共查询到20条相似文献,搜索用时 15 毫秒
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Russell JL Powers JT Rounbehler RJ Rogers PM Conti CJ Johnson DG 《Molecular and cellular biology》2002,22(5):1360-1368
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Murakami T Takagi H Suzuma K Suzuma I Ohashi H Watanabe D Ojima T Suganami E Kurimoto M Kaneto H Honda Y Yoshimura N 《The Journal of biological chemistry》2005,280(36):31841-31849
Oxidative stress activates various signal transduction pathways, including Jun N-terminal kinase (JNK) and its substrates, that induce apoptosis. We reported here the role of angiopoietin-1 (Ang1), which is a prosurvival factor in endothelial cells, during endothelial cell damage induced by oxidative stress. Hydrogen peroxide (H2O2) increased apoptosis of endothelial cells through JNK activation, whereas Ang1 inhibited H2O2-induced apoptosis and concomitant JNK phosphorylation. The inhibition of H2O2-induced JNK phosphorylation was reversed by inhibitors of phosphatidylinositol (PI) 3-kinase and dominant-negative Akt, and constitutively active-Akt attenuated JNK phosphorylation without Ang1. These data suggested that Ang1-dependent Akt phosphorylation through PI 3-kinase leads to the inhibition of JNK phosphorylation. H2O2-induced phosphorylation of SAPK/Erk kinase (SEK1) at Thr261, which is an upstream regulator of JNK, was also attenuated by Ang1-dependent activation of the PI 3-kinase/Akt pathway. In addition, Ang1 induced SEK1 phosphorylation at Ser80, suggesting the existence of an additional signal transduction pathway through which Ang1 attenuates JNK phosphorylation. These results demonstrated that Ang1 attenuates H2O2-induced SEK1/JNK phosphorylation through the PI 3-kinase/Akt pathway and inhibits the apoptosis of endothelial cells to oxidative stress. 相似文献
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Tan J Zhuang L Jiang X Yang KK Karuturi KM Yu Q 《The Journal of biological chemistry》2006,281(15):10508-10515
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Deregulation of the Rb-E2F pathway occurs in many cancers and results in aberrant cell proliferation as well as an increased propensity to undergo apoptosis. In most cases, apoptosis in response to Rb inactivation involves the activation of p53 but the molecular details of the signaling pathway connecting Rb loss to p53 are poorly understood. Here we demonstrate that the E1A oncoprotein, which binds and inhibits Rb family members, induces the accumulation and phosphorylation of p53 through the DNA damage-responsive ATM kinase. As a result, E1A-induced apoptosis is significantly impaired in cells lacking ATM. In contrast, inactivation of ARF, which is widely believed to activate p53 in response to oncogenic stress, has no effect on p53 induction and only a modest effect on apoptosis in response to E1A. Both E2F1 and E2F3 contribute to ATM-dependent phosphorylation of p53 and apoptosis in cells expressing E1A. However, deregulated E2F3 activity is implicated in the DNA damage caused by E1A while E2F1 stimulates ATM- and NBS1-dependent p53 phosphorylation and apoptosis through a mechanism that does not involve DNA damage. 相似文献
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The transcription factor E2F1 modulates apoptosis of neurons 总被引:11,自引:2,他引:9
Hou ST Callaghan D Fournier MC Hill I Kang L Massie B Morley P Murray C Rasquinha I Slack R MacManus JP 《Journal of neurochemistry》2000,75(1):91-100
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ASPP1 and ASPP2 are new transcriptional targets of E2F 总被引:4,自引:0,他引:4
Fogal V Kartasheva NN Trigiante G Llanos S Yap D Vousden KH Lu X 《Cell death and differentiation》2005,12(4):369-376