It is shown here that one can induce prematurely condensed chromosomes (PCCs) in G1-phase human (HeLa) and mouse (FT210) cells by treating them with the protein phosphatase inhibitor calyculin A. However, histone H1 i...It is shown here that one can induce prematurely condensed chromosomes (PCCs) in G1-phase human (HeLa) and mouse (FT210) cells by treating them with the protein phosphatase inhibitor calyculin A. However, histone H1 is not phosphorylated in these G1-PCCs. It has previously been proposed that histone H1 phosphorylation is responsible for mitotic chromosome condensation, but our results suggest that this is not the case. They indicate instead that phosphorylation of histone H1 is not required for chromosome condensation. It is known that the Cdk1 protein kinase, which triggers mitosis and also phosphorylates histone H1, cannot be activated in G1-phase because mitotic cyclins are not present. Since calyculin A induces PCCs in G1-phase in the absence of active Cdk1, our results suggest that inactivation of protein phosphatases may be just as important for the onset of chromosome condensation and other mitotic events as the activation of protein kinases.展开更多
目的:研究非霍奇金淋巴瘤(non-hodgkin's lymphoma,NHL)中微小染色体维持蛋白2(Minichromosome maintenance protein 2,MCM2)与细胞间隙连接蛋白43(Connexin 43,Cx43)以及S期激酶相关蛋白2(S phase kinase-associated protein 2,Sk...目的:研究非霍奇金淋巴瘤(non-hodgkin's lymphoma,NHL)中微小染色体维持蛋白2(Minichromosome maintenance protein 2,MCM2)与细胞间隙连接蛋白43(Connexin 43,Cx43)以及S期激酶相关蛋白2(S phase kinase-associated protein 2,Skp2)在非霍奇金淋巴瘤中的表达及临床意义,以期为临床诊治非霍奇金淋巴瘤提供一定的参考。方法:选取2013年1月至2015年1月间入院诊治的非霍奇金淋巴瘤36例作为实验组,并选取同期入院诊治的淋巴结反应性增生18例作为对照组,应用免疫组化法检测MCM2、Cx43、Skp2的表达情况,同时分析MCM2、Cx43、Skp2的表达与非霍奇金淋巴瘤恶性程度、临床分期等的相关性。结果:实验组NHL患者MCM2阳性表达率为83.33%、Skp2阳性表达率为86.11%,显著高于对照组22.22%与27.78%的阳性表达率(P<0.01);NHL患者Cx43阳性表达率为22.22%,显著低于对照组61.11%阳性表达率(P<0.01)。NHL患者MCM2阳性表达与肿瘤恶性程度、临床分期及Ki67水平密切相关(P<0.05);NHL患者Cx43阳性表达与肿瘤恶性程度呈负相关(P<0.01);NHL患者Skp2阳性表达与肿瘤恶性程度及临床分期密切相关(P<0.05)。结论:MCM2、Cx43、Skp2的异常表达与非霍奇金淋巴瘤的恶性程度密切相关,联合检测MCM2、Cx43、Skp2可为非霍奇金淋巴瘤的诊治提供一定的参考。展开更多
文摘It is shown here that one can induce prematurely condensed chromosomes (PCCs) in G1-phase human (HeLa) and mouse (FT210) cells by treating them with the protein phosphatase inhibitor calyculin A. However, histone H1 is not phosphorylated in these G1-PCCs. It has previously been proposed that histone H1 phosphorylation is responsible for mitotic chromosome condensation, but our results suggest that this is not the case. They indicate instead that phosphorylation of histone H1 is not required for chromosome condensation. It is known that the Cdk1 protein kinase, which triggers mitosis and also phosphorylates histone H1, cannot be activated in G1-phase because mitotic cyclins are not present. Since calyculin A induces PCCs in G1-phase in the absence of active Cdk1, our results suggest that inactivation of protein phosphatases may be just as important for the onset of chromosome condensation and other mitotic events as the activation of protein kinases.
文摘目的:研究非霍奇金淋巴瘤(non-hodgkin's lymphoma,NHL)中微小染色体维持蛋白2(Minichromosome maintenance protein 2,MCM2)与细胞间隙连接蛋白43(Connexin 43,Cx43)以及S期激酶相关蛋白2(S phase kinase-associated protein 2,Skp2)在非霍奇金淋巴瘤中的表达及临床意义,以期为临床诊治非霍奇金淋巴瘤提供一定的参考。方法:选取2013年1月至2015年1月间入院诊治的非霍奇金淋巴瘤36例作为实验组,并选取同期入院诊治的淋巴结反应性增生18例作为对照组,应用免疫组化法检测MCM2、Cx43、Skp2的表达情况,同时分析MCM2、Cx43、Skp2的表达与非霍奇金淋巴瘤恶性程度、临床分期等的相关性。结果:实验组NHL患者MCM2阳性表达率为83.33%、Skp2阳性表达率为86.11%,显著高于对照组22.22%与27.78%的阳性表达率(P<0.01);NHL患者Cx43阳性表达率为22.22%,显著低于对照组61.11%阳性表达率(P<0.01)。NHL患者MCM2阳性表达与肿瘤恶性程度、临床分期及Ki67水平密切相关(P<0.05);NHL患者Cx43阳性表达与肿瘤恶性程度呈负相关(P<0.01);NHL患者Skp2阳性表达与肿瘤恶性程度及临床分期密切相关(P<0.05)。结论:MCM2、Cx43、Skp2的异常表达与非霍奇金淋巴瘤的恶性程度密切相关,联合检测MCM2、Cx43、Skp2可为非霍奇金淋巴瘤的诊治提供一定的参考。
