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F. M. Johnson

Researcher at National Institutes of Health

Publications -  26
Citations -  1367

F. M. Johnson is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Mutant & Globin. The author has an hindex of 15, co-authored 26 publications receiving 1332 citations.

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A sequence-based variation map of 8.27 million SNPs in inbred mouse strains

TL;DR: A dense map of genetic variation in the laboratory mouse genome will provide insights into the evolutionary history of the species and lead to an improved understanding of the relationship between inter-strain genotypic and phenotypic differences.
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A mouse model for β-Thalassemia

TL;DR: Mice homozygous for the mutant allele, designated Hbb th-1 , represent the first animal model of β-thalassemia (Cooley's anemia), a severe genetic disease of humans.
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Electrophoretically detected germinal mutations induced in the mouse by ethylnitrosourea.

TL;DR: A preliminary study conducted concomitantly with the electrophoretic analyses for dominant lethal effects and physical malformation showed no increase over background due to EtNU treatment of spermatogonia, which suggests that mutations induced by EtN U tend not to be expressed in this way.
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Fine Mapping in 94 Inbred Mouse Strains Using a High-density Haplotype Resource

TL;DR: A dense set of genotypes from 94 inbred mouse strains containing 10.77 million genotypes over 121,433 single nucleotide polymorphisms (SNPs) is reported, demonstrating the utility of these data in high-resolution linkage mapping through power simulations and statistical power analysis and providing guidelines for developing such studies.
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ANALYSIS OF A MOUSE α-GLOBIN GENE MUTATION INDUCED BY ETHYLNITROSOUREA

TL;DR: It is proposed that ethylnitrosourea induced an A → T transversion in the histidine codon at position 89 (CAC → CTC) that has apparently not been observed previously in humans, mice or other mammals, and its novel occurrence may be indicative of other unusual mutational events that do not ordinarily occur in the absence of specific mutagen exposure.