ArticleThe Journal of biological chemistry2013
A TRPC1 protein-dependent pathway regulates osteoclast formation and function.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 68 citations in OpenAlex.
- Spectrum and functions of ion channels and transporters in osteoclasts.Bone research · 2026Review
- Physiological functions and pharmacological targeting of transient receptor potential channels.Pharmacological reviews · 2025Review
- I-mfa, Mesangial Cell TRPC1 Channel, and Regulation of GFR.Journal of the American Society of Nephrology : JASN · 2025Article
- Targeting TRPC channels for control of arthritis-induced bone erosion.Science advances · 2025Article
- Non-voltage-gated CaAmerican journal of physiology. Renal physiology · 2024Review
- Engineering approaches to manipulate osteoclast behavior for bone regeneration.Materials today. Bio · 2024Review
- The role of calcium channels in osteoporosis and their therapeutic potential.Frontiers in endocrinology · 2024Review
- Store-operated CaExperimental biology and medicine (Maywood, N.J.) · 2023Review
- TRPC channels blockade abolishes endotoxemic cardiac dysfunction by hampering intracellular inflammation and CaNature communications · 2022Article
- Calcium-Permeable Channels Cooperation for Rheumatoid Arthritis: Therapeutic Opportunities.Biomolecules · 2022Review
- New Insights into TRP Ion Channels in Stem Cells.International journal of molecular sciences · 2022Review
- Roles of calcium signaling in cancer metastasis to bone.Exploration of targeted anti-tumor therapy · 2022Review
- Distribution and Assembly of TRP Ion Channels.Advances in experimental medicine and biology · 2021Article
- Store-Operated Calcium Entry in the Cardiovascular System.Advances in experimental medicine and biology · 2021Review
- Finely-Tuned Calcium Oscillations in Osteoclast Differentiation and Bone Resorption.International journal of molecular sciences · 2020Review
- Opposite Roles of the JMJD1A Interaction Partners MDFI and MDFIC in Colorectal Cancer.Scientific reports · 2020Article
- The Role of CaInternational journal of molecular sciences · 2020Review
- RNA-seq analysis reveals TRPC genes to impact an unexpected number of metabolic and regulatory pathways.Scientific reports · 2020Article
- Control of PTH secretion by the TRPC1 ion channel.JCI insight · 2020Article
- Inhibitor of myogenic differentiation family isoform a, a new positive regulator of fibronectin production by glomerular mesangial cells.American journal of physiology. Renal physiology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Ca(2+) signaling is essential for bone homeostasis and skeletal development. Here, we show that the transient receptor potential canonical 1 (TRPC1) channel and the inhibitor of MyoD family, I-mfa, function antagonistically in the regulation of osteoclastogenesis. I-mfa null mice have an osteopenic phenotype characterized by increased osteoclast numbers and surface, which are normalized in mice lacking both Trpc1 and I-mfa. In vitro differentiation of pre-osteoclasts derived from I-mfa-deficient mice leads to an increased number of mature osteoclasts and higher bone resorption per osteoclast. These parameters return to normal levels in osteoclasts derived from double mutant mice. Consistently, whole cell currents activated in response to the depletion of intracellular Ca(2+) stores are larger in pre-osteoclasts derived from I-mfa knock-out mice compared with currents in wild type mice and normalized in cells derived from double mutant mice, suggesting a cell-autonomous effect of I-mfa on TRPC1 in these cells. A new splice variant of TRPC1 (TRPC1ε) was identified in early pre-osteoclasts. Heterologous expression of TRPC1ε in HEK293 cells revealed that it is unique among all known TRPC1 isoforms in its ability to amplify the activity of the Ca(2+) release-activated Ca(2+) (CRAC) channel, mediating store-operated currents. TRPC1ε physically interacts with Orai1, the pore-forming subunit of the CRAC channel, and I-mfa is recruited to the TRPC1ε-Orai1 complex through TRPC1ε suppressing CRAC channel activity. We propose that the positive and negative modulation of the CRAC channel by TRPC1ε and I-mfa, respectively, fine-tunes the dynamic range of the CRAC channel regulating osteoclastogenesis.
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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.