ArticleMolecular biology of the cell2002
Mutant actins demonstrate a role for unpolymerized actin in control of transcription by serum response factor.
Article in Molecular biology of the cell, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.
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Who cites it
140 citing papers in PubMed, 277 citations in OpenAlex.
- Actin disassembly triggers CNS myelin compaction and wrapping.bioRxiv : the preprint server for biology · 2026Article
- Compartmentalized cytoplasmic tradewinds direct soluble proteins.Nature communications · 2026Article
- Multilayered regulation of cytoskeletal protein abundance: autoregulatory mechanisms of actin and tubulin.Experimental & molecular medicine · 2026Review
- Nuclear rupture in confined cell migration triggers nuclear actin polymerization to limit chromatin leakage.The EMBO journal · 2025Article
- Myocardin-related transcription factor regulates actomyosin contractility and apical junction remodeling during vertebrate neural tube closure.Development (Cambridge, England) · 2025Article
- New insights into the pharmacological inhibition of SRF activity: Key inhibitory targets and mechanisms.Vascular pharmacology · 2024Review
- TORC2 inhibition triggers yeast chromosome fragmentation through misregulated Base Excision Repair of clustered oxidation events.Nature communications · 2024Article
- SUN2 mediates calcium-triggered nuclear actin polymerization to cluster active RNA polymerase II.EMBO reports · 2024Article
- IL-2 delivery to CD8Nature communications · 2024Article
- Recent advances in serum response factor posttranslational modifications and their therapeutic potential in cardiovascular and neurological diseases.Vascular pharmacology · 2024Review
- Nuclear actin is a critical regulator ofbioRxiv : the preprint server for biology · 2024Article
- Nuclear actin assembly is an integral part of decidualization in human endometrial stromal cells.Communications biology · 2024Article
- Aggravated Ulcerative Colitis via circNlgn-Mediated Suppression of Nuclear Actin Polymerization.Research (Washington, D.C.) · 2024Article
- Nuclear actin polymerization rapidly mediates replication fork remodeling upon stress by limiting PrimPol activity.Nature communications · 2023Article
- A defective mechanosensing pathway affects fibroblast-to-myofibroblast transition in the old male mouse heart.iScience · 2023Article
- Actin nucleators safeguard replication forks by limiting nascent strand degradation.Nucleic acids research · 2023Article
- Article
- Actin filaments accumulated in the nucleus remain in the vicinity of condensing chromosomes in the zebrafish early embryo.Biology open · 2023Article
- Activation of an actin signaling pathway in pre-malignant mammary epithelial cells by P-cadherin is essential for transformation.Disease models & mechanisms · 2023Article
- Actin nucleators safeguard replication forks by limiting nascent strand degradation.bioRxiv : the preprint server for biology · 2023Article
80 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signal-induced activation of the transcription factor serum response factor (SRF) requires alterations in actin dynamics. SRF activity can be inhibited by ectopic expression of beta-actin, either because actin itself participates in SRF regulation or as a consequence of cytoskeletal perturbations. To distinguish between these possibilities, we studied actin mutants. Three mutant actins, G13R, R62D, and a C-terminal VP16 fusion protein, were shown not to polymerize in vivo, as judged by two-hybrid, immunofluorescence, and cell fractionation studies. These actins effectively inhibited SRF activation, as did wild-type actin, which increased the G-actin level without altering the F:G-actin ratio. Physical interaction between SRF and actin was not detectable by mammalian or yeast two-hybrid assays, suggesting that SRF regulation involves an unidentified cofactor. SRF activity was not blocked upon inhibition of CRM1-mediated nuclear export by leptomycin B. Two actin mutants were identified, V159N and S14C, whose expression favored F-actin formation and which strongly activated SRF in the absence of external signals. These mutants seemed unable to inhibit SRF activity, because their expression did not reduce the absolute level of G-actin as assessed by DNase I binding. Taken together, these results provide strong evidence that G-actin, or a subpopulation of it, plays a direct role in signal transduction to SRF.
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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.