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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...
Gorde:
| Argitaratua izan da: | J Exp Med |
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| Egile Nagusiak: | , , , , , , , , , , , , , , , , , , , , , , , |
| Formatua: | Artigo |
| Hizkuntza: | Inglês |
| Argitaratua: |
The Rockefeller University Press
2017
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| Gaiak: | |
| Sarrera elektronikoa: | 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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