ArticleNature communications2014
A genetic variant of p53 restricts the mucous secretory phenotype by regulating SPDEF and Bcl-2 expression.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Management of airway mucus hypersecretion in chronic airway inflammatory disease: Chinese expert consensus (English edition).International journal of chronic obstructive pulmonary disease · 2018Guideline
- Mucus plug and lung cancer incidence in patients with COPD.Scientific reports · 2025Article
- The multifunctional proline-rich domain of p53 tumor suppressor.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- Hippo cooperates with p53 to regulate lung airway mucous cell metaplasia.Disease models & mechanisms · 2024Article
- Airway-occluding Mucus Plugs and Cause-specific Mortality in Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2024Article
- Airway Mucus Plugs in Community-Living Adults: A Study Protocol.medRxiv : the preprint server for health sciences · 2024Article
- Galactosylceramide Upregulates the Expression of theCancers · 2024Article
- Airway Mucus Plugs in Community-Living Adults: A Study Protocol.Journal of clinical & experimental pathology · 2024Article
- Bik promotes proteasomal degradation to control low-grade inflammation.The Journal of clinical investigation · 2023Article
- Does Chronic Obstructive Pulmonary Disease Originate from Different Cell Types?American journal of respiratory cell and molecular biology · 2023Article
- Physicochemical and toxicological properties of wood smoke particulate matter as a function of wood species and combustion condition.Journal of hazardous materials · 2023Article
- Development of an Integrated Platform to Assess the Physicochemical and Toxicological Properties of Wood Combustion Particulate Matter.Chemical research in toxicology · 2022Article
- Apoptotic and Necroptotic Mediators are Differentially Expressed in Mucinous and Non-Mucinous Colorectal Cancer.Frontiers in oncology · 2022Article
- Effects of Wood Smoke Constituents on Mucin Gene Expression in Mice and Human Airway Epithelial Cells and on Nasal Epithelia of Subjects with a Susceptibility Gene Variant inEnvironmental health perspectives · 2022Article
- Review
- Article
- A Small Molecule BH3-mimetic Suppresses Cigarette Smoke-Induced Mucous Expression in Airway Epithelial Cells.Scientific reports · 2018Article
- Early Endotyping: A Chance for Intervention in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2018Article
- IL-13 in LPS-Induced Inflammation Causes Bcl-2 Expression to Sustain Hyperplastic Mucous cells.Scientific reports · 2018Article
- Blocking Bcl-2 resolves IL-13-mediated mucous cell hyperplasia in a Bik-dependent manner.The Journal of allergy and clinical immunology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Despite implications for carcinogenesis and other chronic diseases, basic mechanisms of p53 and its variants in suppressing Bcl-2 levels are poorly understood. Bcl-2 sustains mucous cell metaplasia, whereas p53(-/-) mice display chronically increased mucous cells. Here we show that p53 decreases bcl-2 mRNA half-life by interacting with the 5' untranslated region (UTR). The p53-bcl-2 mRNA interaction is modified by the substitution of proline by arginine within the p53 proline-rich domain (PRD). Accordingly, more mucous cells are present in primary human airway cultures with p53(Arg) compared with p53(Pro). Also, the p53(Arg) compared with p53(Pro) displays higher affinity to and activates the promoter region of SAM-pointed domain-containing Ets-like factor (SPDEF), a driver of mucous differentiation. On two genetic backgrounds, mice with targeted replacement of prolines in p53 PRD show enhanced expression of SPDEF and Bcl-2 and mucous cell metaplasia. Together, these studies define the PRD of p53 as a determinant for chronic mucous hypersecretion.
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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.