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新型抗生素 tautomycin 诱导人髓性白血病细胞形态变化及蛋白激酶 C 的激活

Induction of morphological change of human myeloid leukemia and activation of protein kinase C by a novel antibiotic, tautomycin.

作者信息

Magae J, Watanabe C, Osada H, Cheng X C, Isono K

机构信息

Riken, Institute of Physical and Chemical Research, Saitama, Japan.

出版信息

J Antibiot (Tokyo). 1988 Jul;41(7):932-7. doi: 10.7164/antibiotics.41.932.

Abstract

A novel antibiotic tautomycin induced many blebs on the surface of K562 human chronic myeloid leukemia cells, similar to the morphological changes induced by phorbol esters. However, tautomycin did not induce nitroblue tetrazolium reducing activity, when HL60 human promyelocytic leukemia cells were caused to differentiate by quinomycin into mature granulocytes. It did not induce spread of HL60 cells, one of the phenotypes of mature macrophages. In addition, it did not compete with phorbol dibutyrate to bind to the cell surface of K562 cells. However, tautomycin significantly activated protein kinase C (PKC) extracted from K562 cells. These results indicate that tautomycin is a new activator of PKC, distinct from phorbol esters.

摘要

一种新型抗生素 tautomycin 在 K562 人慢性髓性白血病细胞表面诱导出许多泡状突起,类似于佛波酯诱导的形态学变化。然而,当 HL60 人早幼粒细胞白血病细胞被醌霉素诱导分化为成熟粒细胞时,tautomycin 并未诱导硝基蓝四唑还原活性。它也未诱导 HL60 细胞的铺展,而铺展是成熟巨噬细胞的表型之一。此外,它不与二丁酰佛波醇竞争结合 K562 细胞的细胞表面。然而,tautomycin 能显著激活从 K562 细胞中提取的蛋白激酶 C(PKC)。这些结果表明,tautomycin 是一种不同于佛波酯的新型 PKC 激活剂。

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