Regulation of osteoclast differentiation and function by the CaMK-CREB pathway
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Summary
The CaMKIV-CREB pathway biphasically functions to regulate the transcriptional program of osteoclastic bone resorption, by not only enhancing induction of NFATc1 but also facilitating NFAT c1-dependent gene regulation once its expression is induced.
- Type
- article
- Published
- 2006-12-01
- Cited by
- 345
- References
- 30
- OpenAlex
- https://openalex.org/W2030811514
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:28775551
Keywords
CREB, NFAT, RANKL, Cell biology, Transcription factor
References
- The newly synthesized selective Ca2+/calmodulin dependent protein kinase II inhibitor KN-93 reduces dopamine contents in PC12h cells.
- The versatility and universality of calcium signalling
- T-cell-mediated regulation of osteoclastogenesis by signalling cross-talk between RANKL and IFN-γ
- CREB regulates hepatic gluconeogenesis through the coactivator PGC-1
- Impaired Synaptic Plasticity and cAMP Response Element-Binding Protein Activation in Ca2+/Calmodulin-Dependent Protein Kinase Type IV/Gr-Deficient Mice
- NFAT and Osterix cooperatively regulate bone formation
- Nuclear Factor of Activated T Cells (NFAT)-dependent Transactivation Regulated by the Coactivators p300/CREB-binding Protein (CBP)
- STO-609, a Specific Inhibitor of the Ca2+/Calmodulin-dependent Protein Kinase Kinase*
- Calmodulin and Calmodulin-dependent Kinase IIα Regulate Osteoblast Differentiation by Controlling c-fos Expression*
- Induction and activation of the transcription factor NFATc1 (NFAT2) integrate RANKL signaling in terminal differentiation of osteoclasts.
- Calcium/calmodulin‐dependent protein kinase type IV (CaMKIV) inhibits apoptosis induced by potassium deprivation in cerebellar granule neurons
- CREB phosphorylation and dephosphorylation: a Ca(2+)- and stimulus duration-dependent switch for hippocampal gene expression.
- Deficient hippocampal long-term potentiation in alpha-calcium-calmodulin kinase II mutant mice.
- Costimulatory signals mediated by the ITAM motif cooperate with RANKL for bone homeostasis
- Calmodulin-dependent Protein Kinase IV Regulates Hematopoietic Stem Cell Maintenance*
- Structure and regulation of calcium/calmodulin-dependent protein kinases.
- Mechanism of the Generation of Autonomous Activity of Ca2+/Calmodulin-dependent Protein Kinase IV*
- A TNF receptor loop peptide mimic blocks RANK ligand-induced signaling, bone resorption, and bone loss.
- The regulation and function of c-fos and other immediate early genes in the nervous system.
- Calmodulin is a critical regulator of osteoclastic differentiation, function, and survival
Cited by
- The role of T cells in osteoporosis, an update.
- Review Article Stem Cells, Phenotypic Inversion, and Differentiation
- RANKL-induced schlafen2 is a positive regulator of osteoclastogenesis.
- Inhibition of the classical NF-κB pathway prevents osteoclast bone-resorbing activity
- Osteoclast‐targeting small molecules for the treatment of neoplastic bone metastases
- Osteocyte Control of Osteoclastogenesis
- Regulation of type 1 IP₃ receptor expression by dopamine D2-like receptors via AP-1 and NFATc4 activation.
- [Osteoclast biology and osteoimmunology].
- Xanthotoxin prevents bone loss in ovariectomized mice through the inhibition of RANKL-induced osteoclastogenesis
- Ubiquitin-dependent proteolysis of CXCL7 leads to posterior longitudinal ligament ossification
- Afamin stimulates osteoclastogenesis and bone resorption via Gi-coupled receptor and Ca2+/calmodulin-dependent protein kinase (CaMK) pathways
- Stem cells, phenotypic inversion, and differentiation.
- Calcium signaling in osteoclast differentiation and bone resorption.
- Effects of the ω-3 Polyunsaturated Fatty Acid, EPA, in Suppressing Abdominal Aortic Aneurysm Formation
- Dopamine D1 receptors regulate type 1 inositol 1,4,5‐trisphosphate receptor expression via both AP‐1‐ and NFATc4‐mediated transcriptional processes
- New immune connections in osteoclast formation
- The activation of type 1 corticotropin releasing factor receptor (CRF-R1) inhibits proliferation and promotes differentiation of neuroblastoma cells in vitro via p27(Kip1) protein up-regulation and c-Myc mRNA down-regulation.
- New regulation mechanisms of osteoclast differentiation
- Calcium citrate: a new biomaterial that can enhance bone formation in situ.
- The unexpected link between osteoclasts and the immune system.
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