ArticleFree radical biology & medicine2010
Disruption of Sag/Rbx2/Roc2 induces radiosensitization by increasing ROS levels and blocking NF-kappaB activation in mouse embryonic stem cells.
Article in Free radical biology & medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The trial behind it
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
- An integrative pan-cancer analysis revealing the difference in small ring finger family of SCF E3 ubiquitin ligases.Frontiers in immunology · 2022Article
- Neddylation regulation of mitochondrial structure and functions.Cell & bioscience · 2021Review
- Transgenic expression of Sag/Rbx2 E3 causes early stage tumor promotion, late stage cytogenesis and acinar loss in the Kras-PDAC model.Neoplasia (New York, N.Y.) · 2020Article
- Targeting Cullin-RING E3 Ligases for Radiosensitization: From NEDDylation Inhibition to PROTACs.Frontiers in oncology · 2020Review
- The role of SCF ubiquitin-ligase complex at the beginning of life.Reproductive biology and endocrinology : RB&E · 2019Review
- SAG/RBX2 E3 Ubiquitin Ligase Differentially Regulates Inflammatory Responses of Myeloid Cell Subsets.Frontiers in immunology · 2018Article
- Inhibition of Neddylation Modification Sensitizes Pancreatic Cancer Cells to Gemcitabine.Neoplasia (New York, N.Y.) · 2017Article
- RNF7 knockdown inhibits prostate cancer tumorigenesis by inactivation of ERK1/2 pathway.Scientific reports · 2017Article
- Depletion of SAG/RBX2 E3 ubiquitin ligase suppresses prostate tumorigenesis via inactivation of the PI3K/AKT/mTOR axis.Molecular cancer · 2016Article
- SAG/RBX2 E3 ligase complexes with UBCH10 and UBE2S E2s to ubiquitylate β-TrCP1 via K11-linkage for degradation.Scientific reports · 2016Article
- SAG/Rbx2-Dependent Neddylation Regulates T-Cell Responses.The American journal of pathology · 2016Article
- Erbin is a novel substrate of the Sag-βTrCP E3 ligase that regulates KrasG12D-induced skin tumorigenesis.The Journal of cell biology · 2015Article
- Inactivation of Sag/Rbx2/Roc2 e3 ubiquitin ligase triggers senescence and inhibits kras-induced immortalization.Neoplasia (New York, N.Y.) · 2015Article
- Endothelial deletion of Sag/Rbx2/Roc2 E3 ubiquitin ligase causes embryonic lethality and blocks tumor angiogenesis.Oncogene · 2014Article
- SAG/RBX2 is a novel substrate of NEDD4-1 E3 ubiquitin ligase and mediates NEDD4-1 induced chemosensitization.Oncotarget · 2014Article
- Ubiquitination involved enzymes and cancer.Medical oncology (Northwood, London, England) · 2014Review
- Tat-fused recombinant human SAG prevents dopaminergic neurodegeneration in a MPTP-induced Parkinson's disease model.Molecules and cells · 2014Article
- Inactivation of SAG/RBX2 E3 ubiquitin ligase suppresses KrasG12D-driven lung tumorigenesis.The Journal of clinical investigation · 2014Article
- Genetically engineered mouse models for functional studies of SKP1-CUL1-F-box-protein (SCF) E3 ubiquitin ligases.Cell research · 2013Review
- Role of SKP1-CUL1-F-box-protein (SCF) E3 ubiquitin ligases in skin cancer.Journal of genetics and genomics = Yi chuan xue bao · 2013Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
SAG (sensitive to apoptosis gene; also known as RBX2 or ROC2) is a dual-function protein with antioxidant activity when acting alone or E3 ligase activity when complexed with other components of SCF (Skp1, cullins, F-box proteins) E3 ubiquitin ligases. SAG acts as a survival protein to inhibit apoptosis induced by a variety of stresses. Our recent work showed that SAG siRNA silencing sensitized cancer cells to radiation but the mechanism responsible remains elusive. Here we report that complete elimination of Sag expression via a gene-trapping strategy significantly sensitized mouse embryonic stem (ES) cells to radiation, with a sensitizing enhancement rate of 1.5-1.6. Radiosensitization was associated with increased steady-state levels of intracellular ROS (including superoxide) 24h after irradiation as well as enhancement of radiation-induced apoptosis. Furthermore, Sag elimination abrogated IkappaBalpha degradation leading to inhibition of NF-kappaB activation. Further detailed analysis revealed that IkappaBalpha is a direct substrate of SAG-SCF(beta-TrCP) E3 ubiquitin ligase. Taken together, these results support the hypothesis that Sag elimination via gene disruption sensitizes ES cells to radiation-induced cell killing by mechanisms that involve increased steady-state levels of ROS and decreased activation of NF-kappaB.
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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.