ArticleAntioxidants & redox signaling2010
SECIS-binding protein 2 promotes cell survival by protecting against oxidative stress.
Article in Antioxidants & redox signaling, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Culture-dependent baseline states and drug response programs in myxofibrosarcoma models across 2D and 3D systems.Human cell · 2026Article
- Article
- Nrf2 in Cancer, Detoxifying Enzymes and Cell Death Programs.Antioxidants (Basel, Switzerland) · 2021Review
- Article
- Selenium and hydrogen selenide: essential micronutrient and the fourth gasotransmitter?Intensive care medicine experimental · 2019Review
- The hsa-miR-181a-5p reduces oxidation resistance by controlling SECISBP2 in osteoarthritis.BMC musculoskeletal disorders · 2018Article
- Amblyomma maculatum SECIS binding protein 2 and putative selenoprotein P are indispensable for pathogen replication and tick fecundity.Insect biochemistry and molecular biology · 2017Article
- Diverse role of survival motor neuron protein.Biochimica et biophysica acta. Gene regulatory mechanisms · 2017Review
- Oxidative Stress Triggers Body-Wide Skipping of Multiple Exons of the Spinal Muscular Atrophy Gene.PloS one · 2016Article
- Selective up-regulation of human selenoproteins in response to oxidative stress.The Journal of biological chemistry · 2014Article
- Characterization of the UGA-recoding and SECIS-binding activities of SECIS-binding protein 2.RNA biology · 2014Article
- Comparative protein interactomics of neuroglobin and myoglobin.Journal of neurochemistry · 2012Article
- Selenium compounds, apoptosis and other types of cell death: an overview for cancer therapy.International journal of molecular sciences · 2012Review
- Selenium, selenoproteins and the thyroid gland: interactions in health and disease.Nature reviews. Endocrinology · 2011Review
- Mutations in the selenocysteine insertion sequence-binding protein 2 gene lead to a multisystem selenoprotein deficiency disorder in humans.The Journal of clinical investigation · 2010Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Reactive oxygen species (ROS) are a primary cause of cellular damage that leads to cell death. In cells, protection from ROS-induced damage and maintenance of the redox balance is mediated to a large extent by selenoproteins, a distinct family of proteins that contain selenium in form of selenocysteine (Sec) within their active site. Incorporation of Sec requires the Sec-insertion sequence element (SECIS) in the 3'-untranslated region of selenoproteins mRNAs and the SECIS-binding protein 2 (SBP2). Previous studies have shown that SBP2 is required for the Sec-incorporation mechanism; however, additional roles of SBP2 in the cell have remained undefined. We herein show that depletion of SBP2 by using antisense oligonucleotides (ASOs) causes oxidative stress and induction of caspase- and cytochrome c-dependent apoptosis. Cells depleted of SBP2 have increased levels of ROS, which lead to cellular stress manifested as 8-oxo-7,8-dihydroguanine (8-oxo-dG) DNA lesions, stress granules, and lipid peroxidation. Small-molecule antioxidants N-acetylcysteine, glutathione, and alpha-tocopherol only marginally reduced ROS and were unable to rescue cells fully from apoptosis, indicating that apoptosis might be directly mediated by selenoproteins. Our results demonstrate that SBP2 is required for protection against ROS-induced cellular damage and cell survival.
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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.