Can prion formation be induced in a non prion forming protein in non prion forming proteins in humans? If yes, what will be the conditions for the prion to be induced?
My next query is how to count the constitutive expression level of a protein in cell and calculate the threshold expression after which prion formation will be induced in that particular protein (take prion forming protein for instance)?
I guess I can understand what you mean with your question, although there might be some misunderstanding.
PrP (Prion protein) is normally expressed in humans and in its normal conformation may not make the disease, until it is changed or induced into the disease-related conformation. As far as I understand, this can be done by another PrP, which already has the "wrong" conformation, for example after eating some burger in the 1980s, eating human brain (as some cannibals in the south sea), or having a brain operation with not fully autoclaved instruments (decades ago). Some people have point mutations in the PrP and can develop easier the "wrong" conformation (GSS, gerstmann-sträussler-syndrome), some people are heterozygous for some variant of the PrP gene and may get easier the wrong conformation, either randomly or by any of the other factors.
I think not much is known, how the random change in conformation will occur.
Thanks for your opinion. In simple words, I want to know if some non prion forming protein, let's take the c-milk protein. Is it possible to induce the "wrong conformation" in this protein?
Secondly, I want to know is there a particular threshold in the level of PrP, which triggers it to fold in the "wrong conformation"?
Sorry for misinterpreting your question regarding non-prion proteins. It would be very interesting to find any other proteins with a conformation similar to prions, i.e. making them resistant to high-temperatures and able to transmit a disease - although, it would be difficult to exclude that.
Concerning the other part of your question, I think there were mathematical models around some decades ago, since the (classical) human disease Creutzfeld-Jacob (or Jacob-Creutzfeld) usually appeared only in older patients, i.e. most likely in a random fashion, which may address your point of "treshold" as a probability of change in conformation of the first molecule. I think it was believed that it would need 3 decades to develop JCD, but with the BSE and the new variant developing within maybe 5 years after eating a burger, i.e. preferentially even in young adults, some of such models may have become useless.
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