ReviewBiomolecules2026
Outside-In Signaling as a Detonator-like Stimulus of Integrin Activation by Promoting Both Affinity and Avidity.
Review in Biomolecules, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
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Authors and funding
2 authors.
Funding
Abstract
Integrins play a central role in a wide range of biological processes, including development, tissue homeostasis, immune responses, and disease progression. Their activation is traditionally explained by two major signaling modes: inside-out signaling, which converts integrins to ligand-competent and high-affinity states through intracellular activators, including the Rap1-talin-kindlin axis, and outside-in signaling, which transduces ligand engagement into cytoskeletal coupling and downstream signaling. Recent findings indicate that this division is incomplete. Ligand-engaged integrins can also generate spatially organized signaling platforms that feed back to enhance integrin adhesiveness
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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.