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High-level expression of human calmodulin in E.coli and its effects on cell proliferation 被引量:3
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作者 li xj Wu JG +2 位作者 Si JL Guo DW Xu JP 《World Journal of Gastroenterology》 SCIE CAS CSCD 2000年第4期588-592,共5页
Calmodulin (CaM), widely distributed in almost all eukaryotic cells, is a major intracellular calcium receptor responsible for mediating the Ca2 + signal to a multitude of different enzyme systems and is thought to pl... Calmodulin (CaM), widely distributed in almost all eukaryotic cells, is a major intracellular calcium receptor responsible for mediating the Ca2 + signal to a multitude of different enzyme systems and is thought to play a vital role in the regulation of cell proliferative cycle[1,2]. Recently, many studies showed that CaM is also present in extracellular fluid such as cell culture media and normal body fluid and has been reported to stimulate proliferation in a range of normal and neoplastic cells, apparently acting as an autocrine growth factor[3-11]. In 1988, Crocker et al reported for the first time that addition of extracellular pure pig brain CaM could promote DNA synthesis and cell [7]proliferation in K562 human leukaemic lymphocytes[7].After that, more and more research was done on extracellular CaM and evidences demonstrated that extracellular CaM could also stimulate cell proliferation in normal human umbilical vein endothelial cells[5], keratinocytes[4], suspension-cultured cells of Angelica Dahurica, etc[6]. CaM is a monomeric protein of 148 amino acids that contains four homologous Ca2 + -binding domains. CaM has been highly conserved throughout the evolution. Only 1 out of 148 amino acids of human CaM is different from that of fish CaM. Complementary DNAs encoding rat, eel, chicken, human, and trypanosome CaM have been cloned. 展开更多
关键词 CALMODULIN gene expression biological activity ESCHERICHIA COLI cell proliferation TRIFLUOPERAZINE POLYMERASE chain reaction MONOCLONAL antibodies
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组蛋白甲基转移酶SETD2在肝组织中的缺陷导致脂质代谢异常及肝癌 被引量:7
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作者 li xj li QL +1 位作者 JU LG 吴旻 《临床肝胆病杂志》 CAS 北大核心 2021年第6期1308-1308,共1页
【据Hepatology 2021年5月报道】题:组蛋白甲基转移酶SETD2在肝组织中的缺陷导致脂质代谢异常及肝癌(作者Li XJ等)组蛋白甲基转移酶SETD2所催化的H3K36me3是从酵母到哺乳动物都保守的表观遗传修饰之一。SETD2可以抑制肿瘤发生且在多种... 【据Hepatology 2021年5月报道】题:组蛋白甲基转移酶SETD2在肝组织中的缺陷导致脂质代谢异常及肝癌(作者Li XJ等)组蛋白甲基转移酶SETD2所催化的H3K36me3是从酵母到哺乳动物都保守的表观遗传修饰之一。SETD2可以抑制肿瘤发生且在多种癌症中频繁发生突变。来自武汉大学生命科学学院免疫与代谢前沿科学中心的Li等利用SETD2肝脏特异性敲除的小鼠模型发现,SETD2缺失可导致自发性肝癌。 展开更多
关键词 脂质代谢异常 组蛋白甲基转移酶 表观遗传修饰 抑制肿瘤 小鼠模型 前沿科学 肝癌 肝组织
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