ArticleBlood2015
Interaction of kindlin-2 with integrin β3 promotes outside-in signaling responses by the αVβ3 vitronectin receptor.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 34 citations in OpenAlex.
- Multi-Omics and Experimental Validation Reveal the Protective Effect of Paeoniflorin Against Coronary Heart Disease in Mice via Inhibiting the C3-Cfd-C3aR Pathway.International journal of molecular sciences · 2026Article
- Kindlins in the cardiovascular system: from development to pathogenesis.Frontiers in cardiovascular medicine · 2026Review
- Kindlin-2 Deletion in Mural Cells Leads to Vascular Instability.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Integrins as Drug Targets in Vascular and Related Diseases.International journal of drug discovery and pharmacology · 2024Article
- Kindlin-2 controls angiogenesis through modulating Notch1 signaling.Cellular and molecular life sciences : CMLS · 2023Article
- Integrin-based mechanosensing through conformational deformation.Biophysical journal · 2021Article
- miRNA-200c-3p promotes endothelial to mesenchymal transition and neointimal hyperplasia in artery bypass grafts.The Journal of pathology · 2021Article
- Elevated kindlin-2 promotes tumour progression and angiogenesis through the mTOR/VEGFA pathway in melanoma.Aging · 2019Article
- Review
- uPAR isoform 2 forms a dimer and induces severe kidney disease in mice.The Journal of clinical investigation · 2019Article
- Site-specific phosphorylation regulates the functions of kindlin-3 in a variety of cells.Life science alliance · 2019Article
- Cellular tension encodes local Src-dependent differential βMolecular biology of the cell · 2019Article
- Knockdown of the KINDLIN-2 Gene and Reduced Expression of Kindlin-2 Affects Vascular Permeability in Angiogenesis in a Mouse Model of Wound Healing.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Peptides derived from the integrin β cytoplasmic tails inhibit angiogenesis.Cell communication and signaling : CCS · 2018Article
- Optogenetic interrogation of integrin αVβ3 function in endothelial cells.Journal of cell science · 2017Article
- Structural basis of kindlin-mediated integrin recognition and activation.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Force regulated conformational change of integrin αMatrix biology : journal of the International Society for Matrix Biology · 2017Article
- Phosphatidylinositol 3-Kinase/Akt Mediates Integrin Signaling To Control RNA Polymerase I Transcriptional Activity.Molecular and cellular biology · 2016Article
- Kindlin-3 Is Essential for the Resting α4β1 Integrin-mediated Firm Cell Adhesion under Shear Flow Conditions.The Journal of biological chemistry · 2016Article
- Kindlin-2 directly binds actin and regulates integrin outside-in signaling.The Journal of cell biology · 2016Article
Corrections and comments
- Commented on by
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The bidirectional signaling and hemostatic functions of platelet αIIbβ3 are regulated by kindlin-3 through interactions with the β3 cytoplasmic tail. Little is known about kindlin regulation of the related "vitronectin receptor," αVβ3. These relationships were investigated in endothelial cells, which express αVβ3 and kindlin-2 endogenously. "β3ΔRGT" knock-in mice lack the 3 C-terminal β3 tail residues, whereas in "β3/β1(EGK)" mice, RGT is replaced by the corresponding residues of β1. The wild-type β3 tail pulled down kindlin-2 and c-Src in vitro, whereas β3ΔRGT bound neither protein and β3/β1(EGK) bound kindlin-2, but not c-Src. β3ΔRGT endothelial cells, but not β3/β1(EGK) endothelial cells, exhibited migration and spreading defects on vitronectin and reduced sprouting in 3-dimensional fibrin. Short hairpin RNA silencing of kindlin-2, but not c-Src, blocked sprouting by β3 wild-type endothelial cells. Moreover, defective sprouting by β3ΔRGT endothelial cells could be rescued by conditional, forced interaction of αVβ3ΔRGT with kindlin-2. Stimulation of β3ΔRGT endothelial cells led to normal extracellular ligand binding to αVβ3, pin-pointing their defect to one of outside-in αVβ3 signaling. β3ΔRGT mice, but not β3/β1(EGK) mice, exhibited defects in both developmental and tumor angiogenesis, responses that require endothelial cell function. Thus, the β3/kindlin-2 interaction promotes outside-in αVβ3 signaling selectively, with biological consequences in vivo.
Indexed as
Identifiers
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.