ArticleThe Journal of cell biology2011
Kindlin-3-mediated signaling from multiple integrin classes is required for osteoclast-mediated bone resorption.
Article in The Journal of cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 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.
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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
90 citing papers in PubMed, 164 citations in OpenAlex.
- Beyond Integrin Activation: Kindlin-3 as an Organiser of Immune Receptor Signalling.International journal of molecular sciences · 2026Review
- CFTR dictates monocyte adhesion by facilitating integrin clustering but not activation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Nanoscopy reveals integrin clustering reliant on kindlin-3 but not talin-1.Cell communication and signaling : CCS · 2025Article
- Review
- Mesenchymal stem cell-derived apoptotic bodies alleviate alveolar bone destruction by regulating osteoclast differentiation and function.International journal of oral science · 2023Article
- Clinical and Osteopetrosis-Like Radiological Findings in Patients with Leukocyte Adhesion Deficiency Type III.Journal of clinical immunology · 2023Article
- Proteomic Markers for Mechanobiological Properties of Metastatic Cancer Cells.International journal of molecular sciences · 2023Review
- Roles of focal adhesion proteins in skeleton and diseases.Acta pharmaceutica Sinica. B · 2023Review
- A novel compound heterozygous mutation of theFrontiers in pediatrics · 2023Article
- Article
- Kindlin-2 preserves integrity of the articular cartilage to protect against osteoarthritis.Nature aging · 2022Article
- The extracellular matrix of hematopoietic stem cell niches.Advanced drug delivery reviews · 2022Review
- Role of the Interaction of Tumor Necrosis Factor-α and Tumor Necrosis Factor Receptors 1 and 2 in Bone-Related Cells.International journal of molecular sciences · 2022Review
- PDGFRα reporter activity identifies periosteal progenitor cells critical for bone formation and fracture repair.Bone research · 2022Article
- Article
- Inhibition of NFAM1 suppresses phospho-SAPK/JNK signaling during osteoclast differentiation and bone resorption.Journal of cellular biochemistry · 2021Article
- L-Plastin Phosphorylation: Possible Regulation by a TNFR1 Signaling Cascade in Osteoclasts.Cells · 2021Article
- Cellular and molecular actors of myeloid cell fusion: podosomes and tunneling nanotubes call the tune.Cellular and molecular life sciences : CMLS · 2021Review
- Autosomal recessive osteopetrosis: mechanisms and treatments.Disease models & mechanisms · 2021Review
- Role of vasodilator-stimulated phosphoprotein in RANKL-differentiated murine macrophage RAW264.7 cells: Modulation of NF-κB, c-Fos and NFATc1 transcription factors.Experimental and therapeutic medicine · 2021Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The blood cell-specific kindlin-3 protein is required to activate leukocyte and platelet integrins. In line with this function, mutations in the KINDLIN-3 gene in man cause immunodeficiency and severe bleeding. Some patients also suffer from osteopetrosis, but the underlying mechanism leading to abnormal bone turnover is unknown. Here we show that kindlin-3-deficient mice develop severe osteopetrosis because of profound adhesion and spreading defects in bone-resorbing osteoclasts. Mechanistically, loss of kindlin-3 impairs the activation of β1, β2, and β3 integrin classes expressed on osteoclasts, which in turn abrogates the formation of podosomes and sealing zones required for bone resorption. In agreement with these findings, genetic ablation of all integrin classes abolishes the development of podosomes, mimicking kindlin-3 deficiency. Although loss of single integrin classes gives rise to podosomes, their resorptive activity is impaired. These findings show that osteoclasts require their entire integrin repertoire to be regulated by kindlin-3 to orchestrate bone homeostasis.
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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.