Pathways - manually collected, often from reviews:
OpenBEL Selventa BEL large corpus:
NOS3
→
TERT
(increases, TERT Activity)
Evidence: The introduction of telomerase into human endothelial cells in vitro prevents progression to senescence-associated endothelial dysfunction, including the decrease in endothelial nitric oxide synthase activity and increase in monocyte adhesion to endothelial cells.10,23
OpenBEL Selventa BEL large corpus:
NOS3
→
TERT
(increases, TERT Activity)
Evidence: Introduction of TERT prevents endothelial dysfunction associated with senescence such as decreased eNOS activity and increased monocyte binding to endothelial cells (14, 85).
OpenBEL Selventa BEL large corpus:
NOS3
→
TERT
(increases, TERT Activity, NOS3 Activity)
Evidence: Introduction of TERT prevents endothelial dysfunction associated with senescence, such as a decrease in eNOS activity and an increase in monocyte binding to ECs [19,26].
OpenBEL Selventa BEL large corpus:
NOS3
→
TERT
(increases, TERT Activity, NOS3 Activity)
Evidence: Stable expression of hTERT, which increases telomerase activity and induces a younger phenotype in endothelial cells, restores eNOS activity, reestablishing properly functioning endothelium. 71
OpenBEL Selventa BEL large corpus:
TERT
→
NOS3
(increases, NOS3 Activity, TERT Activity)
Evidence: In addition, increasing NO bioavailability or eNOS activity activates telomerase and delays endothelial cell senescence.72,73