טוען...
Genetic deletion of p66(Shc) adaptor protein prevents hyperglycemia-induced endothelial dysfunction and oxidative stress
Increased production of reactive oxygen species (ROS) and loss of endothelial NO bioavailability are key features of vascular disease in diabetes mellitus. The p66(Shc) adaptor protein controls cellular responses to oxidative stress. Mice lacking p66(Shc) (p66(Shc−/−)) have increased resistance to R...
שמור ב:
| Main Authors: | , , , , , , , , , , , |
|---|---|
| פורמט: | Artigo |
| שפה: | Inglês |
| יצא לאור: |
National Academy of Sciences
2007
|
| נושאים: | |
| גישה מקוונת: | https://ncbi.nlm.nih.gov/pmc/articles/PMC1829289/ https://ncbi.nlm.nih.gov/pubmed/17360381 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1073/pnas.0609656104 |
| תגים: |
הוספת תג
אין תגיות, היה/י הראשונ/ה לתייג את הרשומה!
|