ArticleCell death & disease2013
GADD45β mediates p53 protein degradation via Src/PP2A/MDM2 pathway upon arsenite treatment.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- GADD45β inhibits hepatic lipogenesis through the AMPK/SREBP1 pathway via reducing the ubiquitination-mediated degradation of SIRT1.Scientific reports · 2025Article
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- CAR requires Gadd45β to promote phenobarbital-induced mouse liver tumors in early stage.Frontiers in oncology · 2023Article
- Role of Non-Coding RNA in Neurological Complications Associated With Enterovirus 71.Frontiers in cellular and infection microbiology · 2022Review
- GADD45B Transcript Is a Prognostic Marker in Papillary Thyroid Carcinoma Patients Treated With Total Thyroidectomy and Radioiodine Therapy.Frontiers in endocrinology · 2020Article
- Cytokinesis Failure Leading to Chromosome Instability in v-Src-Induced Oncogenesis.International journal of molecular sciences · 2017Review
- FMRP-dependent Mdm2 dephosphorylation is required for MEF2-induced synapse elimination.Human molecular genetics · 2017Article
- Review
- Andrographolide induces vascular smooth muscle cell apoptosis through a SHP-1-PP2A-p38MAPK-p53 cascade.Scientific reports · 2014Article
- Hydrogen peroxide/ATR-Chk2 activation mediates p53 protein stabilization and anti-cancer activity of cheliensisin A in human cancer cells.Oncotarget · 2014Article
- p63 threonine phosphorylation signals the interaction with the WW domain of the E3 ligase Itch.Cell cycle (Georgetown, Tex.) · 2014Article
- Novel predication of protein biomarkers in interferon-gamma-stimulated breast cancer cells.International journal of health sciencesArticle
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Growth arrest and DNA-damage-inducible, beta (GADD45β) has been reported to inhibit apoptosis via attenuating c-Jun N-terminal kinase (JNK) activation. We demonstrated here that GADD45β mediated its anti-apoptotic effect via promoting p53 protein degradation following arsenite treatment. We found that p53 protein expression was upregulated in GADD45β-/- cells upon arsenite exposure as compared with those in GADD45β+/+ cells. Further studies showed that GADD45β attenuated p53 protein expression through Src/protein phosphatase 2A/murine double minute 2-dependent p53 protein-degradation pathway. Moreover, we identified that GADD45β-mediated p53 protein degradation was crucial for its anti-apoptotic effect due to arsenite exposure, whereas increased JNK activation was not involved in the increased cell apoptotic response in GADD45β-/- cells under same experimental conditions. Collectively, our results demonstrate a novel molecular mechanism responsible for GADD45β protection of arsenite-exposed cells from cell death, which provides insight into our understanding of GADD45β function and a unique compound arsenite as both a cancer therapeutic reagent and an environmental carcinogen. Those novel findings may also enable us to design more effective strategies for utilization of arsenite for the treatment of cancers.
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