E
Erika Kague
Researcher at University of Bristol
Publications - 43
Citations - 904
Erika Kague is an academic researcher from University of Bristol. The author has contributed to research in topics: Zebrafish & Gene. The author has an hindex of 13, co-authored 37 publications receiving 578 citations. Previous affiliations of Erika Kague include University of Pennsylvania & University of São Paulo.
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Journal ArticleDOI
Skeletogenic fate of zebrafish cranial and trunk neural crest.
Erika Kague,Michael D. Gallagher,Sally Burke,Michael J. Parsons,Tamara A. Franz-Odendaal,Shannon Fisher +5 more
TL;DR: A two–transgene system based on Cre recombinase is employed to genetically label NC in the zebrafish, demonstrating that cells in the cranial ganglia and peripheral nervous system known to be NC–derived have the ability to form bone during normal vertebrate development.
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Zebrafish as an emerging model for osteoporosis: a primary testing platform for screening new osteo-active compounds
TL;DR: The zebrafish is outlined as a powerful model for osteoporosis research to validate potential therapeutic candidates, and the tools and assays that can be used to study bone homeostasis, and affordable (semi-)high-throughput compound testing are described.
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Osterix/Sp7 limits cranial bone initiation sites and is required for formation of sutures.
Erika Kague,Paula R. Roy,Garrett Asselin,Gui Hu,Jacqueline C. Simonet,Alexandra Stanley,R. Craig Albertson,Shannon Fisher +7 more
TL;DR: It is proposed that signals from the bone itself are required for orderly recruitment of precursor cells and growth along the edges, and the delay in bone maturation caused by loss of Sp7 leads to unregulated bone formation, revealing a new mechanism for patterning the skull and sutures.
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Wnt signalling controls the response to mechanical loading during zebrafish joint development
TL;DR: It is shown that, in the jaw, Wnt signalling is reduced specifically in regions of high strain in response to loss of muscle activity, and it is demonstrated that Wnt acts downstream of mechanical activity and is required for joint patterning and chondrocyte maturation.
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Giantin-knockout models reveal a feedback loop between Golgi function and glycosyltransferase expression.
Nicola L. Stevenson,Dylan J. M. Bergen,Roderick E. H. Skinner,Erika Kague,Elizabeth Martin-Silverstone,Kate Brown,Chrissy L. Hammond,David J. Stephens +7 more
TL;DR: In this paper, the authors show that the loss of the largest golgin, giantin, leads to substantial changes in gene expression despite only limited effects on the Golgi structure.