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James L. Weber

Researcher at Marshfield Clinic

Publications -  172
Citations -  31142

James L. Weber is an academic researcher from Marshfield Clinic. The author has contributed to research in topics: Gene mapping & Locus (genetics). The author has an hindex of 70, co-authored 172 publications receiving 30301 citations. Previous affiliations of James L. Weber include QIMR Berghofer Medical Research Institute & Walter Reed Army Institute of Research.

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Mapping of human chromosome 5 microsatellite DNA polymorphisms.

TL;DR: Thirteen moderately to highly informative microsatellite DNA polymorphisms based on (dC-dA)n.(dG-dT)n repeats were mapped to segments of human chromosome 5 using both linkage analysis and a panel of somatic cell hybrids which contained rearranged chromosomes.
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Further evidence for linkage of Gilles de la Tourette syndrome (GTS) susceptibility loci on chromosomes 2p11, 8q22 and 11q23-24 in South African Afrikaners

TL;DR: Analysis of DNA samples from 91 Afrikaner nuclear families with one or more affected children provided important additional evidence for the location of GTS susceptibility loci.
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Mapping the Treacher Collins syndrome locus to 5q31.3----q33.3.

TL;DR: Linkage analysis was performed in Treacher Collins families with restriction fragment length or microsatellite polymorphisms associated with eight loci previously mapped to 5q31----qter and there was no evidence for genetic heterogeneity among eight families with variable expression of the condition.
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Autosomal dominant supravalvular aortic stenosis: localization to chromosome 7

TL;DR: Based on preliminary linkage data, the abnormal microscopic appearance of aortic elastic fibers in SVAS, and analogous animal and human diseases associated with elastic fiber and vascular abnormalities, there is indirect evidence suggesting elastin as a possible candidate gene for this disorder.
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Structure of the circumsporozoite protein gene in 18 strains of Plasmodium falciparum.

TL;DR: The cloned circumsporozoite protein gene is highly conserved among strains of Plasmodium falciparum and that malaria vaccine development with the CS protein is unlikely to be complicated by strain variation.