ArticleMolecular and cellular biology2005
Endoplasmic reticulum stress accelerates p53 degradation by the cooperative actions of Hdm2 and glycogen synthase kinase 3beta.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 101 citations in OpenAlex.
- The Role of Endoplasmic Reticulum Stress Response in Liver Regeneration.Seminars in liver disease · 2023Review
- Article
- Gossypol Induces Apoptosis of Human Pancreatic Cancer Cells via CHOP/Endoplasmic Reticulum Stress Signaling Pathway.Journal of microbiology and biotechnology · 2022Article
- Glycogen synthesis and beyond, a comprehensive review of GSK3 as a key regulator of metabolic pathways and a therapeutic target for treating metabolic diseases.Medicinal research reviews · 2022Review
- Review
- The Cross Talk Between p53 and mTOR Pathways in Response to Physiological and Genotoxic Stresses.Frontiers in cell and developmental biology · 2021Review
- Network-based analysis implies critical roles of microRNAs in the long-term cellular responses to gold nanoparticles.Nanoscale · 2020Article
- Review
- Cytoplasmic Restriction of Mutated SOD1 Impairs the DNA Repair Process in Spinal Cord Neurons.Cells · 2019Article
- Autophagy protects HUVECs against ER stress-mediated apoptosis under simulated microgravity.Apoptosis : an international journal on programmed cell death · 2019Article
- Unfolded Protein Response supports endothelial barrier function.Biochimie · 2019Review
- Bi-modal reprogramming of cell cycle by MiRNA-4673 amplifies human neurogenic capacity.Cell cycle (Georgetown, Tex.) · 2019Article
- Peptidylarginine deiminase 4 overexpression resensitizes MCF-7/ADR breast cancer cells to adriamycin via GSK3β/p53 activation.Cancer management and research · 2019Article
- Length and secondary structure of the 5' non-coding regions of mouse p53 mRNA transcripts - mouse as a model organism for p53 gene expression studies.RNA biology · 2019Article
- Clinorotation-induced autophagy via HDM2-p53-mTOR pathway enhances cell migration in vascular endothelial cells.Cell death & disease · 2018Article
- PERK Integrates Oncogenic Signaling and Cell Survival During Cancer Development.Journal of cellular physiology · 2016Review
- Differential Proteomic Analysis of Human Placenta-Derived Mesenchymal Stem Cells Cultured on Normal Tissue Culture Surface and Hyaluronan-Coated Surface.Stem cells international · 2016Article
- Reduction of p53 by knockdown of theCellular and molecular gastroenterology and hepatology · 2016Article
- Alterations in Mitochondrial and Endoplasmic Reticulum Signaling by p53 Mutants.Frontiers in oncology · 2016Review
- Combined regulation of mTORC1 and lysosomal acidification by GSK-3 suppresses autophagy and contributes to cancer cell growth.Oncogene · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inactivation of the tumor suppressor p53 by degradation is a mechanism utilized by cells to adapt to endoplasmic reticulum (ER) stress. However, the mechanisms of p53 destabilization by ER stress are not known. We demonstrate here that the E3 ubiquitin-ligase Hdm2 is essential for the nucleocytoplasmic transport and proteasome-dependent degradation of p53 in ER-stressed cells. We also demonstrate that p53 phosphorylation at S315 and S376 is required for its nuclear export and degradation by Hdm2 without interfering with the ubiquitylation process. Furthermore, we show that p53 destabilization in unstressed cells utilizes the cooperative action of Hdm2 and glycogen synthase kinase 3beta, a process that is enhanced in cells exposed to ER stress. In contrast to other stress pathways that stabilize p53, our findings further substantiate a negative role of ER stress in p53 activation with important implications for the function of the tumor suppressor in cells with a dysfunctional ER.
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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.