ArticleProceedings of the National Academy of Sciences of the United States of America2019
CAP2 deficiency delays myofibril actin cytoskeleton differentiation and disturbs skeletal muscle architecture and function.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. 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, 52 citations in OpenAlex.
- Loss of cyclase-associated protein 2 alters actin cytoskeleton organization and biomechanical properties of the ocular lens.Journal of cell science · 2026Article
- Synaptic and cytoskeletal CSF signatures of motor neuron disease: the role of cyclase-associated protein 2.Scientific reports · 2026Article
- ROS-Drp1-mitophagy feedback loop regulates myogenic differentiation via actin cytoskeleton remodeling-mediated MRTF-A/SRF axis.Redox report : communications in free radical research · 2025Article
- Cyclase associated actin cytoskeleton regulatory protein 2 (CAP2) organizes the actin cytoskeleton to influence the biomechanical properties of the ocular lens.bioRxiv : the preprint server for biology · 2025Article
- Integrative machine learning frameworks to uncover specific protein signature in neuroendocrine cervical carcinoma.BMC cancer · 2025Article
- Advancements in skeletal muscle tissue engineering: strategies for repair and regeneration of skeletal muscle beyond self-repair.Regenerative biomaterials · 2025Review
- Cyclase-associated protein (CAP) inhibits inverted formin 2 (INF2) to induce dendritic spine maturation.Cellular and molecular life sciences : CMLS · 2024Article
- Review
- Cyclase-associated protein interacts with actin filament barbed ends to promote depolymerization and formin displacement.The Journal of biological chemistry · 2023Article
- Article
- Review
- An association study of cyclase-associated protein 2 and frailty.Aging cell · 2023Article
- CAP1 (cyclase-associated protein 1) mediates the cyclic AMP signals that activate Rap1 in stimulating matrix adhesion of colon cancer cells.Cellular signalling · 2023Article
- Integration of Transcriptomics and Non-Targeted Metabolomics Reveals the Underlying Mechanism of Skeletal Muscle Development in Duck during Embryonic Stage.International journal of molecular sciences · 2023Article
- Functional interdependence of the actin regulators CAP1 and cofilin1 in control of dendritic spine morphology.Cellular and molecular life sciences : CMLS · 2022Article
- The Mechanisms of Thin Filament Assembly and Length Regulation in Muscles.International journal of molecular sciences · 2022Review
- miRNA mediated downregulation of cyclase-associated protein 1 (CAP1) is required for myoblast fusion.Frontiers in cell and developmental biology · 2022Article
- Chloroquine Attenuates Asthma Development by Restoring Airway Smooth Muscle Cell PhenotypeFrontiers in pharmacology · 2022Article
- Actin Alpha 2 Downregulation Inhibits Neural Stem Cell Proliferation and Differentiation into Neurons through Canonical Wnt/Oxidative medicine and cellular longevity · 2022Article
- Redefining actin dynamics of the pointed-end complex in striated muscle.Trends in cell biology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Actin filaments (F-actin) are key components of sarcomeres, the basic contractile units of skeletal muscle myofibrils. A crucial step during myofibril differentiation is the sequential exchange of α-actin isoforms from smooth muscle (α-SMA) and cardiac (α-CAA) to skeletal muscle α-actin (α-SKA) that, in mice, occurs during early postnatal life. This "α-actin switch" requires the coordinated activity of actin regulators because it is vital that sarcomere structure and function are maintained during differentiation. The molecular machinery that controls the α-actin switch, however, remains enigmatic. Cyclase-associated proteins (CAP) are a family of actin regulators with largely unknown physiological functions. We here report a function for CAP2 in regulating the α-actin exchange during myofibril differentiation. This α-actin switch was delayed in systemic CAP2 mutant mice, and myofibrils remained in an undifferentiated stage at the onset of the often excessive voluntary movements in postnatal mice. The delay in the α-actin switch coincided with the onset of motor function deficits and histopathological changes including a high frequency of type IIB ring fibers. Our data suggest that subtle disturbances of postnatal F-actin remodeling are sufficient for predisposing muscle fibers to form ring fibers. Cofilin2, a putative CAP2 interaction partner, has been recently implicated in myofibril actin cytoskeleton differentiation, and the myopathies in cofilin2 and CAP2 mutant mice showed striking similarities. We therefore propose a model in which CAP2 and cofilin2 cooperate in actin regulation during myofibril differentiation.
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.