脂肪生成
下调和上调
未折叠蛋白反应
切碎
ATF4
间充质干细胞
基因敲除
细胞生物学
化学
生物
内分泌学
癌症研究
内科学
内质网
细胞凋亡
医学
生物化学
基因
作者
Yueping Chen,Hui Gao,Qingshui Yin,Liang Chen,Panfeng Dong,Xiaoyun Zhang,Jie Kang
摘要
Our data therefore revealed a role of ER stress and ATF4/CHOP in the ethanol-induced inhibition of osteogenesis, and activation of TNF-α signaling by ATF4/CHOP linking ER stress to adipogenic lineage in response to alcohol stimulation. This work should establish a new signaling pathway linking alcohol, ER stress, and TNF-α to loss of bone formation: Ethanol → ER stress↑↑↑ → ATF4 & CHOP↑↑↑ → TNF-α↑↑↑ → Osteoblasts↓↓↓.
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