ArticleThe Journal of biological chemistry2011
14-3-3Gamma inhibition of MDMX-mediated p21 turnover independent of p53.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Reduced structural rigidity of MDMX protein enhances binding to TP53 mRNA.Bioscience reports · 2025Article
- Article
- Evolution of the 14-3-3 gene family in monocotyledons and dicotyledons and validation of MdGRF13 function in transgenic Arabidopsis thaliana.Plant cell reports · 2023Article
- Exploring the Therapeutic Potential ofInternational journal of molecular sciences · 2023Article
- Emerging roles of 14-3-3γ in the brain disorder.BMB reports · 2020Review
- Article
- Mdm2 and MdmX RING Domains Play Distinct Roles in the Regulation of p53 Responses: A Comparative Study of Mdm2 and MdmX RING Domains in U2OS Cells.International journal of molecular sciences · 2020Article
- Retrospective Proteomic Screening of 100 Breast Cancer Tissues.Proteomes · 2017Article
- The p53 inhibitor Mdm4 cooperates with multiple genetic lesions in tumourigenesis.The Journal of pathology · 2017Article
- Phosphorylation-dependent degradation of MEF2C contributes to regulate G2/M transition.Cell cycle (Georgetown, Tex.) · 2015Article
- Plant 14-3-3 proteins as spiders in a web of phosphorylation.Protoplasma · 2013Review
- Delayed cell cycle progression in selenoprotein W-depleted cells is regulated by a mitogen-activated protein kinase kinase 4-p38/c-Jun NH2-terminal kinase-p53 pathway.The Journal of biological chemistry · 2012Article
- Hormone-induced 14-3-3γ adaptor protein regulates steroidogenic acute regulatory protein activity and steroid biosynthesis in MA-10 Leydig cells.The Journal of biological chemistry · 2012Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The stability of p21, a cyclin-dependent kinase inhibitor, is highly regulated by various protein molecules through the cell cycle and in response to extracellular signals. One of the p21 regulators is MDMX, which can directly bind to p21 and mediate its proteasomal degradation in an ubiquitination-independent fashion. The fact that 14-3-3γ binds to the MDMX domain adjacent to p21 binding suggests that this 14-3-3γ may affect MDMX-mediated p21 proteasomal turnover. Indeed, we found that overexpression of 14-3-3γ increased the level of both endogenous and exogenous p21 in p53-null cells by extending its half-life, leading to p21-dependent G1 arrest. Also, 14-3-3γ excluded p21 from binding to MDMX in a dose-dependent manner as determined by co-immunroprecipitation in vitro using purified proteins and in cells. In response to DNA damage, the level of the 14-3-3γ-MDMX complex increased whereas that of the MDMX-p21 complex declined as detected by co-immunoprecipitation assays, leading to the induction of p21 in p53-null cells. Knockdown of 14-3-3γ inversely alleviated the induction of p21 levels by DNA damage. Hence, our study as presented here unravels a new role for 14-3-3γ in protecting p21 from MDMX-mediated proteasomal turnover, which may partially account for DNA damage-induced elevation of p21 levels independent of p53.
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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.