ArticleNature communications2026
Adhesion-derived condensates control component availability to regulate adhesion dynamics.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Reconstituted nascent adhesion condensates drive actin polymerization on supported lipid bilayers.Science advances · 2026Article
- Talin-tensin3 interactions regulate fibrillar adhesion formation and tensin3 phase separation.The Journal of cell biology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Integrin adhesion complexes mediate dynamic cell-matrix interactions to regulate cell adhesion, migration and invasion. While increasing evidence suggests that adhesion components can undergo liquid-liquid phase separation, the functional relevance of adhesion-derived condensates remains elusive. Here, we demonstrate that tensin 1 (TNS1), a multidomain adaptor protein linking active integrins with the actin cytoskeleton, forms condensates in cells to regulate adhesion component availability. We show that endogenous TNS1 condensates are formed upon focal adhesion disassembly or limited integrin-extracellular matrix engagement, acting as reversible reservoirs for unphosphorylated adhesion proteins. We identify the TNS1 intrinsically disordered region as governing TNS1 condensation and condensate biophysical properties. We further demonstrate a negative regulatory role for phosphorylation on condensate assembly upon stress-responsive kinase activation. Finally, we confirm the functional effects of TNS1 condensation on adhesion dynamics and cell migration, identifying a feedback loop acutely regulating kinase-mediated adhesion turnover upon integrin activation.
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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.