ArticleBiophysical journal2003
Avidity modulation activates adhesion under flow and requires cooperativity among adhesion receptors.
Article in Biophysical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Actin cortex formation is required for integrin clustering but not activation during leukocyte adhesion.International journal of biological sciences · 2026Article
- Nanoscopy reveals integrin clustering reliant on kindlin-3 but not talin-1.Cell communication and signaling : CCS · 2025Article
- Integrin Regulated Autoimmune Disorders: Understanding the Role of Mechanical Force in Autoimmunity.Frontiers in cell and developmental biology · 2022Review
- Multiple lupus-associated ITGAM variants alter Mac-1 functions on neutrophils.Arthritis and rheumatism · 2013Article
- Increased extracellular pressure enhances cancer cell integrin-binding affinity through phosphorylation of beta1-integrin at threonine 788/789.American journal of physiology. Cell physiology · 2009Article
- Membrane mobility of beta2 integrins and rolling associated adhesion molecules in resting neutrophils.Biophysical journal · 2008Article
- Alterations in human breast cancer adhesion-motility in response to changes in cell surface glycoproteins displaying alpha-L-fucose moieties.International journal of oncology · 2008Article
- The tumor cell-host organ interface in the early onset of metastatic organ colonisation.Clinical & experimental metastasis · 2008Review
- The primacy of affinity over clustering in regulation of adhesiveness of the integrin {alpha}L{beta}2.The Journal of cell biology · 2004Article
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 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An early step in activation of leukocyte adhesion is a release of integrins from cytoskeletal constraints on their diffusion, leading to rearrangement and, consequently, increased avidity. Static adhesion assays using purified ligand as a substrate have demonstrated that very low doses of cytochalasin D disconnect beta2-integrins from their cytoskeletal links, allowing rearrangement and activating adhesion. The adhesion process in blood vessels is poorly simulated by these assays, however, for two reasons: leukocyte adhesion to endothelium 1), occurs in the presence of blood flow and 2), involves the simultaneous interactions of multiple sets of adhesion molecules. We investigated the effect of cytochalasin D, at concentrations that increase integrin diffusion but do not alter leukocyte shape and surface features, on adhesion of leukocytes to endothelial cells under flow. Cytochalasin D increased the number of rolling cells, the number of firmly adherent cells, and the duration of both rolling and firm adhesion. These effects required endothelial cell expression of ICAM-1, the ligand for leukocyte beta2-integrins. The beta2-integrin-ICAM-1 interaction alone was not sufficient, however. Experiments using purified substrates demonstrated that avidity effects on activation of adhesion under flow require functional cooperativity between integrins and other adhesion receptors.
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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.