作为主要的阿迪波内克丁结合伙伴的T-cadherin抑制了代谢组织中的ERK信号传递
Hirofumi Nagao1,2, Yuta Kondo2, Keitaro Kawada2
1Department of Metabolism and Atherosclerosis, Graduate School of Medicine, The University of Osaka, Suita, Osaka 565-0871, Japan.
概括
T-cadherin抑制ERK信号传递,影响心脏和骨肌肉平衡. 阿迪波内克丁维持T-cadherin,这会影响细胞内通路和外体细胞的产生.
科学领域:
- 细胞生物学 细胞生物学
- 分子信号传递是分子信号传递.
- 代谢研究的研究.
背景情况:
- T-cadherin 是一种具有器官保护作用的阿迪波内克丁结合伙伴.
- 代谢组织中T-cadherin诱导的细胞内信号变化尚未得到充分理解.
研究的目的:
- 研究T-cadherin在调节细胞内信号通路中的作用.
- 为了阐明T-cadherin对心脏和骨肌肉平衡的作用.
主要方法:
- 细胞培养实验 (C2C12肌细胞,F2内皮细胞) 使用T-cadherin敲击和过度表达.
- 蛋白质组分析以确定ERK信号的下游目标.
- 在心脏和骨肌肉中,T-cadherin被淘汰的小鼠模型.
主要成果:
- 在培养细胞和小鼠组织中,T-cadherin抑制ERK (细胞外信号调节激酶) 信号传递.
- 降低T-cadherin增加了ERK的酸化,并对下游目标进行了上调.
- 在小鼠中,T-cadherin的切除导致ERK信号的增加,心脏缩,并在饥饿期间改变肌肉缩.
结论:
- T-cadherin调节细胞内信号,特别是抑制ERK通路.
- T-cadherin在维持心脏和骨肌肉平衡方面发挥着作用.
- 亚迪波涅克丁维持的T-cadherin会影响外体细胞的产生和细胞信号传递.
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