ArticleThe Biochemical journal2013
ATP-dependent regulation of actin monomer-filament equilibrium by cyclase-associated protein and ADF/cofilin.
Article in The Biochemical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Mechanisms of actin disassembly and turnover.The Journal of cell biology · 2023Review
- Cyclase-associated protein interacts with actin filament barbed ends to promote depolymerization and formin displacement.The Journal of biological chemistry · 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
- Cofilin1 oxidation links oxidative distress to mitochondrial demise and neuronal cell death.Cell death & disease · 2021Article
- Dynamic Phosphorylation and Dephosphorylation of Cyclase-Associated Protein 1 by Antagonistic Signaling through Cyclin-Dependent Kinase 5 and cAMP Are Critical for the Protein Functions in Actin Filament Disassembly and Cell Adhesion.Molecular and cellular biology · 2020Article
- CAPt'n of Actin Dynamics: Recent Advances in the Molecular, Developmental and Physiological Functions of Cyclase-Associated Protein (CAP).Frontiers in cell and developmental biology · 2020Review
- Mechanism of CAP1-mediated apical actin polymerization in pollen tubes.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Conserved hydrophobic residues in the CARP/β-sheet domain of cyclase-associated protein are involved in actin monomer regulation.Cytoskeleton (Hoboken, N.J.) · 2017Article
- The C-terminal dimerization motif of cyclase-associated protein is essential for actin monomer regulation.The Biochemical journal · 2016Article
- Neuronal Actin Dynamics, Spine Density and Neuronal Dendritic Complexity Are Regulated by CAP2.Frontiers in cellular neuroscience · 2016Article
- Regulation of structure and function of sarcomeric actin filaments in striated muscle of the nematode Caenorhabditis elegans.Anatomical record (Hoboken, N.J. : 2007) · 2014Review
- The role of cyclase-associated protein in regulating actin filament dynamics - more than a monomer-sequestration factor.Journal of cell science · 2013Review
- Native cyclase-associated protein and actin from Xenopus laevis oocytes form a unique 4:4 complex with a tripartite structure.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
CAP (cyclase-associated protein) is a conserved regulator of actin filament dynamics. In the nematode Caenorhabditis elegans, CAS-1 is an isoform of CAP that is expressed in striated muscle and regulates sarcomeric actin assembly. In the present study, we report that CAS-2, a second CAP isoform in C. elegans, attenuates the actin-monomer-sequestering effect of ADF (actin depolymerizing factor)/cofilin to increase the steady-state levels of actin filaments in an ATP-dependent manner. CAS-2 binds to actin monomers without a strong preference for either ATP- or ADP-actin. CAS-2 strongly enhances the exchange of actin-bound nucleotides even in the presence of UNC-60A, a C. elegans ADF/cofilin that inhibits nucleotide exchange. UNC-60A induces the depolymerization of actin filaments and sequesters actin monomers, whereas CAS-2 reverses the monomer-sequestering effect of UNC-60A in the presence of ATP, but not in the presence of only ADP or the absence of ATP or ADP. A 1:100 molar ratio of CAS-2 to UNC-60A is sufficient to increase actin filaments. CAS-2 has two independent actin-binding sites in its N- and C-terminal halves, and the C-terminal half is necessary and sufficient for the observed activities of the full-length CAS-2. These results suggest that CAS-2 (CAP) and UNC-60A (ADF/cofilin) are important in the ATP-dependent regulation of the actin monomer-filament equilibrium.
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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.