CaMKIV negatively regulates osteoblast differentiation by modulating c-Fos and NFATc1 signaling: an in vitro and in vivo mechanistic study.

Jung Ha Kim, Kabsun Kim, Inyoung Kim, Semun Seong, Wonbong Lim, Jeong-Tae Koh, Nacksung Kim

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Article in BMB reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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7 authors.

Jung Ha KimLaboratory of Orthopaedic Research, Chosun University, Gwangju 61453; Regional Leading Research Center, Chonnam National University, Yeosu 59626, Korea.

Kabsun KimLaboratory of Orthopaedic Research, Chosun University, Gwangju 61453; Regional Leading Research Center, Chonnam National University, Yeosu 59626, Korea.

Inyoung KimDepartment of Pharmacology, Chonnam National University Medical School, Gwangju 61469; Hard-Tissue Biointerface Research Center, School of Dentistry, Chonnam National University, Gwangju 61186, Korea.

Semun SeongDepartment of Pharmacology, Chonnam National University Medical School, Gwangju 61469; Hard-Tissue Biointerface Research Center, School of Dentistry, Chonnam National University, Gwangju 61186, Korea.

Wonbong LimLaboratory of Orthopaedic Research, Chosun University, Gwangju 61453; Regional Leading Research Center, Chonnam National University, Yeosu 59626, Korea.

Jeong-Tae KohHard-Tissue Biointerface Research Center, School of Dentistry, Chonnam National University, Gwangju 61186; Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University, Gwangju 61186, Korea.

Nacksung KimDepartment of Pharmacology, Chonnam National University Medical School, Gwangju 61469; Hard-Tissue Biointerface Research Center, School of Dentistry, Chonnam National University, Gwangju 61186, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The CaMKIV-c-Fos-NFATc1 axis is established in osteoclastogenesis, but its role in osteoblasts is largely unexplored. We show that this axis suppresses osteoblast differentiation and bone formation. Silencing CaMKIV increased osteogenic gene expression and mineralization, whereas overexpressing c-Fos or NFATc1 reduced osteoblast activity. Mechanistically, CaMKIV binds c-Fos and inhibits its ubiquitination, stabilizing c-Fos and elevating NFATc1. NFATc1, in turn, impairs Runx2 acetylation by competing for PCAF, thereby attenuating osteoblast maturation. Pharmacological CaMKIV inhibition with STO-609 increased bone formation in vitro and enhanced ectopic bone formation in vivo, supporting CaMKIV as a potential anabolic target for bone regeneration. [BMB Reports 2026; 59(4): 235-241].

Indexed as

NFATC Transcription FactorsOsteoblastsProto-Oncogene Proteins c-fosAnimalsCell DifferentiationCore Binding Factor Alpha 1 SubunitHumansMiceOsteogenesisSignal TransductionCore Binding Factor Alpha 1 SubunitNFATC Transcription FactorsProto-Oncogene Proteins c-fos

Identifiers

PMID41655987

PMCPMC13126065

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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.