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Alison L. Ruhe
Researcher at University of California, Davis
Publications - 10
Citations - 595
Alison L. Ruhe is an academic researcher from University of California, Davis. The author has contributed to research in topics: Sanger sequencing & Point mutation. The author has an hindex of 7, co-authored 9 publications receiving 515 citations. Previous affiliations of Alison L. Ruhe include Translational Genomics Research Institute.
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Journal ArticleDOI
Tracking footprints of artificial selection in the dog genome
Joshua M. Akey,Alison L. Ruhe,Dayna Akey,Aaron K. Wong,Caitlin F. Connelly,Jennifer Madeoy,Thomas J. Nicholas,Mark W. Neff +7 more
TL;DR: A genome-wide scan for selection in 275 dogs from 10 phenotypically diverse breeds that were genotyped for over 21,000 autosomal SNPs is described and 155 genomic regions that possess strong signatures of recent selection and contain candidate genes for phenotypes that vary most conspicuously among breeds are identified.
Journal ArticleDOI
A Comprehensive Linkage Map of the Dog Genome
Aaron K. Wong,Alison L. Ruhe,Beth L. Dumont,Kathryn R. Robertson,Giovanna Guerrero,Sheila M. Shull,Janet S. Ziegle,L. V. Millon,Karl W. Broman,Bret A. Payseur,Mark W. Neff +10 more
TL;DR: The reference sequence of a boxer is leveraged to construct the first complete linkage map for the domestic dog, which will enable empiric coverage estimates and multipoint linkage analysis, and benefit association, selective sweep, and phylogenetic mapping approaches.
Journal ArticleDOI
Necrotizing meningoencephalitis of Pug Dogs associates with dog leukocyte antigen class II and resembles acute variant forms of multiple sclerosis
Kimberly A. Greer,Aaron K. Wong,Hongwei Liu,Thomas R. Famula,Niels C Pedersen,Alison L. Ruhe,M. Wallace,Mark W. Neff +7 more
TL;DR: P Pug Dog encephalitis (PDE) shares clinical features with the less common acute variant forms of MS, and NME of Pug Dogs may represent a naturally occurring canine model of certain idiopathic inflammatory disorders of the human central nervous system.
Journal ArticleDOI
Somatic inactivating PTPRJ mutations and dysregulated pathways identified in canine malignant melanoma by integrated comparative genomic analysis.
William P.D. Hendricks,Victoria Zismann,Karthigayini Sivaprakasam,Karthigayini Sivaprakasam,Christophe Legendre,Kelsey Poorman,Kelsey Poorman,Waibhav Tembe,Nieves Perdigones,Jeff Kiefer,Winnie S. Liang,Valerie DeLuca,Valerie DeLuca,Mitchell S. Stark,Alison L. Ruhe,Roe Froman,Nicholas S. Duesbery,Megan Washington,Jessica Aldrich,Mark W. Neff,Matthew J. Huentelman,Nicholas K. Hayward,Kevin N. Brown,Douglas H. Thamm,G. S. Post,Chand Khanna,Barbara Davis,Matthew Breen,Alexander Sekulic,Alexander Sekulic,Jeffrey M. Trent +30 more
TL;DR: The genomic landscape of canine melanoma is mapped through multi-platform analysis of 37 tumors and matching constitutional samples and identifies novel predominantly truncating mutations in the putative tumor suppressor gene PTPRJ, which resembles that seen in BRAF wild-type and sun-shielded human melanoma subtypes.
Journal ArticleDOI
An ADAMTSL2 founder mutation causes Musladin-Lueke Syndrome, a heritable disorder of beagle dogs, featuring stiff skin and joint contractures.
Hannah L. Bader,Alison L. Ruhe,Lauren W. Wang,Aaron K. Wong,Kari F. Walsh,Rebecca A. Packer,Jonathan Mitelman,Kathryn R. Robertson,Dennis P. O'Brien,Karl W. Broman,G. Diane Shelton,Suneel S. Apte,Mark W. Neff +12 more
TL;DR: The genetic basis of MLS is a founder mutation in ADAMTSL2, previously shown to interact with latent TGF-β binding protein, which binds fibrillin-1, and the molecular effect of the founder mutation on ADAMtsL2 is formation of disulfide-bonded dimers.