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delayed intervention) influence long-term neurological outcomes
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D51.9 serves as the unspecified variant when clinical documentation fails to identify the deficiency mechanism
The mechanism study revealed that GCN5L specifically acetylates the K268 site of PPAR, enhancing its interaction with PGC-1, promoting mitochondrial biogenesis in adipocytes and increasing the expression of UCP1 in brown adipose tissue (Miao, , 2023)
J Pharmacol Toxicol Methods 41:5558
Hendriks VM, Van den Brink W, Blanken P, Bosman IJ, Van Ree JM
