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Satoshi Takaki

Researcher at University of Tokyo

Publications -  78
Citations -  4956

Satoshi Takaki is an academic researcher from University of Tokyo. The author has contributed to research in topics: Haematopoiesis & Stem cell. The author has an hindex of 34, co-authored 76 publications receiving 4629 citations. Previous affiliations of Satoshi Takaki include Kumamoto University.

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Severe osteopetrosis, defective interleukin-1 signalling and lymph node organogenesis in TRAF6-deficient mice.

TL;DR: TRAF6, a member of the tumour necrosis factor receptor‐associated factor family, was first identified as a transducer ofCD40 and interleukin‐1 receptor (IL‐1R) signals based on the interaction of TRAF6 with the cytoplasmic tail of CD40 and with the IL-1R associated kinase in vitro.
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Differential signaling by lymphocyte antigen receptors

TL;DR: Evidence is outlined supporting the view that the nature of the ligand/receptor interaction directs the physical recruitment of signaling pathways differentially inside the lymphocyte and hence defines thenature of the subsequent immune response.
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Identification of Innate IL-5–Producing Cells and Their Role in Lung Eosinophil Regulation and Antitumor Immunity

TL;DR: It is shown that innate IL-5–producing cells were increased in response to tumor invasion, and their regulation of eosinophils is critical to suppress tumor metastasis and contribute to development of novel immunotherapies for cancer.
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Quantification of Self-Renewal Capacity in Single Hematopoietic Stem Cells from Normal and Lnk-Deficient Mice

TL;DR: Establishment of a clonal and quantitative assay for HSC function permitted demonstration that adult mouse HSCs are significantly heterogeneous in degree of multilineage repopulation and that higher repopulating potential reflects higher self-renewal activity.
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Adipose Natural Regulatory B Cells Negatively Control Adipose Tissue Inflammation

TL;DR: Adipose tissue Breg cells are a naturally occurring regulatory B cell subset that maintains homeostasis within adipose tissue and that Breg cell dysfunction contributes pivotally to the progression of adipose tissues inflammation in obesity.