiliations of Naoto Hirano include Harvard University.

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A novel signaling molecule, p130, forms stable complexes in vivo with v-Crk and v-Src in a tyrosine phosphorylation-dependent manner.

TL;DR: The p130 (designated Cas for Crk‐associated substrate) is a common cellular target of phosphorylation signal via v‐Crk and v‐Src oncoproteins, and its unique structure indicates the possible role of p130Cas in assembling signals from multiple SH2‐containing molecules.
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Transplantation of anergic histoincompatible bone marrow allografts.

TL;DR: Donor bone marrow treated ex vivo to induce anergy to alloantigens from the recipient can reconstitute hematopoiesis in vivo with a relatively low risk of GVHD.
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Tob is a negative regulator of activation that is expressed in anergic and quiescent T cells

TL;DR: T cell quiescence is an actively maintained phenotype that must be suppressed for T cell activation to occur and Tob, a member of an anti-proliferative gene family, was highly expressed in anergic T cell clones.
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Human primary and memory cytotoxic T lymphocyte responses are efficiently induced by means of CD40-activated B cells as antigen-presenting cells: potential for clinical application.

TL;DR: This work demonstrates that CD40-B cells from healthy donors and cancer patients are fully functional and equally expanded in long-term cultures, and are an excellent source of professional APCs for immune assessment, antigen discovery, and antigen-specific immunotherapy.
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Homozygous loss of the cyclin-dependent kinase 4-inhibitor (p16) gene in human leukemias

TL;DR: The results suggest that loss of the CDK4I function may contribute to immortalization of human leukemia cells and play a causative role at least in development of human lymphocytic leukemias.