细胞质超氧化物歧化酶缺陷小鼠的脾脏和肾脏中假定原癌基因 Pir 的表达显著上调。
Putative proto-oncogene Pir expression is significantly up-regulated in the spleen and kidney of cytosolic superoxide dismutase-deficient mice.
机构信息
Centre for Radiobiology and Biological Dosimetry, Warsaw, Poland.
出版信息
Redox Rep. 2011;16(3):129-33. doi: 10.1179/1351000211Y.0000000002.
Abstract
Iron binding protein pirin was isolated as an interactor of the NFIX transcription factor but it can also form complexes with Bcl3 and NF-κB1(p50). Alterations of pirin expression were observed in various tumors and after exposure to pro-carcinogenic oxidative stressors. The aim of the present work was to study the level of pirin transcription in an in vivo model of oxidative stress, namely, in Sod1-deficient mice. We have found that Sod1(-/-) mice have a significantly elevated level of Pir mRNA in the spleen and kidney but not in the liver, heart, or/and brain. We have also shown that similarly to its human ortholog, the mouse Pir gene transcription level varies significantly between organs. The highest expression was found in the liver and the lowest in the spleen and kidney. Based on literature data, we propose the involvement of Nrf2, AP-1, and NF-κB transcription factors in Pir up-regulation in Sod1(-/-) mice.
摘要
铁结合蛋白吡林被分离出来作为 NFIX 转录因子的相互作用物，但它也可以与 Bcl3 和 NF-κB1(p50)形成复合物。在各种肿瘤和暴露于致癌性氧化应激物后，观察到吡林表达的改变。本研究的目的是研究氧化应激体内模型中吡林转录的水平，即 Sod1 缺陷型小鼠。我们发现，Sod1(-/-)小鼠的脾脏和肾脏中 Pir mRNA 的水平显著升高，但肝脏、心脏和/或大脑中没有升高。我们还表明，与人类同源物一样，小鼠 Pir 基因的转录水平在器官之间差异很大。在肝脏中的表达最高，在脾脏和肾脏中的表达最低。根据文献数据，我们提出 Nrf2、AP-1 和 NF-κB 转录因子参与了 Sod1(-/-)小鼠中 Pir 的上调。
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