ArticleThe Journal of cell biology2019
Rap1 binding and a lipid-dependent helix in talin F1 domain promote integrin activation in tandem.
Article in The Journal of cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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Who cites it
43 citing papers in PubMed, 51 citations in OpenAlex.
- Optimization of stapled peptide inhibitors reveals design principles for targeting talin-induced integrin activation.bioRxiv : the preprint server for biology · 2026Article
- TLN1 interacts with NGFR and suppresses the development of castration-resistant prostate cancer by upregulating NGFR.Frontiers in immunology · 2026Article
- From inflammatory effectors to tissue sculptors: non-canonical functions of neutrophils in repair, barrier remodelling and fibrosis.Frontiers in immunology · 2026Review
- Inside-out integrin activation is essential for early mammalian development.Molecular biology of the cell · 2025Article
- Divergent Functions of Rap1A and Rap1B in Endothelial Biology and Disease.International journal of molecular sciences · 2025Review
- Deletion of the plexin-D1 ectodomain leads to anoikis by suppressing integrin inside-out signaling.Molecular biology of the cell · 2025Article
- Molecular basis of β2 integrin activation by talin unveils subunit-specific mechanisms of integrin signaling.Cell reports · 2025Article
- Talin, a Rap1 effector for integrin activation at the plasma membrane, also promotes Rap1 activity by disrupting sequestration of Rap1 by SHANK3.Journal of cell science · 2025Article
- TLN1: an oncogene associated with tumorigenesis and progression.Discover oncology · 2024Review
- Evidence that inositol 1,4,5-trisphosphate 3-kinase and inositol 1,3,4,5-tetrakisphosphate are negative regulators of platelet function.Research and practice in thrombosis and haemostasis · 2024Article
- Spatial Mechano-Signaling Regulation of GTPases through Non-Degradative Ubiquitination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- [Molecular dynamics simulation of force-regulated interaction between talin and Rap1b].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2023Article
- Article
- ConFERMing the role of talin in integrin activation and mechanosignaling.Journal of cell science · 2023Article
- CAP1 (cyclase-associated protein 1) mediates the cyclic AMP signals that activate Rap1 in stimulating matrix adhesion of colon cancer cells.Cellular signalling · 2023Article
- Talin variant P229S compromises integrin activation and associates with multifaceted clinical symptoms.Human molecular genetics · 2022Article
- Review
- Epithelial JAM-A is fundamental for intestinal wound repair in vivo.JCI insight · 2022Article
- Integrin Regulators in Neutrophils.Cells · 2022Review
- Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Rap1 GTPases bind effectors, such as RIAM, to enable talin1 to induce integrin activation. In addition, Rap1 binds directly to the talin1 F0 domain (F0); however, this interaction makes a limited contribution to integrin activation in CHO cells or platelets. Here, we show that talin1 F1 domain (F1) contains a previously undetected Rap1-binding site of similar affinity to that in F0. A structure-guided point mutant (R118E) in F1, which blocks Rap1 binding, abolishes the capacity of Rap1 to potentiate talin1-induced integrin activation. The capacity of F1 to mediate Rap1-dependent integrin activation depends on a unique loop in F1 that has a propensity to form a helix upon binding to membrane lipids. Basic membrane-facing residues of this helix are critical, as charge-reversal mutations led to dramatic suppression of talin1-dependent activation. Thus, a novel Rap1-binding site and a transient lipid-dependent helix in F1 work in tandem to enable a direct Rap1-talin1 interaction to cause integrin activation.
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What OpenQuestion holds
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.