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Hajime Karasuyama

Researcher at Tokyo Medical and Dental University

Publications -  240
Citations -  21865

Hajime Karasuyama is an academic researcher from Tokyo Medical and Dental University. The author has contributed to research in topics: Immunoglobulin E & Basophil. The author has an hindex of 65, co-authored 231 publications receiving 20535 citations. Previous affiliations of Hajime Karasuyama include Tokyo University of Science & Institute of Medical Science.

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Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice

TL;DR: CPP32 is shown to play a critical role during morphogenetic cell death in the mammalian brain during embryonic day 12, resulting in a variety of hyperplasias and disorganized cell deployment.
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Reduced Apoptosis and Cytochrome c-Mediated Caspase Activation in Mice Lacking Caspase 9

TL;DR: Results indicate that Casp9 is a critical upstream activator of the caspase cascade in vivo, as indicated by the absence of Casp3-like cleavage and the restoration of cytochrome c-mediated cleavage after addition of in vitro-translated Casp 9.
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Establishment of mouse cell lines which constitutively secrete large quantities of interleukin 2, 3, 4 or 5, using modified cDNA expression vectors

TL;DR: Mouse cell lines of different lineages have been established which constitutively secrete large quantities of recombinant mouse interleukins, and an existing bovine papilloma virus‐based expression vector was modified to allow transformed X63Ag8‐653 myeloma cells, NIH 3T3 fibroblasts and C127 mammary tumor cells to stably carry multiple copies of the vector.
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Interleukin-2 production by tumor cells bypasses T helper function in the generation of an antitumor response

TL;DR: These findings demonstrate that the failure of an effective antitumor immune response may be primarily due to a helper arm deficiency of the immune system rather than a paucity of tumor-specific cytotoxic effector cells and outline a novel strategy for augmenting tumor immunity.
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Dominant-negative mutations in the DNA-binding domain of STAT3 cause hyper-IgE syndrome

TL;DR: It is shown that dominant-negative mutations in the human signal transducer and activator of transcription 3 (STAT3) gene result in the classical multisystem HIES, highlighting the multiple roles played by STAT3 in humans, and underline the critical involvement of multiple cytokine pathways in the pathogenesis of HIES.