医学
安普克
PI3K/AKT/mTOR通路
FOXP3型
结肠炎
炎症性肠病
车站3
免疫学
RAR相关孤儿受体γ
溃疡性结肠炎
炎症
磷酸化
内科学
信号转导
疾病
蛋白激酶A
免疫系统
生物
生物化学
作者
Ying Xue Yang,Yuan Yuan,Boning Xia
标识
DOI:10.15586/aei.v50i5.654
摘要
These findings established that CTD1 improved DSS-induced colitis by suppressing Th17-Treg cells balance by activating the AMPK/mTOR pathway. This study provided a new strategy for developing novel treatments for patients with IBD.
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