HMI 115 sembra funzionare, ma non si capisce perchè!!
"I think we should take another look at PRLR cofactors again and cleaved Prl fragments. We know acetylation is implicated in AGA, and this affects dimerization along with FOX01 and part of NF-kB which is altered by EDA2R, which has a variant that confers near-immunity to AGA.
There's no association between PRLR and AGA in any GWAS, and it's not differentially expressed in bald scalp.
Prolactin binding might be greatly increased, but if that's all it is then I would expect STAT3 to be upregulated instead of downregulated in Chew et al. analysis. So if that's accurate we have to be looking at altered PRLR signaling instead of upregulated. Unless blocking the PRLR is a cheat code to restore expression of some vital protein like BMP4 that's suppressed by another pathway rather than the PRLR being causal. Or PRLR expression is required for transcription of some causal protein downstream of AR"
"I think we should take another look at PRLR cofactors again and cleaved Prl fragments. We know acetylation is implicated in AGA, and this affects dimerization along with FOX01 and part of NF-kB which is altered by EDA2R, which has a variant that confers near-immunity to AGA.
There's no association between PRLR and AGA in any GWAS, and it's not differentially expressed in bald scalp.
Prolactin binding might be greatly increased, but if that's all it is then I would expect STAT3 to be upregulated instead of downregulated in Chew et al. analysis. So if that's accurate we have to be looking at altered PRLR signaling instead of upregulated. Unless blocking the PRLR is a cheat code to restore expression of some vital protein like BMP4 that's suppressed by another pathway rather than the PRLR being causal. Or PRLR expression is required for transcription of some causal protein downstream of AR"