ArticlePloS one2009
Filamins regulate cell spreading and initiation of cell migration.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
What it found
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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.
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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.
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Who cites it
82 citing papers in PubMed, 143 citations in OpenAlex.
- Comprehensive analysis of RNA sequencing reveals DNA damage response and immune-associated alternative splicing and RBP regulators contributing to preeclampsia.BMC genomics · 2026Article
- Filamin A editing in myeloid cells reduces intestinal inflammation and protects from colitis.The Journal of experimental medicine · 2025Article
- Unveiling the multifaceted role of the FLNC gene: implications for cancer diagnosis and prognosis.European journal of medical research · 2025Article
- Mutations in Filamin C Associated with Both Alleles Do Not Affect the Functioning of Mice Cardiac Muscles.International journal of molecular sciences · 2025Article
- Fine-tuning levels of filamins a and b as a specific mechanism sustaining Th2 lymphocyte functions.Nature communications · 2024Article
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- Filamin B restricts vaccinia virus spread and is targeted by vaccinia virus protein C4.Journal of virology · 2024Article
- Mining proteomics data to extract post-translational modifications associated with gastric cancer.Amino acids · 2023Article
- Contrasting effects of filamin A and B proteins in modulating filovirus entry.PLoS pathogens · 2023Article
- Proteomic analysis of the effect of hemin in breast cancer.Scientific reports · 2023Article
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- Single-cell transcriptomics in ovarian cancer identify a metastasis-associated cell cluster overexpressed RAB13.Journal of translational medicine · 2023Article
- Age and Blood Pressure Contribute to Aortic Cell and Tissue Stiffness Through Distinct Mechanisms.Hypertension (Dallas, Tex. : 1979) · 2022Article
- BCL11A promotes myeloid leukemogenesis by repressing PU.1 target genes.Blood advances · 2022Article
- Methamphetamine induces transcriptional changes in cultured HIV-infected mature monocytes that may contribute to HIV neuropathogenesis.Frontiers in immunology · 2022Article
- Role of filamin A in the pathogenesis of neuroendocrine tumors and adrenal cancer.Endocrine oncology (Bristol, England) · 2022Review
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- Dynamic Changes in the Proteome of Early Bovine Embryos DevelopedFrontiers in cell and developmental biology · 2022Article
- Systematic analysis of migration factors by MigExpress identifies essential cell migration control genes in non-small cell lung cancer.Molecular oncology · 2021Article
22 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
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Mammalian filamins (FLNs) are a family of three large actin-binding proteins. FLNa, the founding member of the family, was implicated in migration by cell biological analyses and the identification of FLNA mutations in the neuronal migration disorder periventricular heterotopia. However, recent knockout studies have questioned the relevance of FLNa to cell migration. Here we have used shRNA-mediated knockdown of FLNa, FLNb or FLNa and FLNb, or, alternatively, acute proteasomal degradation of all three FLNs, to generate FLN-deficient cells and assess their ability to migrate. We report that loss of FLNa or FLNb has little effect on migration but that knockdown of FLNa and FLNb, or proteolysis of all three FLNs, impairs migration. The observed defect is primarily a deficiency in initiation of motility rather than a problem with maintenance of locomotion speed. FLN-deficient cells are also impaired in spreading. Re-expression of full length FLNa, but not re-expression of a mutated FLNa lacking immunoglobulin domains 19 to 21, reverts both the spreading and the inhibition of initiation of migration.Our results establish a role for FLNs in cell migration and spreading and suggest that compensation by other FLNs may mask phenotypes in single knockout or knockdown cells. We propose that interactions between FLNs and transmembrane or signalling proteins, mediated at least in part by immunoglobulin domains 19 to 21 are important for both cell spreading and initiation of migration.
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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.