NDLI: Putative proto-oncogene Pir expression is significantly up-regulated in the spleen and kidney of cytosolic superoxide dismutase-deficient mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Brzóska, Kamil Stepkowski, Tomasz M. Kruszewski, Marcin
Description	Country affiliation: Poland Author Affiliation: Brzóska K ( Centre for Radiobiology and Biological Dosimetry, Warsaw, Poland.)
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.
File Format	HTM / HTML
ISSN	13510002
e-ISSN	17432928
Journal	Redox Report
Issue Number	3
Volume Number	16
Language	English
Publisher	Taylor & Francis
Publisher Date	2011-01-01
Publisher Place	Great Britain (UK)
Access Restriction	Subscribed
Subject Keyword	Discipline Metabolism Discipline Biochemistry Carrier Proteins Metabolism Kidney Nuclear Proteins Spleen Superoxide Dismutase Deficiency Animals Gene Expression Regulation Genotype Liver Mice Mice, 129 Strain Mice, Knockout Models, Animal Nf-kappa B P50 Subunit Genetics Nfi Transcription Factors Oxidative Stress Promoter Regions, Genetic Rna, Messenger Transcription Factor Ap-1 Transcription, Genetic Up-regulation Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Biochemistry (medical) Cell Biology Physiology Biochemistry Clinical Biochemistry

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