ArticleThe Journal of biological chemistry2013
Depletion of the ubiquitin-binding adaptor molecule SQSTM1/p62 from macrophages harboring cftr ΔF508 mutation improves the delivery of Burkholderia cenocepacia to the autophagic machinery.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 58 citations in OpenAlex.
- Restoration of CFTR function in patients with cystic fibrosis carrying the F508del-CFTR mutation.Autophagy · 2014Trial
- The phospholipase PlcP mediates membrane lipid remodeling required for the intracellular survival of Burkholderia cenocepacia.The Journal of biological chemistry · 2026Article
- Mitochondria Meet the Lung Microbiome: A Bidirectional Dialogue in Inflammation and Respiratory Diseases.Biomedicines · 2026Review
- SARS-CoV-2 nonstructural protein 6 triggers endoplasmic reticulum stress-induced autophagy to degrade STING1.Autophagy · 2023Article
- The versatile defender: exploring the multifaceted role of p62 in intracellular bacterial infection.Frontiers in cellular and infection microbiology · 2023Review
- Emerging Concepts in Defective Macrophage Phagocytosis in Cystic Fibrosis.International journal of molecular sciences · 2022Review
- Autophagy-Inflammation Interplay During Infection: Balancing Pathogen Clearance and Host Inflammation.Frontiers in pharmacology · 2022Review
- Role of inflammation and oxidative stress in tissue damage associated with cystic fibrosis: CAPE as a future therapeutic strategy.Molecular and cellular biochemistry · 2022Review
- CFTR Modulators Restore Acidification of Autophago-Lysosomes and Bacterial Clearance in Cystic Fibrosis Macrophages.Frontiers in cellular and infection microbiology · 2022Article
- Review
- The regulatory effect of acetylation of HMGN2 and H3K27 on pyocyanin-induced autophagy in macrophages by affecting Ulk1 transcription.Journal of cellular and molecular medicine · 2021Article
- Defective immunometabolism pathways in cystic fibrosis macrophages.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2021Article
- Gasdermin D restricts Burkholderia cenocepacia infection in vitro and in vivo.Scientific reports · 2021Article
- Bacterial Subversion of Autophagy in Cystic Fibrosis.Frontiers in cellular and infection microbiology · 2021Review
- Roles of Specialized Pro-Resolving Lipid Mediators in Autophagy and Inflammation.International journal of molecular sciences · 2020Review
- Review
- CFTR Modulators DampenFrontiers in cellular and infection microbiology · 2020Article
- Autophagy, Unfolded Protein Response and Lung Disease.Current research in cell biology · 2020Article
- Caspase-11 counteracts mitochondrial ROS-mediated clearance of Staphylococcus aureus in macrophages.EMBO reports · 2019Article
- HDAC6 depletion improves cystic fibrosis mouse airway responses to bacterial challenge.Scientific reports · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 4 countries.
Funding
Abstract
Cystic fibrosis is the most common inherited lethal disease in Caucasians. It is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR), of which the cftr ΔF508 mutation is the most common. ΔF508 macrophages are intrinsically defective in autophagy because of the sequestration of essential autophagy molecules within unprocessed CFTR aggregates. Defective autophagy allows Burkholderia cenocepacia (B. cepacia) to survive and replicate in ΔF508 macrophages. Infection by B. cepacia poses a great risk to cystic fibrosis patients because it causes accelerated lung inflammation and, in some cases, a lethal necrotizing pneumonia. Autophagy is a cell survival mechanism whereby an autophagosome engulfs non-functional organelles and delivers them to the lysosome for degradation. The ubiquitin binding adaptor protein SQSTM1/p62 is required for the delivery of several ubiquitinated cargos to the autophagosome. In WT macrophages, p62 depletion and overexpression lead to increased and decreased bacterial intracellular survival, respectively. In contrast, depletion of p62 in ΔF508 macrophages results in decreased bacterial survival, whereas overexpression of p62 leads to increased B. cepacia intracellular growth. Interestingly, the depletion of p62 from ΔF508 macrophages results in the release of the autophagy molecule beclin1 (BECN1) from the mutant CFTR aggregates and allows its redistribution and recruitment to the B. cepacia vacuole, mediating the acquisition of the autophagy marker LC3 and bacterial clearance via autophagy. These data demonstrate that p62 differentially dictates the fate of B. cepacia infection in WT and ΔF508 macrophages.
Indexed as
Identifiers
What OpenQuestion holds
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.