ArticleCell death & disease2026
K48 and K63 linkage-competed ubiquitination of BECN1 promotes circPDE4D-mediated autophagy in chronic obstructive pulmonary disease.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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1 citing paper in PubMed.
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8 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Chronic obstructive pulmonary disease (COPD) is a progressive inflammatory lung disease with limited clinical therapeutic effects to suspend its progression. Circular RNAs (circRNAs) possess regulatory effects in various diseases. However, circRNA-involved regulatory mechanisms in COPD are largely unknown. This study reveals the mechanism of SMURF1-mediated BECN1 ubiquitination, which is competed by Ub-K48 and Ub-K63, driving the circPDE4D-regulated autophagy. Here, circPDE4D is first identified as a downregulated circRNA in COPD. Among patients with COPD, the lower expression of circPDE4D is associated with the reduced lung function values of FEV
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