ArticleNature cell biology2009
p53-cofactor JMY is a multifunctional actin nucleation factor.
Article in Nature cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 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
154 citing papers in PubMed, 250 citations in OpenAlex.
- Review
- Autophagosome turnover requires Arp2/3 complex-mediated maintenance of lysosomal integrity.Molecular biology of the cell · 2026Article
- Junction-mediating and regulatory protein (JMY) is a promoting protein for radial migration of cortical neurons.Cell death discovery · 2026Article
- When two worlds collide: actin dynamics on endomembranes regulates membrane trafficking.Current opinion in cell biology · 2025Review
- The actin nucleation promoting factor WASH facilitates clathrin-independent endocytosis of human papillomaviruses.EMBO reports · 2025Article
- Agent-based modelling of the early stages of actin polymerisation required to drive endocytosis in Saccharomyces cerevisiae.Scientific reports · 2025Article
- Liquid-like condensates that bind actin promote assembly and bundling of actin filaments.Developmental cell · 2025Article
- JMY powers dendritogenesis and is regulated by CaM revealing a general, critical principle in neuromorphogenesis.Communications biology · 2025Article
- Article
- Identification and Preliminary Analysis of Granulosa Cell Biomarkers to Predict Oocyte In Vitro Maturation Outcome in the Southern White Rhinoceros (Animals : an open access journal from MDPI · 2024Article
- Membrane Ruffles: Composition, Function, Formation and Visualization.International journal of molecular sciences · 2024Review
- Disulfidptosis: a novel cell death modality induced by actin cytoskeleton collapse and a promising target for cancer therapeutics.Cell communication and signaling : CCS · 2024Review
- Granulosa cells provide transcriptomic information on ovarian follicle dynamics in southern white rhinoceros.Scientific reports · 2024Article
- WHAMM functions in kidney reabsorption and polymerizes actin to promote autophagosomal membrane closure and cargo sequestration.Molecular biology of the cell · 2024Article
- NPFs-mediated actin cytoskeleton: a new viewpoint on autophagy regulation.Cell communication and signaling : CCS · 2024Review
- WHAMM functions in kidney reabsorption and polymerizes actin to promote autophagosomal membrane closure and cargo sequestration.bioRxiv : the preprint server for biology · 2024Article
- Changes of Ex Vivo Cervical Epithelial Cells Due to Electroporation with JMY.International journal of molecular sciences · 2023Article
- p53-dependent DNA repair during the DNA damage response requires actin nucleation by JMY.Cell death and differentiation · 2023Article
- Branching out in different directions: Emerging cellular functions for the Arp2/3 complex and WASP-family actin nucleation factors.European journal of cell biology · 2023Article
- F-actin-rich territories coordinate apoptosome assembly and caspase activation during DNA damage-induced intrinsic apoptosis.Molecular biology of the cell · 2023Article
94 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Many cellular structures are assembled from networks of actin filaments, and the architecture of these networks depends on the mechanism by which the filaments are formed. Several classes of proteins are known to assemble new filaments, including the Arp2/3 complex, which creates branched filament networks, and Spire, which creates unbranched filaments. We find that JMY, a vertebrate protein first identified as a transcriptional co-activator of p53, combines these two nucleating activities by both activating Arp2/3 and assembling filaments directly using a Spire-like mechanism. Increased levels of JMY expression enhance motility, whereas loss of JMY slows cell migration. When slowly migrating HL-60 cells are differentiated into highly motile neutrophil-like cells, JMY moves from the nucleus to the cytoplasm and is concentrated at the leading edge. Thus, JMY represents a new class of multifunctional actin assembly factor whose activity is regulated, at least in part, by sequestration in the nucleus.
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.