Mot-2 protein is shown to interact with p53 and inhibit its transcriptional activation function. Mot-2 overexpressing stable clones of NIH 3T3 cells were malignantly transformed, however, they had a high level of expr...Mot-2 protein is shown to interact with p53 and inhibit its transcriptional activation function. Mot-2 overexpressing stable clones of NIH 3T3 cells were malignantly transformed, however, they had a high level of expression of a p53 downstream gene, p21WAF1. The present study was undertaken to elucidate possible molecular mechanism(s) of such upregulation. An inCreased level of p21WAF1, expression was detected in sta- ble transfectants although an exogenous reporter gene driven by p21WAF1, promoter exhibited lower activity in these cells suggesting that some post-transcriptional mechanism contributes to upregulation. Western analyses of transient and stable clones revealed that upregulation of p21WAF1, in stable NIH 3T3/mot-2 cells may be mediated by cyclin D1 and cdk-2.展开更多
This study investigated the relationship between human papillomavirus (HPV) genotype and expression of p53and p21^(WAF1) Expression of p53 and p2l^(WAF1) in 35 cases ofcondyloma acuminatum specimens infected by HPV6/1...This study investigated the relationship between human papillomavirus (HPV) genotype and expression of p53and p21^(WAF1) Expression of p53 and p2l^(WAF1) in 35 cases ofcondyloma acuminatum specimens infected by HPV6/11andHPV16/18 were studied using immunohistochemical staining.All specimens of the condyloma acuminatum case were positivefor expression of p53 and p21^(WAF1). The expression of p53 incondyloma acuminatum infected by HPV16/18 wassignificantly lower than that in specimens infected byHPV6/11.However, expression of p21^(WAF1) between the twogroups was not significantly different. Expression of p53 incondyloma acuminatum is likely related to HPV genotype,exoression of p21^(WAF1) was not related to HPV genotype.展开更多
Objective To investigate the protective effects of hydrogen peroxide preconditioning （HPP） on the pheochromocytoma （PC12） cells treated with 1-methyl-4-phenylpyridinium （MPP^＋） and to explore the potential mech...Objective To investigate the protective effects of hydrogen peroxide preconditioning （HPP） on the pheochromocytoma （PC12） cells treated with 1-methyl-4-phenylpyridinium （MPP^＋） and to explore the potential mechanisms. Methods The viability and apoptosis of PC 12 cells were determinded by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay and 4′,6′-diamidino-2-phenylindole （DAPI） staining, respectively. The expressions of 14-3-3 protein and phospholylated p38 mitogen-activated protein kinase （MAPK） were determined by Western blot. Enzyme-linked immunosorbent assay （ELISA） was used to measure the activity of extracellular signal-regulated protein kinase 1/2 （ERK1/2）. Results The cell viability decreased and the number of apoptotic cells increased dramatically in MPP^＋ group compared with that in Control group. HPP induced a significant increase in cell viability and a marked decrease in population of apoptotic cells of the MPP^＋- treated PC 12 cells, accompanied with up-regulation of 14-3-3 protein and increase of ERK 1/2 and p38 MAPK activities. The 14-3-3 protein expression was positively correlated with the phosphorylation of ERK1/2. Furthermore, inhibition of the ERK1/2 with PD98059 abolished the 14-3-3 protein up-regulation in PC 12 cells induced by HPP. Conclusion HPP protects PC 12 cells against MPP＋ toxicity by up-regulating 14-3-3 protein expression through the ERK1/2 and p38 MAPK signaling pathways.展开更多
文摘Mot-2 protein is shown to interact with p53 and inhibit its transcriptional activation function. Mot-2 overexpressing stable clones of NIH 3T3 cells were malignantly transformed, however, they had a high level of expression of a p53 downstream gene, p21WAF1. The present study was undertaken to elucidate possible molecular mechanism(s) of such upregulation. An inCreased level of p21WAF1, expression was detected in sta- ble transfectants although an exogenous reporter gene driven by p21WAF1, promoter exhibited lower activity in these cells suggesting that some post-transcriptional mechanism contributes to upregulation. Western analyses of transient and stable clones revealed that upregulation of p21WAF1, in stable NIH 3T3/mot-2 cells may be mediated by cyclin D1 and cdk-2.
文摘This study investigated the relationship between human papillomavirus (HPV) genotype and expression of p53and p21^(WAF1) Expression of p53 and p2l^(WAF1) in 35 cases ofcondyloma acuminatum specimens infected by HPV6/11andHPV16/18 were studied using immunohistochemical staining.All specimens of the condyloma acuminatum case were positivefor expression of p53 and p21^(WAF1). The expression of p53 incondyloma acuminatum infected by HPV16/18 wassignificantly lower than that in specimens infected byHPV6/11.However, expression of p21^(WAF1) between the twogroups was not significantly different. Expression of p53 incondyloma acuminatum is likely related to HPV genotype,exoression of p21^(WAF1) was not related to HPV genotype.
基金the National Natural Science Foundation of China (No. 30570627)
文摘Objective To investigate the protective effects of hydrogen peroxide preconditioning （HPP） on the pheochromocytoma （PC12） cells treated with 1-methyl-4-phenylpyridinium （MPP^＋） and to explore the potential mechanisms. Methods The viability and apoptosis of PC 12 cells were determinded by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay and 4′,6′-diamidino-2-phenylindole （DAPI） staining, respectively. The expressions of 14-3-3 protein and phospholylated p38 mitogen-activated protein kinase （MAPK） were determined by Western blot. Enzyme-linked immunosorbent assay （ELISA） was used to measure the activity of extracellular signal-regulated protein kinase 1/2 （ERK1/2）. Results The cell viability decreased and the number of apoptotic cells increased dramatically in MPP^＋ group compared with that in Control group. HPP induced a significant increase in cell viability and a marked decrease in population of apoptotic cells of the MPP^＋- treated PC 12 cells, accompanied with up-regulation of 14-3-3 protein and increase of ERK 1/2 and p38 MAPK activities. The 14-3-3 protein expression was positively correlated with the phosphorylation of ERK1/2. Furthermore, inhibition of the ERK1/2 with PD98059 abolished the 14-3-3 protein up-regulation in PC 12 cells induced by HPP. Conclusion HPP protects PC 12 cells against MPP＋ toxicity by up-regulating 14-3-3 protein expression through the ERK1/2 and p38 MAPK signaling pathways.
