多巴胺D4受体下调节脏的化对运输器通过UBIQUITINATION-ASSOCIATED Lysosome降解
bioRxiv : the preprint server for biology
|February 26, 2024
概括
多巴胺受体D4 (Drd4) 缺乏增加了小鼠对 thiazide 敏感的化共运输体 (NCC),导致高血压. Drd4的激活通过二维基因化和溶酶体降解来降低NCC的调节,这表明了新的治疗点.
科学领域:
- 脏生理学和分子生物学
- 心血管研究的心血管研究.
- 内分泌学 在内分泌学.
背景情况:
- 对 thiazide 敏感的化共运输体 (NCC) 对于在远端卷状管 (DCT) 中的再吸收至关重要,调节血压.
- 多巴胺受体D4 (Drd4) 在脏抗高血压系统中发挥作用,其干扰导致高血压,但潜在的机制尚不清楚.
结论:
- 多巴胺受体D4 (Drd4) 在脏中负面调节化共运输体 (NCC).
- 这种调节通过促进USP48相关的二维基因化发生,从而导致NCC内部化,溶酶体降解和活性降低.
- 这些发现阐明了一种新的机制,通过NCC调制将Drd4信号与血压调节联系起来.
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