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二丁酰环磷酸腺苷抑制培养的成纤维细胞和动脉平滑肌细胞中的低密度脂蛋白结合。

Dibutyryl cyclic AMP inhibits LDL binding in cultured fibroblasts and arterial smooth muscle cells.

作者信息

Stout R W, Bierman E L

出版信息

Atherosclerosis. 1983 Jan;46(1):13-20. doi: 10.1016/0021-9150(83)90159-4.

Abstract

The interaction of low density lipoproteins (LDL) with cell membrane receptors is regulated by certain hormones. To test whether LDL receptor activity is influenced by cyclic AMP, the effect of dibutyryl cyclic AMP on LDL binding uptake and degradation was studied in cultured human skin fibroblasts and in rat and human arterial smooth muscle cells. Dibutyryl cyclic AMP in concentrations of 10(-3) to 10(-7)M inhibited LDL binding and degradation in fibroblasts and rat arterial smooth muscle cells, and degradation in human arterial smooth muscle cells. Inhibition of LDL receptor activity by dibutyryl cyclic AMP did not appear to be due to a non-specific toxic effect of the nucleotide. It appeared to be mediated on the affinity of the receptor for LDL rather than receptor number.

摘要

低密度脂蛋白(LDL)与细胞膜受体的相互作用受某些激素调节。为了检测LDL受体活性是否受环磷酸腺苷(cAMP)影响,研究了二丁酰环磷腺苷对培养的人皮肤成纤维细胞以及大鼠和人动脉平滑肌细胞中LDL结合、摄取和降解的作用。浓度为10^(-3)至10^(-7)M的二丁酰环磷腺苷抑制了成纤维细胞和大鼠动脉平滑肌细胞中LDL的结合与降解,以及人动脉平滑肌细胞中LDL的降解。二丁酰环磷腺苷对LDL受体活性的抑制似乎并非由于该核苷酸的非特异性毒性作用。它似乎是通过受体对LDL的亲和力而非受体数量来介导的。

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