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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Bibliografske podrobnosti
izdano v:J Exp Med
Main Authors: 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
Format: Artigo
Jezik:Inglês
Izdano: The Rockefeller University Press 2017
Teme:
Research Articles
Online dostop:https://ncbi.nlm.nih.gov/pmc/articles/PMC5551565/
https://ncbi.nlm.nih.gov/pubmed/28724617
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1084/jem.20160875
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