ArticleScientific reports2017
Cofilin-mediated Neuronal Apoptosis via p53 Translocation and PLD1 Regulation.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 32 citations in OpenAlex.
- Cofilin 1-138 Promotes Mitochondrial Dysfunction and Synaptic Degeneration in Parkinson's Disease.Molecular neurobiology · 2026Article
- Cofilin-1 Exacerbates Tau-Induced Mitochondrial Damage, Oxidative Stress, and Apoptosis in Alzheimer's Disease.Neurochemical research · 2026Article
- Role of LIMK1-cofilin-actin axis in dendritic spine dynamics in Alzheimer's disease.Cell death & disease · 2025Review
- Multi-target neuroprotection by dl-PHPB in APP/PS1 mice: a proteomic analysis.Frontiers in pharmacology · 2025Article
- Enhanced cell survival in prepubertal testicular tissue cryopreserved with membrane lipids and antioxidants rich cryopreservation medium.Cell and tissue research · 2025Article
- Effect of Kruppel-like factor 4 on PTZ-induced acute seizure mice.Journal of cellular and molecular medicine · 2024Article
- α-Synuclein-mediated mitochondrial translocation of cofilin-1 leads to oxidative stress and cell apoptosis in PD.Frontiers in neuroscience · 2024Article
- Article
- Slingshot homolog-1 mediates the secretion of small extracellular vesicles containing misfolded proteins by regulating autophagy cargo receptors and actin dynamics.Frontiers in aging neuroscience · 2022Article
- Cofilin1 oxidation links oxidative distress to mitochondrial demise and neuronal cell death.Cell death & disease · 2021Article
- Review
- Cofilin and Neurodegeneration: New Functions for an Old but Gold Protein.Brain sciences · 2021Review
- The actin nucleation factors JMY and WHAMM enable a rapid Arp2/3 complex-mediated intrinsic pathway of apoptosis.PLoS genetics · 2021Article
- Role of cofilin‑1 in arsenic trioxide‑induced apoptosis of NB4‑R1 cells.Molecular medicine reports · 2020Article
- Loss of non-canonical KCC2 functions promotes developmental apoptosis of cortical projection neurons.EMBO reports · 2020Article
- Involvement of the Actin Machinery in Programmed Cell Death.Frontiers in cell and developmental biology · 2020Review
- Dual role of cofilin in APP trafficking and amyloid-β clearance.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Activated cofilin exacerbates tau pathology by impairing tau-mediated microtubule dynamics.Communications biology · 2019Article
- Cofilin, a Master Node Regulating Cytoskeletal Pathogenesis in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2019Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Amyloid β (Aβ) accumulation is an early event in the pathogenesis of Alzheimer's disease (AD), leading to mitochondrial and synaptic dysfunction, tau accumulation, and eventual neuronal death. While the p53 apoptotic pathway has clearly been associated with Aβ deposits and neuronal apoptosis, the critical upstream factors contributing to p53 activation in AD are not well understood. We have previously shown that cofilin activation plays a pivotal role in Aβ-induced mitochondrial and synaptic dysfunction. In this study, we show that activated cofilin (S3A) preferentially forms a complex with p53 and promotes its mitochondrial and nuclear localization, resulting in transcription of p53-responsive genes and promotion of apoptosis. Conversely, reduction of endogenous cofilin by knockdown or genetic deficiency inhibits mitochondrial and nuclear translocation of p53 in cultured cells and in APP/PS1 mice. This cofilin-p53 pro-apoptotic pathway is subject to negative regulation by PLD1 thorough cofilin inactivation and inhibition of cofilin/p53 complex formation. Finally, activated cofilin is unable to induce apoptosis in cells genetically lacking p53. These findings taken together indicate that cofilin coopts and requires the nuclear and mitochondrial pro-apoptotic p53 program to induce and execute apoptosis, while PLD1 functions in a regulatory multi-brake capacity in this pathway.
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.