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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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The unusual properties of mtDNA from a "low-density" petite mutant of yeast.

TL;DR: It is proposed that most of the isolated RD1A mtDNA is present in large fishnets concatenanes; the unwinding restriction imposed on DNA of which the strands are plaited into a fishnet concatenate explains the restricted ethidium uptake.
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ICOS is essential for the development of experimental autoimmune myasthenia gravis

TL;DR: Following immunization with Torpedo acetylcholine receptor (AChR), ICOS gene knockout mice were highly resistant to clinical experimental autoimmune myasthenia gravis (EAMG) development, had less serum AChR-specific immunoglobulins (Igs), and exhibited a diminutive germinal center (GC) reaction in secondary lymphoid tissues.
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OspA vaccination of mice with established Borrelia burgdorferi infection alters disease but not infection.

TL;DR: C3H mice vaccinated with outer surface protein A at different intervals after infection with Borrelia burgdorferi reduced both the number of mice and individual joints with arthritis, a result suggesting an acceleration of the resolution phase of the disease.
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Yeast mitochondrial RNA does not contain poly(A)

TL;DR: The finding that poly(A) was also present in mitochondrial RNA from animal cells suggested a simple means of isolating mitochondrial mRNAs and suggested that the similarity between prokaryotes and mitochondria might not be as close as previously suggested4.
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Truncated form of TGF-βRII, but not its absence, induces memory CD8+ T cell expansion and lymphoproliferative disorder in mice

TL;DR: A previously unrecognized dominant function of the dnTGFβRII is uncovers in CD8+ T cell proliferation and cellular transformation, which is caused by a mechanism that is different from the absence of TGF-β signaling.