Induction of apoptosis in p53-deficient L1210 cells by an I-kappa-B-alpha-inhibitor (Bay 11-7085) via a NF-kappa-B-independent mechanism.

Cory AH; Cory JG

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Induction of apoptosis in p53-deficient L1210 cells by an I-kappa-B-alpha-inhibitor (Bay 11-7085) via a NF-kappa-B-independent mechanism.

机译：I-κB-α-抑制剂（Bay 11-7085）通过独立于NF-κB的机制诱导p53缺陷L1210细胞凋亡。

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The effects of Bay 11-7085, an inhibitor of I-kappa-B-alpha kinase, were compared in the wild-type and deoxyadenosine-resistant mouse leukemia cell lines. At higher concentrations, Bay 11-7085 caused apoptosis and necrosis in the two cell lines. However, at much lower concentrations of Bay 11-7085, the deoxyadenosine-resistant cells became much more apoptotic than the parental wild-type L1210 cells. Under these conditions (low drug concentrations), the level of apoptotic cells far exceeded the fraction of necrotic cells. The apoptotic effects of Bay 11-7085 on the deoxyadenosine-resistant cells was both time- and concentration-dependent. Caspase-3 activity was activated in the Bay 11-7085-treated cells. The molecular basis for the difference in the apoptotic response between the wild-type and deoxyadenosine-resistant L1210 cells is not defined at this time, but these cell lines may provide a comparative model system in which differences in the cells that lead to apoptotic or necrotic responses to drugscan be defined and used in development of appropriate drugs for clinical use.

机译：在野生型和抗脱氧腺苷的小鼠白血病细胞系中比较了I-κB-α激酶抑制剂Bay 11-7085的作用。在较高浓度下，Bay 11-7085导致两种细胞系发生凋亡和坏死。但是，在较低的Bay 11-7085浓度下，耐脱氧腺苷的细胞比亲本野生型L1210细胞凋亡的要多得多。在这些条件下（低药物浓度），凋亡细胞的水平远远超过了坏死细胞的比例。 Bay 11-7085对抗脱氧腺苷的细胞的凋亡作用是时间依赖性和浓度依赖性的。在Bay 11-7085处理的细胞中，Caspase-3活性被激活。目前尚不确定野生型和抗脱氧腺苷的L1210细胞之间凋亡反应差异的分子基础，但是这些细胞系可能提供了一个比较模型系统，其中导致凋亡或坏死的细胞差异可以定义对药物的反应，并将其用于开发适合临床的药物。

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《Advances in enzyme regulation》 |2005年第0期|共9页
作者
Cory AH; Cory JG;
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正文语种 eng
中图分类基础医学;
关键词
Apoptosis; I-kappa B Kinase; Leukemia L1210; NF-kappa B; Nitriles; Sulfones; 脱噬作用; 白血病 L1210; NF-κB; 腈类; 砜类;

机译：Apoptosis;I-kappa B Kinase;Leukemia L1210;NF-kappa B;Nitriles;Sulfones;脱噬作用;白血病 L1210;NF-κB;腈类;砜类;

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1. Induction of apoptosis in p53-deficient L1210 cells by an I-kappa-B-alpha-inhibitor (Bay 11-7085) via a NF-kappa-B-independent mechanism. [J] . Cory AH, Cory JG Advances in enzyme regulation . 2005,第0期

机译：I-κB-α-抑制剂（Bay 11-7085）通过独立于NF-κB的机制诱导p53缺陷L1210细胞凋亡。
2. Augmentation of apoptosis responses in p53-deficient L1210 cells by compounds directed at blocking NFkappaB activation. [J] . Cory-A H, Cory-J G Anticancer Research: International Journal of Cancer Research and Treatment . 2001,第6Appa期

机译：针对p53缺陷的L1210细胞中的凋亡反应，通过针对NFkappaB激活的阻断化合物来增强。
3. Induction of apoptosis by pectenotoxin-2 is mediated with the induction of DR4/DR5, Egr-1 and NAG-1, activation of caspases and modulation of the Bcl-2 family in p53-deficient Hep3B hepatocellular carcinoma cells. [J] . Shin DY, Kim GY, Kim ND, Oncology reports . 2008,第2期

机译：通过果胶毒素2诱导的细胞凋亡与DR4 / DR5，Egr-1和NAG-1的诱导，胱天蛋白酶的激活以及Bcl-2家族在p53缺陷的Hep3B肝癌细胞中的介导有关。
4. Induction of apoptosis in p53-deficient L1210cells by an I-К-B-α-inhibitor (Bay 11-7085)via a NF-К-B-independent mechanism [C] . Ann H. Cory, Joseph G. Cory International Symposium on Regulation of Enzyme Activity and Synthesis in Normal and Neoplastic Tissues . 2005

机译：通过NF-к-b-β-抑制剂（Bay 11-7085）通过NF-к-B-B-B-B-B-B-β-β-抑制剂诱导P53缺陷L1210Cells的凋亡
5. Induction and inhibition of apoptosis: A study of a key immune mechanism. [D] . Chaudhuri, Aniruddho R. 1999

机译：诱导和抑制细胞凋亡：关键免疫机制的研究。
6. BAY 11-7085 induces glucocorticoid receptor activation and autophagy that collaborate with apoptosis to induce human synovial fibroblast cell death [O] . Biserka Relic, Edith Charlier, Celine Deroyer, 2016

机译：BAY 11-7085诱导糖皮质激素受体激活和自噬与细胞凋亡协同作用诱导人滑膜成纤维细胞死亡
7. Induction of CHOP and apoptosis by nitric oxide in p53-deficient microglial cells [O] . Kawahara Kohichi, Oyadomari Seiichi, Gotoh Tomomi, 2001

机译：一氧化氮在p53缺陷型小胶质细胞中诱导CHOP和凋亡
8. Role of Cell-Cell Signalling in the Induction of Apoptosis in Human Breast Cancer Cells. [R] . Chrysogelos, S. A. 1996

机译：细胞信号在诱导人乳腺癌细胞凋亡中的作用。

Induction of apoptosis in p53-deficient L1210 cells by an I-kappa-B-alpha-inhibitor (Bay 11-7085) via a NF-kappa-B-independent mechanism.

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