ArticleMolecular endocrinology (Baltimore, Md.)2009
Apurinic/apyrimidinic endonuclease 1 alters estrogen receptor activity and estrogen-responsive gene expression.
Article in Molecular endocrinology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Nanoscale Interaction of Endonuclease APE1 with DNA.International journal of molecular sciences · 2024Article
- The human AP-endonuclease 1 (APE1) is a DNA G-quadruplex structure binding protein and regulates KRAS expression in pancreatic ductal adenocarcinoma cells.Nucleic acids research · 2022Article
- Beyond the Double-Strand Breaks: The Role of DNA Repair Proteins in Cancer Stem-Cell Regulation.Cancers · 2021Review
- EtMIC3 and its receptors BAG1 and ENDOUL are essential for site-specific invasion of Eimeria tenella in chickens.Veterinary research · 2020Article
- 17β-Estradiol alters oxidative damage and oxidative stress response protein expression in the mouse mammary gland.Molecular and cellular endocrinology · 2016Article
- Regulation of limited N-terminal proteolysis of APE1 in tumor via acetylation and its role in cell proliferation.Oncotarget · 2016Article
- Estrogen Receptor Expression Is Associated with DNA Repair Capacity in Breast Cancer.PloS one · 2016Article
- Expression of estrogen receptor α in the mouse cerebral cortex.Molecular and cellular endocrinology · 2015Article
- Suppression of choroidal neovascularization through inhibition of APE1/Ref-1 redox activity.Investigative ophthalmology & visual science · 2014Article
- Modulation of nuclear receptor function by cellular redox poise.Journal of inorganic biochemistry · 2014Review
- 17β-Estradiol alters oxidative stress response protein expression and oxidative damage in the uterus.Molecular and cellular endocrinology · 2014Article
- Estrogen signaling and the DNA damage response in hormone dependent breast cancers.Frontiers in oncology · 2014Review
- Prognostic value of human apurinic/apyrimidinic endonuclease 1 (APE1) expression in breast cancer.PloS one · 2014Article
- Protein-disulfide isomerase regulates the thyroid hormone receptor-mediated gene expression via redox factor-1 through thiol reduction-oxidation.The Journal of biological chemistry · 2013Article
- APE1/Ref-1 role in redox signaling: translational applications of targeting the redox function of the DNA repair/redox protein APE1/Ref-1.Current molecular pharmacology · 2012Review
- Apurinic/Apyrimidinic endonuclease 1 regulates inflammatory response in macrophages.Anticancer research · 2011Article
- Article
- Understanding different functions of mammalian AP endonuclease (APE1) as a promising tool for cancer treatment.Cellular and molecular life sciences : CMLS · 2010Review
- Immunohistochemical analysis of oxidative stress and DNA repair proteins in normal mammary and breast cancer tissues.BMC cancer · 2010Article
- Thioredoxin and thioredoxin reductase influence estrogen receptor alpha-mediated gene expression in human breast cancer cells.Journal of molecular endocrinology · 2009Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Apurinic/apyrimidinic endonuclease 1 or redox factor-1 (Ape1/Ref-1) is a pleiotropic cellular protein involved in DNA repair and, through its redox activity, enhances the binding of a select group of transcription factors to their cognate recognition sequences in DNA. Thus, we were intrigued when we identified Ape1/Ref-1 and a number of DNA repair and oxidative stress proteins in a complex associated with the DNA-bound estrogen receptor alpha (ERalpha). Because Ape1/Ref-1 interacts with a number of transcription factors and influences their activity, we determined whether it might also influence ERalpha activity. We found that endogenously expressed Ape1/Ref-1 and ERalpha from MCF-7 human breast cancer cells interact and that Ape1/Ref-1 enhances the interaction of ERalpha with estrogen-response elements (EREs) in DNA. More importantly, Ape1/Ref-1 alters expression of the endogenous, estrogen-responsive progesterone receptor and pS2 genes in MCF-7 cells and associates with ERE-containing regions of these genes in native chromatin. Interestingly, knocking down Ape1/Ref-1 expression or inhibiting its redox activity with the small molecule inhibitor E3330 enhances estrogen responsiveness of the progesterone receptor and pS2 genes but does not alter the expression of the constitutively active 36B4 gene. Additionally, the reduced form of Ape1/Ref-1 increases and E3330 limits ERalpha-ERE complex formation in vitro and in native chromatin. Our studies demonstrate that Ape1/Ref-1 mediates its gene-specific effects, in part, by associating with endogenous, estrogen-responsive genes and that the redox activity of Ape1/Ref-1 is instrumental in altering estrogen-responsive gene expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.