" Additional experiments showed that OEA activation of the Erk pathway involved activation of Neu/ErbB2 receptor, which suggests OEA actions in cardiac muscle might require activation of Neu/ErbB2."
OK, I need help understanding this one. Doesn't nue/ErbB2 = HER2??
Then why would we want to stock-up on OEA which according to the quote above, activates Nue/erbB2?
From another article:
"Interestingly, overexpression especially of ErbB2, appears to force the equilibrium toward spontaneous homodimer formation leading to activation in the absence of ligands (Samanta
et al., 1994). This situation is often present in a variety of human cancers (Klapper et al., 2000)."
Correct me if I am wrong but the way I read this is in order to correct cardio problems, you should take OEA which has been shown to activate HER2?
Here is the essence of the problem: I've read a lot of studies and xonsider myself fairly literate however, in my attempt to understand exactly what is being said here, I question my interpretation. I wonder about the rest of the people on this site who are struggling to make sence out of this stuff because, as far as they can see; their lives depend on it.
I can't help but wonder if posting these studies is doing anyone any favours?? I am as guilty as anyone else but I am just thinking about this with all due respect to others who post. I would hate to see others start taking OEA when it might up-regulate HER2/neu.
I'm sure I'm going to get slammed for my comments but pre-trial information just doesn't make a lot of sence sometimes. Maybe we should stick to hard in vivo facts and as a curtosy, translate this into terms we can all understand.
Respectfully,
Al
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