Niebvll
Stop the rHGH Cope
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@claygo funny high iq larp you posted
Lets see what kind of info he's gonna "spoonfeed" us
Perhaps a humble genius?
Regarding the other claim that type x collagen somehow noticeably influences the chondrocyte differentiation, theres a reason why literally 0 evidence is given. Type x collagen is primarily a marker of hypertrophy and is exclusively secreted in chondrocytes that have entered senescence. The deletion of Col10a1 proved that type x collagen is completely dispensable for differentiation but also that absence of the former faciliates the latter. Showing that the absence of type x collagen increases chondrocyte differentiation into hypertrophy, it's presence leads to a longer stay in a proliferative phase. Both FGFR1 and FGFR2 primarily cause collagen x downregulation by affecting the responsible transcription factors, this would again faciliate differentiation and thus be counterproductive. FGFR3 Inhibition however consistently upregulates it which results in greater proliferation before hypertrophy. Whether this has any significant effects is very questionable and would presume that the secretion has noticeable effects extracellularly, I would argue most of the matters have already been decided by pathways upstream. Observations like this could also be reverse causality.
You also didnt really give any specification or go into detail on how this would work? I would kind of expect that when putting forth such a ground breaking theory.
And how does "erda doesnt work as you think it does" conclude in "erda has more roi than all other compounds"
Big ego for just joining
Lets see what kind of info he's gonna "spoonfeed" us
Okay backing down a little bit
Perhaps a humble genius?
Bold claim when literally all of literature supports that it is
I would guess because the potency with tyra is worse lol. Others like infig also have metabolism issues that Erda doesnt have.
saying this as if fgfr3 inhibition isnt potent
FGFR1 signalling is indeed thought of to be growth-inhibiting, however loss of function shows 0 increase in adult height (so it's inhibition is fairly useless) and only a transient increase in hypertrophic zone height, not even anything permanent lol. FGFR2 signalling however is seen to be growth-promoting and it's msc inactivation actually led to dwarfism [PMC4133284, PMC8965158], its shown in people with both fgfr2 gain or loss of function mutations that they end up with significantly decreased adult heights, while we see a clear differentiation between height results with fgfr3 overexpression and deletion. That does imply that it is fgfr3 inhibition which leads to the actual height increases while fgfr2 must be balanced out.
Regarding the other claim that type x collagen somehow noticeably influences the chondrocyte differentiation, theres a reason why literally 0 evidence is given. Type x collagen is primarily a marker of hypertrophy and is exclusively secreted in chondrocytes that have entered senescence. The deletion of Col10a1 proved that type x collagen is completely dispensable for differentiation but also that absence of the former faciliates the latter. Showing that the absence of type x collagen increases chondrocyte differentiation into hypertrophy, it's presence leads to a longer stay in a proliferative phase. Both FGFR1 and FGFR2 primarily cause collagen x downregulation by affecting the responsible transcription factors, this would again faciliate differentiation and thus be counterproductive. FGFR3 Inhibition however consistently upregulates it which results in greater proliferation before hypertrophy. Whether this has any significant effects is very questionable and would presume that the secretion has noticeable effects extracellularly, I would argue most of the matters have already been decided by pathways upstream. Observations like this could also be reverse causality.
You also didnt really give any specification or go into detail on how this would work? I would kind of expect that when putting forth such a ground breaking theory.
what the fuck is this reasoning LOL
And how does "erda doesnt work as you think it does" conclude in "erda has more roi than all other compounds"
Please dont
Because you made it all up?
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