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百日咳毒素对3T3-L1脂肪细胞中胰岛素诱导的颗粒型环磷酸腺苷磷酸二酯酶活性激活的选择性调节。

Selective regulation by pertussis toxin of insulin-induced activation of particulate cAMP phosphodiesterase activity in 3T3-L1 adipocytes.

作者信息

Elks M L, Watkins P A, Manganiello V C, Moss J, Hewlett E, Vaughan M

出版信息

Biochem Biophys Res Commun. 1983 Oct 31;116(2):593-8. doi: 10.1016/0006-291x(83)90565-x.

Abstract

Incubation of 3T3-L1 adipocytes with insulin or isoproterenol for 10 min increased particulate "low Km" cAMP phosphodiesterase activity by 42% and 50%, respectively. Pertussis toxin catalyzed the [32P]-ADP ribosylation of a 41,000 dalton protein in adipocyte particulate fractions; prior incubation of adipocytes with toxin markedly reduced incorporation of radiolabel. Exposure of adipocytes to pertussis toxin (0.3 microgram, 18 hr) increased glycerol production and inhibited activation of cAMP phosphodiesterase by insulin, but not by isoproterenol. These results suggest that pertussis toxin can interfere with receptor-mediated processes that stimulate cAMP hydrolysis as well as those that inhibit cAMP formation.

摘要

将3T3-L1脂肪细胞与胰岛素或异丙肾上腺素孵育10分钟,分别使微粒体“低Km”环磷酸腺苷(cAMP)磷酸二酯酶活性提高了42%和50%。百日咳毒素催化脂肪细胞微粒体部分中一种41,000道尔顿蛋白质的[32P]-ADP核糖基化;预先将脂肪细胞与毒素孵育可显著减少放射性标记的掺入。将脂肪细胞暴露于百日咳毒素(0.3微克,18小时)可增加甘油生成,并抑制胰岛素对cAMP磷酸二酯酶的激活,但不抑制异丙肾上腺素的激活。这些结果表明,百日咳毒素可干扰受体介导的刺激cAMP水解以及抑制cAMP形成的过程。

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