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ToolsGray, Caroline, Bratt, David, Lees, Julie, daCosta, Marc, Plant, Karen, Watson, Oliver J, Solaymani-Kohal, Sara, Tazzyman, Simon, Serbanovic-Canic, Jovana, Crossman, David C, Keavney, Bernard D, Haase, Andrea, McMahon, Kathryn, Gering, Martin, Roehl, Henry, Evans, Paul C and Chico, Timothy J A (2013) Loss of function of parathyroid hormone receptor 1 induces Notch-dependent aortic defects during zebrafish vascular development. Arteriosclerosis, Thrombosis, and Vascular Biology, 33 (6). pp. 1257-63. ISSN 1079-5642
Full text not available from this repository.Abstract
Coarctation of the aorta is rarely associated with known gene defects. Blomstrand chondrodysplasia, caused by mutations in the parathyroid hormone receptor 1 (PTHR1) is associated with coarctation of the aorta in some cases, although it is unclear whether PTHR1 deficiency causes coarctation of the aorta directly. The zebrafish allows the study of vascular development using approaches not possible in other models. We therefore examined the effect of loss of function of PTHR1 or its ligand parathyroid hormone-related peptide (PTHrP) on aortic formation in zebrafish.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | animals,aorta,aortic coarctation,female,gene expression regulation, developmental,homeodomain proteins,male,models, animal,mutation,neovascularization, physiologic,nerve tissue proteins,receptor, notch1,receptor, parathyroid hormone, type 1,reference values,signal transduction,up-regulation,zebrafish,zebrafish proteins |
| Faculty \ School: | Faculty of Medicine and Health Sciences > Norwich Medical School |
| UEA Research Groups: | Faculty of Medicine and Health Sciences > Research Groups > Norwich Clinical Trials Unit |
| Depositing User: | Pure Connector |
| Date Deposited: | 20 Jan 2014 16:02 |
| Last Modified: | 24 Oct 2022 05:33 |
| URI: | https://ueaeprints.uea.ac.uk/id/eprint/46175 |
| DOI: | 10.1161/ATVBAHA.112.300590 |
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