ArticleRedox report : communications in free radical research2011
Putative proto-oncogene Pir expression is significantly up-regulated in the spleen and kidney of cytosolic superoxide dismutase-deficient mice.
Article in Redox report : communications in free radical research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Role of the redox state of the Pirin-bound cofactor on interaction with the master regulators of inflammation and other pathways.PloS one · 2023Article
- Disparities in COVID-19 severities and casualties across ethnic groups around the globe and patterns of ACE2 and PIR variants.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2021Article
- Review
- Article
- Effect of full flavor and denicotinized cigarettes exposure on the brain microvascular endothelium: a microarray-based gene expression study using a human immortalized BBB endothelial cell line.BMC neuroscience · 2015Article
- Basal PIR expression in HeLa cells is driven by NRF2 via evolutionary conserved antioxidant response element.Molecular and cellular biochemistry · 2014Article
- Article
- Pirin is an iron-dependent redox regulator of NF-κB.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Curcumin protects human keratinocytes against inorganic arsenite-induced acute cytotoxicity through an NRF2-dependent mechanism.Oxidative medicine and cellular longevity · 2013Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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