You can’t be serious.
You appear to have a strong tendency to misrepresent qualified statements as not qualified. What drives this?
“Basically 50/50” in opposite directions is not a trend. 70/30 in opposite directions is not a trend, either.
Why did you omit “basically”?
5 years later, we don’t have encyclopedic knowledge.
Really? What kind of proteins? All? Average ones, or only a particular type? It’s literally there in the first word of the Introduction.
What do we know about the biophysical process by which that particular type of protein folds?
Again, you employ a blatant straw man fallacy. My pointing out that 8 for 8 is unremarkable is not a claim that it demonstrates “50/50.” How could it? What did I write in the discussion of that paper? Did you forget that they also had opposite effects on contractility?
Your pretending that a study explicitly limited to a specific structural subset of proteins is universal isn’t cherrypicking?
IMO, the best we’ve got to reflect what’s going on in vivo are the collections of GOF and hypomorphic alleles. As @swamidass noted, P53 mutations are about 50/50, and I notice that you completely ignored the G6PD ones. Why?
No. The reality is that no study can do all that work. All of them are limited in some way. The in vitro ones are necessarily highly biased in favor of those proteins that are easier to purify. Guess what kind those are?
Collections of hypomorphic and GOF mutants are not limited in that way.
In what type of proteins? A specific type, no?
In what type of proteins? IDPs? What’s the antecedent of “it,” precisely and literally?
Not for surface residues, for which the mean was basically 0. You are missing so much by trying to win arguments with this lame cherrypicking. You can’t even see it in the data you are presenting!
I don’t know of any that are comprehensive. Certainly none you cited were.
Because you’re not explaining anything. You appear to be arguing for the sake of arguing, particularly obvious from your repeated straw men.
See above.