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Hyperphosphorylation of retinoblastoma protein and p53 by okadaic acid, a tumor promoter.

作者信息

Yatsunami J, Komori A, Ohta T, Suganuma M, Fujiki H

机构信息

Cancer Prevention Division, National Cancer Center Research Institute, Tokyo Japan.

出版信息

Cancer Res. 1993 Jan 15;53(2):239-41.

PMID:8417815
Abstract

A potent tumor promoter, okadaic acid, induced hyperphosphorylation of tumor suppressor proteins, retinoblastoma protein and p53, by in vitro incubation with nuclei isolated from rat regenerating liver as well as by incubation with primary human fibroblasts. Most of the retinoblastoma protein migrated to a hyperphosphorylated position in electrophoresis. The phosphorylation of p53 was increased at a rate 8 times that in non-treated primary human fibroblasts. Hyperphosphorylation of tumor suppressor proteins, mediated through inhibition of protein phosphatases 1 and 2A, is involved in tumor promotion by okadaic acid. The significance of hyperphosphorylation of the retinoblastoma protein and p53 is discussed in relation to the regulation of the cell cycle.

摘要

相似文献

1
Hyperphosphorylation of retinoblastoma protein and p53 by okadaic acid, a tumor promoter.
Cancer Res. 1993 Jan 15;53(2):239-41.
2
Hyperphosphorylation of p53 induced by okadaic acid attenuates its transcriptional activation function.冈田酸诱导的p53过度磷酸化减弱其转录激活功能。
Cancer Res. 1994 Aug 15;54(16):4448-53.
3
Hyperphosphorylation of cytokeratins by okadaic acid class tumor promoters in primary human keratinocytes.冈田酸类肿瘤启动子在原代人角质形成细胞中对角蛋白的过度磷酸化作用。
Cancer Res. 1993 Mar 1;53(5):992-6.
4
Inhibition of histone H1 kinase expression, retinoblastoma protein phosphorylation, and cell proliferation by the phosphatase inhibitor okadaic acid.磷酸酶抑制剂冈田酸对组蛋白H1激酶表达、视网膜母细胞瘤蛋白磷酸化及细胞增殖的抑制作用
Oncogene. 1993 Feb;8(2):433-41.
5
Inhibition of PP2A, but not PP5, mediates p53 activation by low levels of okadaic acid in rat liver epithelial cells.在大鼠肝上皮细胞中,抑制蛋白磷酸酶2A(PP2A)而非蛋白磷酸酶5(PP5)介导了低水平冈田酸对p53的激活作用。
J Cell Biochem. 2006 Sep 1;99(1):241-55. doi: 10.1002/jcb.20919.
6
Effects of the tumour promoter okadaic acid on intracellular protein phosphorylation and metabolism.肿瘤启动子冈田酸对细胞内蛋白质磷酸化和代谢的影响。
Nature. 1989 Jan 5;337(6202):78-81. doi: 10.1038/337078a0.
7
Complex regulation of the DNA-binding activity of p53 by phosphorylation: differential effects of individual phosphorylation sites on the interaction with different binding motifs.
Oncogene. 1996 Mar 7;12(5):953-61.
8
The effect of phosphorylation on the antigenic reactivity of p53 in cultured human keratinocytes.磷酸化对培养的人角质形成细胞中p53抗原反应性的影响。
Biochem Biophys Res Commun. 1995 Sep 14;214(2):744-53. doi: 10.1006/bbrc.1995.2348.
9
Reversible hyperphosphorylation and reorganization of vimentin intermediate filaments by okadaic acid in 9L rat brain tumor cells.冈田酸诱导9L大鼠脑肿瘤细胞中波形蛋白中间丝的可逆性过度磷酸化和重组
J Cell Biochem. 1992 Aug;49(4):378-93. doi: 10.1002/jcb.240490408.
10
Absence of synergistic effects on tumor promotion in CD-1 mouse skin by simultaneous applications of two different types of tumor promoters, okadaic acid and teleocidin.
Cancer Res. 1993 Mar 1;53(5):1012-6.

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A specific PP2A regulatory subunit, B56gamma, mediates DNA damage-induced dephosphorylation of p53 at Thr55.一种特定的蛋白磷酸酶2A(PP2A)调节亚基B56γ介导DNA损伤诱导的p53在苏氨酸55位点的去磷酸化。
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Protein phosphatase 2A: a highly regulated family of serine/threonine phosphatases implicated in cell growth and signalling.蛋白磷酸酶2A:一个与细胞生长和信号传导相关的丝氨酸/苏氨酸磷酸酶的高度调控家族。
Biochem J. 2001 Feb 1;353(Pt 3):417-39. doi: 10.1042/0264-6021:3530417.
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Okadaic acid suppresses TPA-induced differentiation by stimulating G1/S transition in human myeloblastic leukaemia ML-1 cells.冈田酸通过刺激人髓性白血病ML-1细胞中的G1/S期转换来抑制佛波酯诱导的分化。
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Carcinogenic potential of benzene and toluene when evaluated using cyclin-dependent kinase activation and p53-DNA binding.使用细胞周期蛋白依赖性激酶激活和p53-DNA结合评估苯和甲苯的致癌潜力。
Environ Health Perspect. 1996 Dec;104 Suppl 6(Suppl 6):1289-92. doi: 10.1289/ehp.961041289.
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Hyperphosphorylation of retinoblastoma protein and stimulation of growth by okadaic acid in human pancreatic cancer.人胰腺癌中视网膜母细胞瘤蛋白的过度磷酸化及冈田酸对生长的刺激作用
Dig Dis Sci. 1996 Oct;41(10):1975-80. doi: 10.1007/BF02093599.