Human venous valve disease caused by mutations in FOXC2 and GJC2

Venous valves (VVs) prevent venous hypertension and ulceration. We report that FOXC2 and GJC2 mutations are associated with reduced VV number and length. In mice, early VV formation is marked by elongation and reorientation (“organization”) of Prox1(hi) endothelial cells by postnatal day 0. The expr...

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Detalles Bibliográficos
Autores principales: Lyons, Oliver, Saha, Prakash, Seet, Christopher, Kuchta, Adam, Arnold, Andrew, Grover, Steven, Rashbrook, Victoria, Sabine, Amélie, Vizcay-Barrena, Gema, Patel, Ash, Ludwinski, Francesca, Padayachee, Soundrie, Kume, Tsutomu, Kwak, Brenda R., Brice, Glen, Mansour, Sahar, Ostergaard, Pia, Mortimer, Peter, Jeffery, Steve, Brown, Nigel, Makinen, Taija, Petrova, Tatiana V., Modarai, Bijan, Smith, Alberto
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2017
Materias:
Research Articles
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5551565/
https://www.ncbi.nlm.nih.gov/pubmed/28724617
http://dx.doi.org/10.1084/jem.20160875

Internet

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5551565/
https://www.ncbi.nlm.nih.gov/pubmed/28724617
http://dx.doi.org/10.1084/jem.20160875

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