G
Gerlinde R. Van de Walle
Researcher at Cornell University
Publications - 122
Citations - 3045
Gerlinde R. Van de Walle is an academic researcher from Cornell University. The author has contributed to research in topics: Virus & Mesenchymal stem cell. The author has an hindex of 29, co-authored 111 publications receiving 2428 citations. Previous affiliations of Gerlinde R. Van de Walle include Ghent University & Eötvös Loránd University.
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Journal ArticleDOI
Markers of stemness in equine mesenchymal stem cells: a plea for uniformity
TL;DR: It is mandatory to define a set of CD markers which can be uniformly applied for the identification of equine MSC, as the expression of certain adult stem cell markers may differ between species.
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Virus complement evasion strategies
TL;DR: This review will focus on the different strategies that viruses use to avoid recognition by one of the components of the immune system: the complement system.
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In search for cross‐reactivity to immunophenotype equine mesenchymal stromal cells by multicolor flow cytometry
Catharina De Schauwer,Sofie Piepers,Gerlinde R. Van de Walle,Kristel Demeyere,Maarten Hoogewijs,Jan Govaere,Kevin Braeckmans,Ann Van Soom,Evelyne Meyer +8 more
TL;DR: It is suggested that this selected nine‐marker panel can be used for the adequate immunophenotyping of equine MSC.
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Investigation of the prevalence of neurologic equine herpes virus type 1 (EHV-1) in a 23-year retrospective analysis (1984-2007).
Gillian A. Perkins,Laura B. Goodman,Koji Tsujimura,Gerlinde R. Van de Walle,Sung G. Kim,Edward J. Dubovi,Nikolaus Osterrieder,Nikolaus Osterrieder +7 more
TL;DR: The odds of having neurologic disease with the ORF30 G(2254) genotype were computed as 162 times greater than those with the opposite allele OrF30 A( 2254) (95% confidence interval: 35-742), suggesting that other factors may also contribute to the onset of EHM.
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The role of BRCA1 in DNA double-strand repair: past and present.
TL;DR: The questions as to what extent HR repair cannot be properly fulfilled when breast cancer related mutations in the BRCA1 gene occur are posed and how the recent and excessive studied poly-ADP ribose polymerase (PARP) inhibiting therapy approach links with the proposed tumor suppression function of the different BRCa1 domains are posed.