[-Clelia-]

Hi Lotus, here I am
This is another paper about palmitoylation:

Palmitoylation regulates 17β-estradiol-induced estrogen receptor-α degradation and transcriptional activity.
http://www.ncbi.nlm.nih.gov/pubmed/22446104

[...]
The lack of palmitoylation renders ERα more susceptible to E2-dependent degradation, blocks ERα S118 phosphorylation and prevents E2-induced ERα estrogen-responsive element-containing promoter occupancy. Consequently, ERα transcriptional activity is prevented and the receptor addressed to the nuclear matrix subnuclear compartment. These data uncover a circuitry in which receptor palmitoylation links E2-dependent ERα degradation, S118 phosphorylation, and transcriptional activity in a unique molecular mechanism. We propose that rapid E2-dependent signaling could be considered as a prerequisite for ERα transcriptional activity and suggest an integrated model of ERα intracellular signaling where E2-dependent early extranuclear effects control late receptor-dependent nuclear actions.

ok palmitoylation is good for a good estrogen activity, you ask: "the palmitoylation of estrogen receptor alpha (ER-a) is (or can be) mediated by oxidative phosphorylation?"
my answer is: I don't know...what do you mean?

Oxidative phosphorylation, wiki (not my favourite source, but this time i can use it):
Oxidative phosphorylation (or OXPHOS in short) is the metabolic pathway in which the mitochondria in cells use their structure, enzymes, and energy released by the oxidation of nutrients to reform ATP. Although the many forms of life on earth use a range of different nutrients, ATP is the molecule that supplies energy to metabolism. Almost all aerobic organisms carry out oxidative phosphorylation.[...]. Although oxidative phosphorylation is a vital part of metabolism, it produces reactive oxygen species such as superoxide and hydrogen peroxide, which lead to propagation of free radicals, damaging cells and contributing to disease and, possibly, aging (senescence). The enzymes carrying out this metabolic pathway are also the target of many drugs and poisons that inhibit their activities.


in the paper above, it says: These E2 rapid effects require a population of the ERα located at the cell plasma membrane through palmitoylation, a dynamic enzymatic modification mediated by palmitoyl-acyl-transferases.

We should find how this enzyme palmitoyl-acyl-transferases works, if you want to gain estrogen activity (and maybe is not enough, as you see our bodies are quite complicated... )
indeed from your link: "E2 reduces both ERalpha palmitoylation and its interaction with caveolin-1, in a time- and dose-dependent manner"
So, if you want you can increase estrogen receptor expression, but there is a negative feedback as well from estradiol. This is good for the body, to regulate his pathways....and try to keep some equilibrium. We just want to move some of it to favor breast growth, and if estrogen receptor is stronger than negative feedback of estradiol, than it should be worthy the way of palmitoylation.

I think the best way to try to gain some breast is in my previous link, and you noticed that: we should just low the androgen activity in breast, to have breast growth. This is quite simpler than taking account of all the other biological pathways, that's why i started from that (anyway, everything is important, also estrogen, and food, and enzymes.... but i think that the king to fight here is DHT)
I didn't know about DHT metabolites, my thoughs are: if DHT (and metabolite) is more androgenic, then estrogenic in breast tissue, than it could be helpful low it.

I'm sure you're aware that fatty acids synthesize aromatase, (what are your thoughts?)."

ehm... nope. I'm just a scientist, not omniscient :-P
i didn't find this before. I read something on your A.A. thread, but now i missed it. Could you link some source? I tried to have a look but i couldn't find much.
Then i will tell you what I think, but for sure, if fatty acids can promote aromatase expression, that would be great!

"On another note....I've seen that EPA and DHA reduces the risk of breast cancer by as much as a 32% reduction, I don't know the dosage."

Where did you see that? which paper? i quickly had a look on the one you linked before, but i didn't find that information

thank you Lotus, I'm ready to go. Happy me!
yep you gave to a scientist a good homework

Did i?..... cool, I thought I might have insulted you lol.

no worries, of course not

How come, am I the only one? Where are all the others? There is a lot of people here.

Don't know....but I'm glad you're here. I have all kinds of crazy ideas and only myself to entertain them, lmao."

eheh, i'm glad as well, but there is other people that contributed sometimes. Anyway I understand the way you feel. I'm crazy almost like you, and i like scientific research, so I can make good company (Imao)

Anyway, you could be a scientist.

You think so?, nah....... I'm not worthy although I'd love to be one. and thank you so much for saying so.

Your knowledge is becoming huge, also you research a lot, so there is no big difference between you and a scientist. You could apply to a University if you wanted.

Finally, could you help me? I'm looking information for "bad estrogen" that make growth faster,
what is its name? I saw it somewhere but I don't remember.
Thank you very much
See you,
bye!