INT246763
From wiki-pain
|
|
|
|
|
Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
However, studies in normal primary human coronary artery endothelial cells in vitro have demonstrated a similar lack of overt exenatide effect on eNOS and AKT2 protein expression on a background of enhanced activation of both proteins [39]. | |||||||||||||||
| |||||||||||||||
|
No differences in the protein expression of AKT2, SERCA2a, or PI3Kbeta were observed, and the observed trend towards reduction in eNOS expression might be expected to diminish cardiac function rather than improve it. | |||||||||||||||
| |||||||||||||||
|
Immunoblot analysis of cardiac tissue did not demonstrate any significant changes in expression of GLUT4, AKT2, SERCA2a or PI3Kbeta with GLP-1 or AC3174 treatment (Figure 4), although trends towards decreased GLUT1 and eNOS expression were noted.
| |||||||||||||||
| |||||||||||||||
|
The concept that the PI 3-kinase/Akt pathway regulates tuberin is supported by other observations that the expression of a constitutively active PI 3-kinase or active Akt, including Akt1 or Akt2, induce tuberin phosphorylation (27). | |||||||||||||||
| |||||||||||||||
|
General Comments
This test has worked.