ArticleJournal of cell science2013
Rac function is crucial for cell migration but is not required for spreading and focal adhesion formation.
Article in Journal of cell science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 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
96 citing papers in PubMed, 150 citations in OpenAlex.
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- Sensing molecular carbon dioxide: a translational focus for respiratory disease.Physiological reviews · 2025Review
- Cross-talk between Rac and Rap GTPases in migrating cells.Molecular biology of the cell · 2025Article
- The role of abnormal epigenetic regulation of small GTPases in glioma (Review).International journal of oncology · 2025Review
- Tbx1 plays a critical role in focal adhesion dynamics through paxillin regulation.Life science alliance · 2025Article
- Formation control between leader and migratory follower tissues allows coordinated growth.Science advances · 2025Article
- Distinct roles of protrusions and collagen deformation in collective invasion of cancer cell types.Biophysical journal · 2025Article
- RAC2 inhibition enhances tumor sensitivity to NK cell-mediated cytotoxicity.Journal for immunotherapy of cancer · 2025Article
- Nance-Horan-syndrome-like 1b controls mesodermal cell migration by regulating protrusion and actin dynamics during zebrafish gastrulation.Communications biology · 2025Article
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- Navigating the Collective: Nanoparticle-Assisted Identification of Leader Cancer Cells During Migration.Life (Basel, Switzerland) · 2025Article
- Roles played by IL-8 in altering dynamics of trabecular meshwork cells after human cytomegalovirus infection.Frontiers in cellular and infection microbiology · 2025Article
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- Genome-Wide Association Studies Reveal Candidate Genes Associated with Pigmentation Patterns of Single Feathers of Tianfu Nonghua Ducks.Animals : an open access journal from MDPI · 2023Article
- Expression Analysis of the Small GTP-Binding Protein Rac in PterygiumTurkish journal of ophthalmology · 2023Article
- Phosphoinositide Signaling in Immune Cell Migration.Biomolecules · 2023Review
- Role of RhoG as a regulator of cellular functions: integrating insights on immune cell activation, migration, and functions.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
36 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
16 authors at 7 institutions in 3 countries.
Funding
Abstract
Cell migration is commonly accompanied by protrusion of membrane ruffles and lamellipodia. In two-dimensional migration, protrusion of these thin sheets of cytoplasm is considered relevant to both exploration of new space and initiation of nascent adhesion to the substratum. Lamellipodium formation can be potently stimulated by Rho GTPases of the Rac subfamily, but also by RhoG or Cdc42. Here we describe viable fibroblast cell lines genetically deficient for Rac1 that lack detectable levels of Rac2 and Rac3. Rac-deficient cells were devoid of apparent lamellipodia, but these structures were restored by expression of either Rac subfamily member, but not by Cdc42 or RhoG. Cells deficient in Rac showed strong reduction in wound closure and random cell migration and a notable loss of sensitivity to a chemotactic gradient. Despite these defects, Rac-deficient cells were able to spread, formed filopodia and established focal adhesions. Spreading in these cells was achieved by the extension of filopodia followed by the advancement of cytoplasmic veils between them. The number and size of focal adhesions as well as their intensity were largely unaffected by genetic removal of Rac1. However, Rac deficiency increased the mobility of different components in focal adhesions, potentially explaining how Rac - although not essential - can contribute to focal adhesion assembly. Together, our data demonstrate that Rac signaling is essential for lamellipodium protrusion and for efficient cell migration, but not for spreading or filopodium formation. Our findings also suggest that Rac GTPases are crucial to the establishment or maintenance of polarity in chemotactic 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.