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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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Repeated sequence DNA comparisons between Triticum and Aegilops species

TL;DR: The results are consistent with the hypothesis that speciation is accompanied by quantitative changes in the repeated sequence complements of genomes, and using a DNA probe from Aegilops speltoides that contains the most highly repeated sequences, diploid Aegilop species could be distinguished from diploids Triticum species.
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The I region of the C57BL/10 mouse: characterization and physical linkage to H-2K of an SB beta-like class II pseudogene, psi A beta 3.

TL;DR: Comparison of the DNA sequence of the exon encoding the beta 2 domain of psi A beta 3 in the b or k haplotypes with functional class II genes shows that a deletion of eight nucleotides has occurred, such that the psi Abeta 3 sequence cannot be translated into afunctional class II protein, which suggests that psi A Beta 3 is a pseudogene.
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Structure of the human G gamma-A gamma-delta-beta-globin gene locus

TL;DR: A physical map of the human G gamma-, A gamma-, delta-, and beta-globin genes is constructed, which spans more than 40 kilobases and shows the following intergene distances.
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Molecular analysis of antigen recognition by insulin-specific T-cell hybridomas from B6 wild-type and bm12 mutant mice.

TL;DR: Molecular analysis of the heterodimeric T- cell antigen receptor of insulin-specific class II-restricted T-cell hybridomas derived from C57BL/6 (B6) wild-type and B6.C-H-2bm12 (bm12) mutant mice revealed that such T cells use a diverse V gene repertoire.
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Preferential Th1 immune response in invariant chain-deficient mice.

TL;DR: It is suggested that defective Ag presentation in Ii−/− mice leads selectively to a Th1 effector response.