ArticleJournal of signal transduction2012
Oxidative Stress Induced by MnSOD-p53 Interaction: Pro- or Anti-Tumorigenic?
Article in Journal of signal transduction, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 36 citations in OpenAlex.
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- Synthesis and SAR Analysis of Novel 4-Hydroxytamoxifen Analogues Based on Their Cytotoxic Activity and Electron-Donor Character.Molecules (Basel, Switzerland) · 2022Article
- Dexmedetomidine reduces enteric glial cell injury induced by intestinal ischaemia-reperfusion injury through mitochondrial localization of TERT.Journal of cellular and molecular medicine · 2022Article
- Clinical and Apoptotic Factors Defining and Predicting Steroid Resistance in Nephrotic Syndrome in Children.Global pediatric health · 2022Article
- BBS7-SHH Signaling Activity Regulates Primary Cilia for Periodontal Homeostasis.Frontiers in cell and developmental biology · 2021Article
- Induced pluripotent stem cells of patients with Tetralogy of Fallot reveal transcriptional alterations in cardiomyocyte differentiation.Scientific reports · 2020Article
- Cristacarpin promotes ER stress-mediated ROS generation leading to premature senescence by activation of p21(waf-1).Age (Dordrecht, Netherlands) · 2016Article
- Diagnostic and prognostic value of serum thioredoxin and DJ-1 in non-small cell lung carcinoma patients.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Reactivation of p53 by a Cytoskeletal Sensor to Control the Balance Between DNA Damage and Tumor Dissemination.Journal of the National Cancer Institute · 2016Article
- Preparation of a conjugation-ready thiol responsive molecular switch.Tetrahedron letters · 2015Article
- Article
- Does short-term exposure to elevated levels of natural gamma radiation in Ramsar cause oxidative stress?International journal of applied & basic medical research · 2014Article
- Induction of apoptosis through oxidative stress-related pathways in MCF-7, human breast cancer cells, by ethyl acetate extract of Dillenia suffruticosa.BMC complementary and alternative medicine · 2014Article
- Cross Talk between Two Antioxidant Systems, Thioredoxin and DJ-1: Consequences for Cancer.Oncoscience · 2014Review
- Expression of CYP1A1, CYP1B1 and MnSOD in a panel of human cancer cell lines.Molecular and cellular biochemistry · 2013Article
- Redox regulation of T-cell function: from molecular mechanisms to significance in human health and disease.Antioxidants & redox signaling · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The formation of reactive oxygen species (ROS) is a result of incomplete reduction of molecular oxygen during cellular metabolism. Although ROS has been shown to act as signaling molecules, it is known that these reactive molecules can act as prooxidants causing damage to DNA, proteins, and lipids, which over time can lead to disease propagation and ultimately cell death. Thus, restoring the protective antioxidant capacity of the cell has become an important target in therapeutic intervention. In addition, a clearer understanding of the disease stage and molecular events that contribute to ROS generation during tumor promotion can lead to novel approaches to enhance target specificity in cancer progression. This paper will focus on not only the traditional routes of ROS generation, but also on new mechanisms via the tumor suppressor p53 and the interaction between p53 and MnSOD, the primary antioxidant enzyme in mitochondria. In addition, the potential consequences of the p53-MnSOD interaction have also been discussed. Lastly, we have highlighted clinical implications of targeting the p53-MnSOD interaction and discussed recent therapeutic mechanisms utilized to modulate both p53 and MnSOD as a method of tumor suppression.
Identifiers
What OpenQuestion holds
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.