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Richard A. Flavell

Researcher at Yale University

Publications -  1389
Citations -  223064

Richard A. Flavell is an academic researcher from Yale University. The author has contributed to research in topics: Immune system & T cell. The author has an hindex of 231, co-authored 1328 publications receiving 205119 citations. Previous affiliations of Richard A. Flavell include National Institute for Medical Research & University of Michigan.

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Human Hemato-Lymphoid System Mice: Current Use and Future Potential for Medicine

TL;DR: The fundamental requirements and the remarkable progress made over the past few years in improving these models are reviewed, the current major achievements reached by use of these models, and the future challenges to more closely model and study human health and disease are reviewed.
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JNK potentiates TNF-stimulated necrosis by increasing the production of cytotoxic reactive oxygen species

TL;DR: Data indicate that JNK can shift the balance of TNF-stimulated cell death from apoptosis to necrosis, which may represent a contributing factor in stress-induced inflammatory responses mediated by JNK.
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Caspase-3 Controls both Cytoplasmic and Nuclear Events Associated with Fas-Mediated Apoptosis in vivo

TL;DR: It is found that apoptotic caspase-3(-/-) thymocytes exhibited similar "abnormal" morphological changes and delayed DNA fragmentation observed in hepatocytes, and the cleavage of various caspases implicated in mediating apoptotic events, including gelsolin, fodrin, laminB, and DFF45/ICAD was delayed or absent.
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Organization and evolution of the class I gene family in the major histocompatibility complex of the C57BL/10 mouse

TL;DR: The major histocompatibility complex (MHC) encodes several classes of protein vital to the regulation of the immune response and this region in the C57BL/10 mouse is linked into three gene clusters.
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Apoptosis. All's well that ends dead.

TL;DR: People with a disease called type II ALPS cannot efficiently destroy the extra lymphoid cells, and it turns out that this is because they have mutations in a protein at the heart of apoptosis, caspase-10.