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Nancy A. Jenkins

Researcher at Houston Methodist Hospital

Publications -  743
Citations -  105243

Nancy A. Jenkins is an academic researcher from Houston Methodist Hospital. The author has contributed to research in topics: Gene & Gene mapping. The author has an hindex of 155, co-authored 741 publications receiving 101587 citations. Previous affiliations of Nancy A. Jenkins include Institute of Molecular and Cell Biology & University of Texas MD Anderson Cancer Center.

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Accelerated amyloid deposition in the brains of transgenic mice coexpressing mutant presenilin 1 and amyloid precursor proteins

TL;DR: Transgenic animals that coexpress a FAD-linked human PS1 variant (A246E) and a chimeric mouse/human APP harboring mutations linked to Swedish FAD kindreds (APP swe) develop numerous amyloid deposits much earlier than age-matched mice expressing APP swe and wild-type Hu PS1 or APP swe alone.
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Endoproteolysis of presenilin 1 and accumulation of processed derivatives in vivo

TL;DR: It is concluded that PS1 is subject to endoproteolytic processing in vivo, and in brains of transgenic mice expressing human PS1, approximately 17 kDa and approximately 27 kDa PS1 derivatives accumulate to saturable levels, and at approximately 1:1 stoichiometry, independent of transgene-derived mRNA.
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Deletions and a translocation interrupt a cloned gene at the neurofibromatosis type 1 locus.

TL;DR: These findings strongly suggest that the TBR gene is the NF1 gene, and a number of cDNA clones from the translocation breakpoint region (TBR), one of which hybridizes to an approximately 11 kb mRNA.
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Cloning, chromosomal localization, and functional analysis of the murine estrogen receptor β

TL;DR: The results demonstrate that while ER beta shares many of the functional characteristics of ER alpha, the molecular mechanisms regulating the transcriptional activity of mER beta may be distinct from those of ERalpha.
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Limb alterations in brachypodism mice due to mutations in a new member of the TGFβ-superfamily

TL;DR: The isolation of three new members of the transforming growth factor-β (TGF-β) superfamily5 (growth/differentiation factors (GDF) 5, 6 and 7) are reported and it is shown by mapping, expression patterns and sequencing that mutations in Gdf5 are responsible for skeletal alterations in bp mice.