ArticleThe Journal of cell biology1999
Cofilin phosphorylation and actin cytoskeletal dynamics regulated by rho- and Cdc42-activated LIM-kinase 2.
Article in The Journal of cell biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 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
160 citing papers in PubMed, 392 citations in OpenAlex.
- Cytoskeletal disassembly by optogenetic control of RhoA signaling termination.bioRxiv : the preprint server for biology · 2026Article
- Activation of the C3a-C3aReceptor-axis is associated with endothelial dysfunction and glycocalyx damage in ST-elevation myocardial infarction.Basic research in cardiology · 2026Article
- Transsynaptic complex dysfunction in the hippocampus of Alzheimer's disease patients.Frontiers in aging neuroscience · 2026Article
- Exploring diarylheptanoid derivatives to target LIMK1 as potential agents against colorectal cancer.Journal of enzyme inhibition and medicinal chemistry · 2025Article
- Effect of TGF-β mediated phenotypic changes on prostate cancer cell anoikis response.Oncogene · 2025Article
- P21-activated kinase 4: a potent oncogene, molecular mechanisms and opportunities for targeted therapy.Cancer cell international · 2025Review
- Overexpression of Drosophila NUAK or Constitutively-Active Formin-Like Promotes the Formation of Aberrant Myofibrils.Cytoskeleton (Hoboken, N.J.) · 2025Article
- LIMK2 promotes centrosome clustering and cancer progression by activating MST4-mediated phosphorylation of NPM1.Oncogene · 2025Article
- Exploring the Diagnostic Utility of Serum Cofilin-1 and 2 Levels in Patients with Acute Coronary Syndrome: A Case-Control Pilot Study.Indian journal of clinical biochemistry : IJCB · 2025Article
- Role of Maternal Obesity in Offspring Cardiovascular Development and Congenital Heart Defects.Journal of the American Heart Association · 2025Article
- Regulation and signaling of the LIM domain kinases.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- The Mechanisms of Neuroprotection by Topical Rho Kinase Inhibition in Experimental Mouse Glaucoma and Optic Neuropathy.Investigative ophthalmology & visual science · 2024Article
- p57International journal of molecular sciences · 2024Article
- Article
- Mdm2 requires Sprouty4 to regulate focal adhesion formation and metastasis independent of p53.Nature communications · 2024Article
- LIM kinases in cardiovascular health and disease.Frontiers in physiology · 2024Review
- Autoregulation of the LIM kinases by their PDZ domain.Nature communications · 2023Article
- Engineering memory with an extrinsically disordered kinase.Science advances · 2023Article
- Involvement of lncRNAs in cancer cells migration, invasion and metastasis: cytoskeleton and ECM crosstalk.Journal of experimental & clinical cancer research : CR · 2023Review
- LIMK2: A Multifaceted kinase with pleiotropic roles in human physiology and pathologies.Cancer letters · 2023Review
100 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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The rapid turnover of actin filaments and the tertiary meshwork formation are regulated by a variety of actin-binding proteins. Protein phosphorylation of cofilin, an actin-binding protein that depolymerizes actin filaments, suppresses its function. Thus, cofilin is a terminal effector of signaling cascades that evokes actin cytoskeletal rearrangement. When wild-type LIMK2 and kinase-dead LIMK2 (LIMK2/KD) were respectively expressed in cells, LIMK2, but not LIMK2/KD, phosphorylated cofilin and induced formation of stress fibers and focal complexes. LIMK2 activity toward cofilin phosphorylation was stimulated by coexpression of activated Rho and Cdc42, but not Rac. Importantly, expression of activated Rho and Cdc42, respectively, induced stress fibers and filopodia, whereas both Rho- induced stress fibers and Cdc42-induced filopodia were abrogated by the coexpression of LIMK2/KD. In contrast, the coexpression of LIMK2/KD with the activated Rac did not affect Rac-induced lamellipodia formation. These results indicate that LIMK2 plays a crucial role both in Rho- and Cdc42-induced actin cytoskeletal reorganization, at least in part by inhibiting the functions of cofilin. Together with recent findings that LIMK1 participates in Rac-induced lamellipodia formation, LIMK1 and LIMK2 function under control of distinct Rho subfamily GTPases and are essential regulators in the Rho subfamilies-induced actin cytoskeletal reorganization.
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.