The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Structural and functional analysis of an enhancer GPEI having a phorbol 12-O-tetradecanoate 13-acetate responsive element-like sequence found in the rat glutathione transferase P gene
Open accessAbstract
We have recently identified a typical enhancer, termed GPEI, located about 2.5 kilobases upstream from the transcription initiation site of the rat glutathione transferase P gene. Analyses of 5' and 3' deletion mutants revealed that the cis-acting sequence of GPEI contained the phorbol 12-O-tetradecanoate 13-acetate responsive element (TRE)-like sequence in it. For the maximal activity, however, GPEI required an adjacent upstream sequence of about 19 base pairs in addition to the TRE-like sequence. With the DNA binding gel-shift assay, we could detect protein(s) that specifically binds to the TRE-like sequence of GPEI fragment, which was possibly c-jun.c-fos complex or a similar protein complex. The sequence immediately upstream of the TRE-like sequence did not have any activity by itself, but augmented the latter activity by about 5-fold.
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“excess “labile iron” is potentially detrimental to the cell or organism or both because of its propensity to participate in oxidation–reduction reactions that generate harmful free radicals”
From Intracellular iron transport and storage: from molecular mechanisms to health implications (2008) · cites this paper as [229]
In the citing paper
“when ferrous iron interacts with H2O2, it undergoes the Fenton reaction (229). The Fenton reaction produces ferric iron, −OH, and the hydroxyl radical. It may also result in the peroxidation of adjacent lipids and lead to oxidative damage of DNA and other macromolecules.”
From Intracellular iron transport and storage: from molecular mechanisms to health implications (2008) · cites this paper as [229]
In the citing paper
“Resulting iron overload leads to a number of different pathologies, including structural damage from physical iron accumulation and oxidative damage to tissue, protein, lipids, and DNA resulting from iron-induced oxidative stress (229).”
From Intracellular iron transport and storage: from molecular mechanisms to health implications (2008) · cites this paper as [229]
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Metadata
- Authors
- Okuda, A., Imagawa, M., Maeda, Y., Sakai, M., & Muramatsu, M.
- Affiliations
- Hokkaido University (JP)
- ORCID
- Okuda, A
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 1989-10
- Volume
- 264
- Issue
- 28
- Pages
- 16919-16926
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1581676497
- Cited by
- 151
- References
- 31
- Citations by year
- 2022: 1 · 2021: 1 · 2018: 1 · 2016: 2 · 2015: 2 · 2014: 1 · 2013: 2 · 2012: 2
- FWCI
- 2.70
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Glutathione Transferases and Polymorphisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
- Keywords
- cis-acting enhancer, transcriptional regulation, protein-DNA interactions, rat gene
- MeSH terms
- Animals, Base Sequence, Chromosome Deletion, Enhancer Elements, Genetic, Genes, Glutathione Transferase, Molecular Sequence Data, Mutation, Plasmids, Regulatory Sequences, Nucleic Acid, Tetradecanoylphorbol Acetate, Transcription, Genetic, Restriction Mapping, Oligonucleotide Probes, Rats
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