ArticleMolecules and cells2014
Carboxypeptidase E is a novel modulator of RANKL-induced osteoclast differentiation.
Article in Molecules and cells, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Sex differences in the genetic regulation of the human plasma proteome.Nature communications · 2025Article
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- Carboxypeptidase E is a prognostic biomarker co-expressed with osteoblastic genes in osteosarcoma.PeerJ · 2023Article
- CYT387, a JAK-Specific Inhibitor Impedes Osteoclast Activity and Oophorectomy-Induced OsteoporosisFrontiers in pharmacology · 2022Article
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- Nonenzymatic and Trophic Activities of Carboxypeptidase E Regulate Bone Mass and Bioenergetics of Skeletal Stem Cells in Mice.JBMR plus · 2020Article
- Characterisation of genetic regulatory effects for osteoporosis risk variants in human osteoclasts.Genome biology · 2020Article
- Dissecting carboxypeptidase E: properties, functions and pathophysiological roles in disease.Endocrine connections · 2017Review
- Article
- [Screening of Highly Expressed CPEΔN Lung Cancer H1299 Cells].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoclasts are large polykaryons that have the unique capacity to degrade bone and are generated by the differentiation of myeloid lineage progenitors. To identify the genes involved in osteoclast development, we performed microarray analysis, and we found that carboxypeptidase E (CPE), a prohormone processing enzyme, was highly upregulated in osteoclasts compared with their precursors, bone marrow-derived macrophages (BMMs). Here, we demonstrate a novel role for CPE in receptor activator of NF-κB ligand (RANKL)-induced osteoclast differentiation. The overexpression of CPE in BMMs increases the formation of tartrate-resistant acid phosphatase (TRAP)-positive multinuclear osteoclasts and the expression of c-Fos and nuclear factor of activated T cells c1 (NFATc1), which are key regulators in osteoclastogenesis. Furthermore, employing CPE knockout mice, we show that CPE deficiency attenuates osteoclast formation. Together, our data suggest that CPE might be an important modulator of RANKL-induced osteoclast differentiation.
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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.