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Anne M. Latour
Researcher at University of North Carolina at Chapel Hill
Publications - 24
Citations - 5649
Anne M. Latour is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Gene & Gene targeting. The author has an hindex of 18, co-authored 24 publications receiving 5451 citations.
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Journal ArticleDOI
The nuclear receptor PXR is a lithocholic acid sensor that protects against liver toxicity
Jeff L. Staudinger,Jeff L. Staudinger,Bryan Goodwin,Stacey A. Jones,Diane Hawkins-Brown,Kathleen I. MacKenzie,Anne M. Latour,Yaping Liu,Curtis D. Klaassen,Kathleen K. Brown,John F. Reinhard,Timothy M. Willson,Beverly H. Koller,Steven A. Kliewer +13 more
TL;DR: It is proposed that PXR serves as a physiological sensor of LCA, and coordinately regulates gene expression to reduce the concentrations of this toxic bile acid, and suggest that PxR agonists may prove useful in the treatment of human cholestatic liver disease.
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An Animal Model for Cystic Fibrosis Made by Gene Targeting
John N. Snouwaert,Kristen K. Brigman,Anne M. Latour,Nadia N. Malouf,Richard C. Boucher,Oliver Smithies,Beverly H. Koller +6 more
TL;DR: Mice homozygous for the disrupted gene display many features common to young human cystic fibrosis patients, including failure to thrive, meconium ileus, alteration of mucous and serous glands, and obstruction of glandlike structures with inspissated eosinophilic material.
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BRCA1 Required for Transcription-Coupled Repair of Oxidative DNA Damage
TL;DR: It is shown that mouse embryonic stem cells deficient in BRCA1 are defective in the ability to carry out transcription-coupled repair of oxidative DNA damage, and are hypersensitive to ionizing radiation and hydrogen peroxide.
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Brca1 deficiency results in early embryonic lethality characterized by neuroepithelial abnormalities.
TL;DR: Analysis of mice homozygous for the mutant allele indicate that Brcal is critical for normal development, as these mice died in utero between 10 and 13 days of gestation (E10–E13), and abnormalities in Brcal -deficient embryos were most evident in the neural tube.
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Decreased platelet aggregation, increased bleeding time and resistance to thromboembolism in P2Y1-deficient mice.
Jean-Etienne Fabre,MyTrang Nguyen,Anne M. Latour,Jayne A. Keifer,Laurent P. Audoly,Thomas M. Coffman,Beverly H. Koller +6 more
TL;DR: It is shown that the purinoceptor P2Y1 is required for platelet shape change in response to ADP and is also a principal receptor mediating ADP-induced platelet aggregation, which supports the hypothesis that the ATP receptor P2y1 is a principal receptors mediating both physiologic and pathological ADp-induced processes in platelets.