ArticleJournal of cellular biochemistry2016
γ-Secretase Dependent Nuclear Targeting of Dystroglycan.
Article in Journal of cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 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
5 citing papers in PubMed, 11 citations in OpenAlex.
- Social memory maintenance relies on social interaction-induced proteolytic products of neuroligin 1.Signal transduction and targeted therapy · 2025Article
- The Role of β-Dystroglycan in Nuclear Dynamics.Cells · 2024Article
- Profiling of the muscle-specific dystroglycan interactome reveals the role of Hippo signaling in muscular dystrophy and age-dependent muscle atrophy.BMC medicine · 2020Article
- The intracellular domain of β-dystroglycan mediates the nucleolar stress response by suppressing UBF transcriptional activity.Cell death & disease · 2019Article
- γ-Secretase Dependent Nuclear Targeting of Dystroglycan. Daniel Leocadio, Andrew Mitchell, and Steve J. Winder.Journal of cellular biochemistry · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dystroglycan is frequently lost in adenocarcinoma. α-dystroglycan is known to become hypoglycosylated due to transcriptional silencing of LARGE, whereas β-dystroglycan is proteolytically cleaved and degraded. The mechanism and proteases involved in the cleavage events affecting β-dystroglycan are poorly understood. Using LNCaP prostate cancer cells as a model system, we have investigated proteases and tyrosine phosphorylation affecting β-dystroglycan proteolysis and nuclear targeting. Cell density or phorbol ester treatment increases dystroglycan proteolysis, whereas furin or γ-secretase inhibitors decreased dystroglycan proteolysis. Using resveratrol treatment of LNCaP cells cultured at low cell density in order to up-regulate notch and activate proteolysis, we identified significant increases in the levels of a 26 kDa β-dystroglycan fragment. These data, therefore, support a cell density-dependent γ-secretase and furin mediated proteolysis of β-dystroglycan, which could be notch stimulated, leading to nuclear targeting and subsequent degradation. 117: 2149-2157, 2016. © 2016 The Authors. Journal of Cellular Biochemistry Published by Wiley Periodicals, Inc.
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.