ArticleThe Journal of biological chemistry2006
c-Src control of chloride channel support for osteoclast HCl transport and bone resorption.
Article in The Journal of biological chemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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
18 citing papers in PubMed, 51 citations in OpenAlex.
- Proton-activated chloride channel increases endplate porosity and pain in a mouse spine degeneration model.The Journal of clinical investigation · 2024Article
- Osteoclast Signal Transduction During Bone Metastasis Formation.Frontiers in cell and developmental biology · 2020Review
- An exploratory randomized-controlled trial of the efficacy of the Src-kinase inhibitor saracatinib as a novel analgesic for cancer-induced bone pain.Journal of bone oncology · 2019Article
- c-Src kinase is involved in the tyrosine phosphorylation and activity of SLC11A1 in differentiating macrophages.PloS one · 2018Article
- Identification of Chloride Intracellular Channel Protein 3 as a Novel Gene Affecting Human Bone Formation.JBMR plus · 2017Article
- CLIC1 null mice demonstrate a role for CLIC1 in macrophage superoxide production and tissue injury.Physiological reports · 2017Article
- Src inhibitor reduces permeability without disturbing vascularization and prevents bone destruction in steroid-associated osteonecrotic lesions in rabbits.Scientific reports · 2015Article
- Regulation of osteoclasts by membrane-derived lipid mediators.Cellular and molecular life sciences : CMLS · 2013Review
- Computational analysis of the soluble form of the intracellular chloride ion channel protein CLIC1.BioMed research international · 2013Article
- Membrane trafficking in osteoblasts and osteoclasts: new avenues for understanding and treating skeletal diseases.Traffic (Copenhagen, Denmark) · 2012Review
- Dengue-2 structural proteins associate with human proteins to produce a coagulation and innate immune response biased interactome.BMC infectious diseases · 2011Article
- Screening of protein kinase inhibitors identifies PKC inhibitors as inhibitors of osteoclastic acid secretion and bone resorption.BMC musculoskeletal disorders · 2010Article
- S-nitrosylation regulates nuclear translocation of chloride intracellular channel protein CLIC4.The Journal of biological chemistry · 2010Article
- CLIC5 mutant mice are resistant to diet-induced obesity and exhibit gastric hemorrhaging and increased susceptibility to torpor.American journal of physiology. Regulatory, integrative and comparative physiology · 2010Article
- Chloride channels of intracellular membranes.FEBS letters · 2010Review
- A novel role for Stat1 in phagosome acidification and natural host resistance to intracellular infection by Leishmania major.PLoS pathogens · 2009Article
- Calcium signalling and calcium transport in bone disease.Sub-cellular biochemistry · 2007Review
- The CLIC1 chloride channel is regulated by the cystic fibrosis transmembrane conductance regulator when expressed in Xenopus oocytes.The Journal of membrane biology · 2006Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Bone degradation by osteoclasts depends upon active transport of hydrogen ions to solubilize bone mineral. This transport is supported by the parallel actions of a proton ATPase and a chloride channel located in the osteoclast ruffled membrane. We have previously identified a novel chloride channel, p62, which appears to be the avian counterpart to CLIC-5b and is expressed coincident with the appearance of acid secretion as avian osteoclasts differentiate in culture. In this article, we show that suppression of CLIC-5b in differentiating avian osteoclasts results in decreased acidification by vesicles derived from these cells and decreased ability of the cells to resorb bone. Acidification is rescued by the presence of valinomycin, consistent with a selective loss of chloride channel but not proton pump activity. Osteoclast bone resorption is known to be dependent on the expression of the tyrosine kinase, c-Src. We show that CLIC-5b from osteoclasts has affinity for both Src SH2 and SH3 domains. We find that suppression of expression of Src in developing osteoclasts results in decreased vesicular acidification, which is rescued by valinomycin, consistent with the loss of chloride conductance in the proton pump-containing vesicles. Suppression of c-Src causes no change in the steady state level of CLIC-5b expression, but does result in failure of proton pump and CLIC-5b to colocalize in cultured osteoclast precursors. We conclude that suppression of c-Src interferes with osteoclast bone resorption by disrupting functional co-localization of proton pump and CLIC-5b.
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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.