ArticlePloS one2015
Alpha-enolase is upregulated on the cell surface and responds to plasminogen activation in mice expressing a ∆133p53α mimic.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Δ133p53 isoform enhances TLR4 function to promote tumor growth.Carcinogenesis · 2025Article
- The 419th Aspartic Acid of Neural Membrane Protein Enolase 2 Is a Key Residue Involved in the Axonal Growth of Motor Neurons Mediated by Interaction between Enolase 2 Receptor and Extracellular Pgk1 Ligand.International journal of molecular sciences · 2024Article
- Canonical and non-canonical functions of p53 isoforms: potentiating the complexity of tumor development and therapy resistance.Cell death & disease · 2024Review
- Regulation of enolase activation to promote neural protection and regeneration in spinal cord injury.Neural regeneration research · 2023Review
- Increased Expression of the Δ133p53β Isoform Enhances Brain Metastasis.International journal of molecular sciences · 2023Article
- Relationships Between Plasminogen-Binding M-Protein and Surface Enolase for Human Plasminogen Acquisition and Activation inFrontiers in microbiology · 2022Article
- The Δ133p53 Isoforms, Tuners of the p53 Pathway.Cancers · 2020Review
- Silencing of Testin expression is a frequent event in spontaneous lymphomas from Trp53-mutant mice.Scientific reports · 2020Article
- Enolase 1 Correlated With Cancer Progression and Immune-Infiltrating in Multiple Cancer Types: A Pan-Cancer Analysis.Frontiers in oncology · 2020Article
- The Emerging Landscape of p53 Isoforms in Physiology, Cancer and Degenerative Diseases.International journal of molecular sciences · 2019Review
- The Δ133p53β isoform promotes an immunosuppressive environment leading to aggressive prostate cancer.Cell death & disease · 2019Article
- A mouse model of the Δ133p53 isoform: roles in cancer progression and inflammation.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Elevation of the TP53 isoform Δ133p53β in glioblastomas: an alternative to mutant p53 in promoting tumor development.The Journal of pathology · 2018Article
- New Insights into the Role of Neuron-Specific Enolase in Neuro-Inflammation, Neurodegeneration, and Neuroprotection.Brain sciences · 2018Review
- Targeting Enolase in Reducing Secondary Damage in Acute Spinal Cord Injury in Rats.Neurochemical research · 2017Article
- p53 Isoforms: Key Regulators of the Cell Fate Decision.Cold Spring Harbor perspectives in medicine · 2016Review
- Neuron specific enolase: a promising therapeutic target in acute spinal cord injury.Metabolic brain disease · 2016Review
- Progress in the biological function of alpha-enolase.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2016Review
- Δ122p53, a mouse model of Δ133p53α, enhances the tumor-suppressor activities of an attenuated p53 mutant.Cell death & disease · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p53 protein is a master regulator of the stress response. It acts as a tumor suppressor by inducing transcriptional activation of p53 target genes, with roles in apoptosis, cell cycle arrest and metabolism. The discovery of at least 12 isoforms of p53, some of which have tumor-promoting properties, has opened new avenues of research. Our previous work studied tumor phenotypes in four mouse models with different p53 backgrounds: wild-type p53, p53 null, mutant p53 lacking the proline domain (mΔpro), and a mimic for the human Δ133p53α p53 isoform (Δ122p53). To identify the major proteins affected by p53 function early in the response to DNA damage, the current study investigated the entire proteome of bone marrow, thymus, and lung in the four p53 models. Protein extracts from untreated controls and those treated with amsacrine were analyzed using two-dimensional fluorescence difference gel electrophoresis. In the bone marrow, reactive proteins were universally decreased by wild-type p53, including α-enolase. Further analysis of α-enolase in the p53 models revealed that it was instead increased in Δ122p53 hematopoietic and tumor cell cytosol and on the cell surface. Alpha-enolase on the surface of Δ122p53 cells acted as a plasminogen receptor, with tumor necrosis factor alpha induced upon plasminogen stimulation. Taken together, these data identified new proteins associated with p53 function. One of these proteins, α-enolase, is regulated differently by wild-type p53 and Δ122p53 cells, with reduced abundance as part of a wild-type p53 response and increased abundance with Δ122p53 function. Increased cell surface α-enolase on Δ122p53 cells provides a possible explanation for the model's pro-inflammatory features and suggests that p53 isoforms may direct an inflammatory response by increasing the amount of α-enolase on the cell surface.
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