ArticlePloS one2011
Knockdown of dystrophin Dp71 impairs PC12 cells cycle: localization in the spindle and cytokinesis structures implies a role for Dp71 in cell division.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 39 citations in OpenAlex.
- Targeting astrocytic Dp71 attenuates BBB disruption after traumatic brain injury through WTAP-associated mScience advances · 2026Article
- The molecular mechanism underlying the differential subcellular distribution of dystrophin Dp71 isoforms.Cell & bioscience · 2026Article
- Disruption of DMD gene leads to altered calcium homeostasis and metabolic shift impacting gastric Cancer cell proliferation and migration.Cancer cell international · 2025Article
- The role of dystrophin isoforms and interactors in the brain.Brain : a journal of neurology · 2025Review
- Duchenne muscular dystrophy gene product expression is associated with survival in head and neck squamous cell carcinoma.Scientific reports · 2025Article
- The Dystrophin-Dystroglycan complex ensures cytokinesis efficiency in Drosophila epithelia.EMBO reports · 2025Article
- Expression of Dystrophin Dp71 Splice Variants Is Temporally Regulated During Rodent Brain Development.Molecular neurobiology · 2024Article
- Differential expression ofTranslational lung cancer research · 2024Article
- Dp71 Point Mutations Induce Protein Aggregation, Loss of Nuclear Lamina Integrity and Impaired Braf35 and Ibraf Function in Neuronal Cells.International journal of molecular sciences · 2022Article
- Growth pattern trajectories in boys with Duchenne muscular dystrophy.Orphanet journal of rare diseases · 2022Observational
- Dystrophin Dp71 Subisoforms Localize to the Mitochondria of Human Cells.Life (Basel, Switzerland) · 2021Article
- Cellular pathology of the human heart in Duchenne muscular dystrophy (DMD): lessons learned from in vitro modeling.Pflugers Archiv : European journal of physiology · 2021Review
- The Duchenne muscular dystrophy gene and cancer.Cellular oncology (Dordrecht, Netherlands) · 2021Review
- Dystrophin Dp71ab is monoclonally expressed in human satellite cells and enhances proliferation of myoblast cells.Scientific reports · 2020Article
- Dystrophin Dp71 and the Neuropathophysiology of Duchenne Muscular Dystrophy.Molecular neurobiology · 2020Review
- Single-transcript multiplexWellcome open research · 2020Article
- Dp71 Expression in Human Glioblastoma.International journal of molecular sciences · 2019Article
- Recurrent DMD Deletions Highlight Specific Role of Dp71 Isoform in Soft-Tissue Sarcomas.Cancers · 2019Article
- Dp71 depleted HBE cells displayed increased DNA damage and apoptosis induced by HCellular & molecular biology letters · 2019Article
- Detection of Dystrophin Dp71 in Human Skeletal Muscle Using an Automated Capillary Western Assay System.International journal of molecular sciences · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The function of dystrophin Dp71 in neuronal cells remains to be established. Previously, we revealed the involvement of this protein in both nerve growth factor (NGF)-induced neuronal differentiation and cell adhesion by isolation and characterization of PC12 neuronal cells with depleted levels of Dp71. In this work, a novel phenotype of Dp71-knockdown cells was characterized, which is their delayed growth rate. Cell cycle analyses revealed an altered behavior of Dp71-depleted cells, which consists of a delay in G0/G1 transition and an increase in apoptosis during nocodazole-induced mitotic arrest. Dp71 associates with lamin B1 and β-dystroglycan, proteins involved in aspects of the cell division cycle; therefore, we compared the distribution of Dp71 with that of lamin B1 and β-dystroglycan in PC12 cells at mitosis and cytokinesis by means of immunofluorescence and confocal microscopy analysis. All of these three proteins exhibited a similar immunostaining pattern, localized at mitotic spindle, cleavage furrow, and midbody. It is noteworthy that a drastic decreased staining in mitotic spindle, cleavage furrow, and midbody was observed for both lamin B1 and β-dystroglycan in Dp71-depleted cells. Furthermore, we demonstrated the interaction of Dp71 with lamin B1 in PC12 cells by immunoprecipitation and pull-down assays, and importantly, we revealed that knockdown of Dp71 expression caused a marked reduction in lamin B1 levels and altered localization of the nuclear envelope protein emerin. Our data indicate that Dp71 is a component of the mitotic spindle and cytokinesis multi-protein apparatuses that might modulate the cell division cycle by affecting lamin B1 and β-dystroglycan levels.
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.