ArticleJournal of leukocyte biology2012
Regulation of osteoclast structure and function by FAK family kinases.
Article in Journal of leukocyte biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- CXCL5 suppresses osteoclastogenesis and protects against lipoteichoic acid-induced bone loss by modulating PLCγ2 and c-Fos signalling in gram-positive periprosthetic joint infection.Bone & joint research · 2026Article
- The potential key genes within focal adhesion that regulate mesenchymal stem cells osteogenesis or adipogenesis in microgravity related disuse osteoporosis: an integrated analysis.Frontiers in endocrinology · 2025Article
- Integrating network pharmacology, IPA, and molecular docking to reveal the anti-osteoporosis effects of EA and EB via the FAK pathway.Frontiers in pharmacology · 2025Article
- Pharmacoproteogenomic approach identifies on-target kinase inhibitors for cancer drug repositioning.In vitro cellular & developmental biology. Animal · 2024Article
- Cooperative interactions between neurotrophin receptors and CXCR4 regulate macrophage phenotype and susceptibility to activation by HIV.Journal of neurovirology · 2024Article
- Identification of ceRNA networks in type H and L vascular endothelial cells through integrated bioinformatics methods.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Roles of focal adhesion proteins in skeleton and diseases.Acta pharmaceutica Sinica. B · 2023Review
- Serglycin induces osteoclastogenesis and promotes tumor growth in giant cell tumor of bone.Cell death & disease · 2021Article
- Novel Majeed Syndrome-Causing LPIN2 Mutations Link Bone Inflammation to Inflammatory M2 Macrophages and Accelerated Osteoclastogenesis.Arthritis & rheumatology (Hoboken, N.J.) · 2021Article
- Targeting Intercellular Communication in the Bone Microenvironment to Prevent Disseminated Tumor Cell Escape from Dormancy and Bone Metastatic Tumor Growth.International journal of molecular sciences · 2021Review
- Involvement of the FAK Network in Pathologies Related to Altered Mechanotransduction.International journal of molecular sciences · 2020Review
- Gingipains promote RANKL-induced osteoclastogenesis through the enhancement of integrin β3 in RAW264.7 cells.Journal of molecular histology · 2020Article
- Article
- Insulin/IGF-1R, SIRT1, and FOXOs Pathways-An Intriguing Interaction Platform for Bone and Osteosarcoma.Frontiers in endocrinology · 2019Article
- A 15-amino acid C-terminal peptide of beta-defensin-3 inhibits bone resorption by inhibiting the osteoclast differentiation and disrupting podosome belt formation.Journal of molecular medicine (Berlin, Germany) · 2017Article
- The nonreceptor protein tyrosine kinase Pyk2 promotes the turnover of monocytes at steady state.Journal of leukocyte biology · 2017Article
- Sperm-oocyte contact induces outside-in signaling via PYK2 activation.Developmental biology · 2017Article
- An in silico high-throughput screen identifies potential selective inhibitors for the non-receptor tyrosine kinase Pyk2.Drug design, development and therapy · 2017Article
- Article
- DC-STAMP: A Key Regulator in Osteoclast Differentiation.Journal of cellular physiology · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Osteoclasts are highly specialized cells that resorb bone and contribute to bone remodeling. Diseases such as osteoporosis and osteolytic bone metastasis occur when osteoclast-mediated bone resorption takes place in the absence of concurrent bone synthesis. Considerable effort has been placed on identifying molecules that regulate the bone resorption activity of osteoclasts. To this end, we investigated unique and overlapping functions of members of the FAK family (FAK and Pyk2) in osteoclast functions. With the use of a conditional knockout mouse model, in which FAK is selectively targeted for deletion in osteoclast precursors (FAK(Δmyeloid)), we found that loss of FAK resulted in reduced bone resorption by osteoclasts in vitro, coincident with impaired signaling through the CSF-1R. However, bone architecture appeared normal in FAK(Δmyeloid) mice, suggesting that Pyk2 might functionally compensate for reduced FAK levels in vivo. This was supported by data showing that podosome adhesion structures, which are essential for bone degradation, were significantly more impaired in osteoclasts when FAK and Pyk2 were reduced than when either molecule was depleted individually. We conclude that FAK contributes to cytokine signaling and bone resorption in osteoclasts and partially compensates for the absence of Pyk2 to maintain proper adhesion structures in these cells.
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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.